Archive for the ‘Regulated Clinical Trials: Design, Methods, Components and IRB related issues’ Category

EmergingMed has guided more than 170,000 patients through a search for Cancer Clinical Trials

Posted in CANCER BIOLOGY & Innovations in Cancer Therapy, Population Health Management, Genetics & Pharmaceutical, Regulated Clinical Trials: Design, Methods, Components and IRB related issues on May 28, 2014| Leave a Comment »

EmergingMed has guided more than 170,000 patients through a search for Cancer Clinical Trials

Reporter: Aviva Lev-Ari, PhD, RN

 

“We need to explain to the American public that the drugs we are benefiting from today did not come out of thin air,” says Armin Weinberg, director of Baylor College of Medicine’s Chronic Disease Prevention and Control Research Center in Houston. “Their participation in trials is the thing that is going to help us advance in all these battles against cancer, asthma, diabetes and hypertension.”

SOURCE

Matchmakers: Patients Meet Clinical Trials

http://online.wsj.com/news/articles/SB121071901838189901

Since December 2000, EmergingMed has guided more than 170,000 patients through a search for cancer clinical trials. (see WSJ coverage, press release)

EmergingMed’s Navigator service enables you to create a detailed profile to see if you match the eligibility requirements of more than 10,000 trials in the United States and Canada.

Our Clinical Trial Specialists will work with you by telephone to make sure you get the information you need to make important decisions about clinical trial options.

Cancer clinical trials are research studies that test how well new medical approaches work in people with early stage or advanced cancers. Each study answers scientific questions and tries to find better ways to prevent, screen for, diagnose, or treat a disease.

There are more than 250 types of cancer. Every cancer treatment—and every clinical trial—is designed for a very specific type and stage of cancer.

Video: The Cure for Cancer: Why Clinical Trials are Imperative

We suggest that you search for cancer clinical trials every time you review your treatment options. Why? Because studies only enroll patients at very specific times:

• Just before a biopsy (to study tissue from a tumor)
• Just before the first surgery or radiation treatment (neo-adjuvant studies)
• Just after surgery or radiation treatment (adjuvant studies)
• Soon after a cancer has recurred or spread (metastasized)
• Soon after you learn that your cancer is spreading despite current treatment

Step 1: Create a profile online or by phone to find clinical trials that match your specific cancer diagnosis, stage and treatment history.

Step 2: Match your profile to the eligibility criteria of all the cancer clinical trials in our database.

Step 3: Navigation support from our Clinical Trial Specialists will help you connect with the doctors and nurses conducting the trials you match, answer questions during your search, and help you quickly gather information to share with your doctor.

Search Online

Cancer Prevention and Early Detection

• Cancer Treatment – Adults
• Cancer Treatment  – Children and Patients under 18

 Select a Diagnosis

• Cancer Prevention and Early Detection Trials for Men
• Cancer Prevention and Early Detection Trials for Women

 SOURCE

http://www.emergingmed.com/

We’ve all heard of them, but what exactly are clinical trials? Put simply, a clinical trial is a scientific study of how a new medicine or treatment works in people. Through clinical studies, doctors find new and better ways to prevent, detect, diagnose, control, and treat illnesses. People who participate in clinical trials are not guinea pigs. A therapy reaches the point where it can be evaluated in a clinical trial only after it proves successful in animals and the laboratory. The researchers who run the trials are actively trying to offer the participants the best available treatment that will be successful against their disease. New medicines and treatments that are helpful and safe in test tubes and in animals must also prove safe and effective in humans before doctors can prescribe them. This testing in humans is permitted only if a person volunteers to participate and understands the risks and benefits of taking part in a study. This informed consent to participate must be based on a patient volunteer’s understanding of what is involved in the study, including potential risks and benefits. Volunteers may leave a study at any time.
	Types of clinical trials Clinical trial phases Inclusion/exclusion criteria The initial screening visit Informed consent Getting paid to participate in clinical trials Where to go for more information
	Types of clinical trials   Top There are several types of trials, according to the National Institutes of Health: Treatment trials test new therapies that may increase the life expectancy or reduce suffering in people who have a serious illness. Prevention trials test new approaches, such as medicines, vaccines, vitamins, minerals, or other supplements that doctors believe may lower the risk of a certain disease. Screening/early detection trials test the best way to find a disease, especially in its early stages. Quality of Life trials (also called Supportive Care trials) explore ways to improve comfort and quality of life for patients with a disease. Genetics trials are meant to improve the ability to look for an inherited risk of illness.
	Clinical Trial Phases    Top Testing of a new therapy (i.e., treatment trials) progresses in an orderly series of steps, called phases. This allows researchers to ask and answer questions in a way that results in reliable information about the drug and protects the patients. Clinical trials are usually classified into one of four phases by the U.S. Food and Drug Administration, which oversees the approval process: Phase I trials: These first studies in people evaluate how a new drug should be given (by mouth, injected into the blood, or injected into the muscle,) how often, and what dose is safe. In particular, these studies are also looking for the highest dose that can safely be given with the fewest serious side effects (maximum tolerated dose). In addition, a Phase I trial might evaluate a new combination of 2 drugs where one or both of the drugs, alone, might be well known but doctors have never before studied the two together. In these combination studies, doctors are watching closely for potential interactions and new side effects when the two drugs are given together. By the time a new treatment reaches the phase I level, it has proved beneficial in several animal models and in the laboratory. A Phase I trial usually enrolls only a small number of patients, sometimes as few as a dozen, and is offered only at major cancer centers. It is important to realize that there is no chance that a patient will receive a placebo in a Phase I clinical trial. Patients enrolling in Phase I trials are the first to help doctors identify promising new drugs and the scientific knowledge that will ultimately help future patients. Phase I trials usually enroll patients with advanced disease for whom no standard therapies are available. Patients considering Phase I trials should have a reasonable expectation that the new drugs (or drug combinations) might shrink their tumors or reduce their tumor burden. However the risks associated with being one of the first people to try a new drug-or a new drug combination-should be weighed very carefully since the side effects of the new drug/combination will not be well understood at the beginning of a Phase I study. Phase II trials: A phase II trial continues to test the safety of the drug, and begins to evaluate how well the new drug works. Phase II studies usually focus on a particular aspect of a disease. Like phase I trials, these trials do not test the difference between two therapies, so the participants will almost always get the experimental treatment. There is still no chance that a participant in the trial will receive a placebo. Phase III trials: These studies test a new drug, a new combination of drugs, or a new surgical procedure in comparison to the current standard for treatment. A participant will usually be assigned to the standard treatment group or the new treatment group at random (called randomization). Phase III trials often enroll large numbers of people and may be conducted at many doctors’ offices, clinics, and disease centers nationwide. In phase III trials, patients rarely receive a placebo – in fact, only when there is no standard therapy for the disease. Otherwise, people who participate in phase III clinical trials will either receive the best available standard therapy or the experimental therapy, with an equal chance of receiving either treatment. Phase IV trials: These are often required when a drug manufacturer wishes to test an already approved therapy for a different medical condition or in a different formulation than it was originally approved for. The manufacturer is not allowed to make new claims about their product until it is properly tested. It is possible (though unlikely) that a placebo may be used in the control group in a phase IV trial.
	Inclusion/exclusion criteria    Top When designing a clinical research study, an investigator must first decide who should be in the study and who should be excluded. Unless the researchers are very firm and diligent about sticking to those inclusion/exclusion criteria, the entire study can be weakened. The researchers must therefore try and find a balance between identifying those people who are most appropriate to test a new therapy and casting a wide enough net to ensure that they will have enough participants to make the results statistically significant. Inclusion/exclusion criteria might be such factors as the age of the participants – many studies will only include people over 18 years old, for example – the date of diagnosis of the illness, other therapies, and other illnesses that the participant might have. Other inclusion/exclusion criteria might be the stage of the illness – many studies try and exclude patients who have very advanced illnesses – how active the participants are in their day-to-day routines, and the ability to take oral medications. Inclusion/exclusion criteria should be explained to each potential participant in a clinical research trial before they are enrolled in the study.
	The initial screening visit    Top After a person has decided to participate in a clinical study, they will be scheduled by the study coordinator for a preliminary screening visit. During that visit, the inclusion/exclusion criteria will be detailed for the participant. The study coordinator will also explain the study, the procedures that need to be followed and answer any questions that may arise. This process is called informed consent and is essential before any volunteer is enrolled in any clinical trial. More on the concept of informed consent can be found below The initial screening visit is also an opportunity for the study coordinator to obtain a full medical history from the participant. He or she will also usually perform a physical exam and schedule any laboratory tests that may be necessary before participation in the study can begin.
	Informed consent    Top The United States government is very strict about the guidelines of medical research performed on people. An Institutional Review Board (IRB) approves and monitors every clinical trial performed in the US to minimize the risks to the study participants and to make sure that the potential benefits of the new therapy outweigh those risks. An IRB is usually made up of physicians, experts in biomedical ethics, statisticians, and members of the community and its sole charge is to make certain that clinical research adheres to the strictest ethical guidelines. Every participant in a clinical trial in the United States has the right to informed consent. In fact, nobody should even consider joining a trial without access to key information that must be provided by the investigators in easy-to-understand language. This information (adapted from the NIH) includes: why the research is being done what the researchers are hoping to accomplish what the different therapies being tested are and how they are thought to work any risks associated with the therapies the potential benefits for the participant other available treatments (with a discussion of their efficacy and side effects) the fact that participants may leave the study at any time
	Getting paid to participate in clinical trials    Top Some clinical trials will pay people for participating in the research but they are rare, primarily because the National Institutes of Health wish to discourage patients from participating in clinical trials solely for financial purposes. Most clinical trial sponsors, however, will reimburse participants for reasonable travel and food expenses accumulated while they are in the trial. The article below describes specific legislation meant to ensure that people who participate in clinical research are not harmed financially by their involvement.
	Where to go for more information    Top The National Institutes of Health have a very comprehensive website that deals exclusively with clinical trials and the issues described above. It can be found at www.clinicaltrials.gov.

Modified: May 2014

SOURCE

http://www.emergingmed.com/pub_AboutClinicalTrials.asp

 

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Cancer Labs at School of Medicine @ Technion: Janet and David Polak Cancer and Vascular Biology Research Center

Posted in Academic Publishing, Autologous Cell Therapy, Bio Instrumentation in Experimental Life Sciences Research, BioBanking, Biological Networks, Gene Regulation and Evolution, Biomarkers & Medical Diagnostics, Biomedical Measurement Science, BioSimilars, CANCER BIOLOGY & Innovations in Cancer Therapy, Cardiac muscle regeneration, Cardiovascular Pharmacogenomics, Cell Biology, Signaling & Cell Circuits, Chemical Biology and its relations to Metabolic Disease, Chemical Genetics, Circulating Progenitor Cells, Computational Biology/Systems and Bioinformatics, Cytoskeleton, Diagnostic Immunology, Drug Delivery Platform Technology, Drug Toxicity, Frontiers in Cardiology and Cardiovascular Disorders, Genome Biology, Genomic Testing: Methodology for Diagnosis, Human Immune System in Health and in Disease, Immunodiagnostics, Innovation in Immunology Diagnostics, Intellectual Property, Innovations, Commercialization, Investment in technological breakthrough, Interviews with Scientific Leaders, Personalized and Precision Medicine & Genomic Research, Pharmaceutical Analytics, Pharmaceutical R&D Investment, Pharmacogenomics, Pharmacologic toxicities, Population Health Management, Genetics & Pharmaceutical, Proteomics, Regenerative Biology and Medicine, Regulated Clinical Trials: Design, Methods, Components and IRB related issues, Scientist: Career considerations, Signaling, Stem Cells for Regenerative Medicine, Technology Transfer: Biotech and Pharmaceutical, Translational Science, Ubiquitinylation on May 28, 2014| Leave a Comment »

Cancer Labs at School of Medicine @ Technion

Reporter: Aviva Lev-Ari, PhD, RN

Article ID #139: Cancer Labs at School of Medicine @ Technion: Janet and David Polak Cancer and Vascular Biology Research Center. Published on 5/28/2014

WordCloud Image Produced by Adam Tubman

Janet and David Polak Cancer and Vascular Biology Research Center. The Rappaport Faculty of Medicine Research Institute and Faculty of Medicine, Technion – Israel Institute of Technology, Haifa, Israel

The center was established in 2003 to promote an in-depth interdisciplinary basic and clinical research on the control of cellular and molecular processes that are involved in cancer initiation and progression. We strongly believe that the understanding of basic biological processes that underlie normal development and their deregulation in cancer, is crucial for our ability to identify molecular targets for early detection, intervention, and cure of the disease. We are interested in a broad view of cancer – from the single malignantly transformed cell and its microenvironment, through the entire tumor in the animal. We focus on targeted ubiquitin-mediated degradation of key regulatory proteins that are involved in malignant transformation [Prof. Aaron Ciechanover (Nobel Prize in Chemistry 2004)], angiogenesis and cancer progression (Prof. Gera Neufeld), metastasis and tumor microenvironment (Prof. Israel Vlodavsky), as well as genetic and genomic dissection of embryonic and cancer transcriptional networks (Dr. Amir Orian). Towards these objectives, we combine molecular, biochemical, cell biological with Drosophila genetic and genomics experimental approaches, as well as employing advanced models of angiogenesis and metastasis.

We believe that scientific excellence and collegiality go together. Therefore, the center has an open and friendly atmosphere, creating a highly stimulating environment. The center is located in the 11th Floor of the Rappaport Faculty of Medicine building. It currently trains 45 graduate students, post-doctoral fellows, clinicians and researchers that are at the heart of our research. Formal and informal collaborations between individuals and laboratories are on-going and encouraged. We are running a series of joint seminars to which we invite researchers from Israel and abroad. The Center has advanced state-of-the-art microscopic and image analysis equipment, as well as other shared pieces of infrastructural equipment . The center is an integral part of the Faculty of Medicine and the Rappaport Research Institute which are home for excellent research groups, and enjoys their advanced Interdepartmental Equipment Unit. It is also adjacent to the Rambam Medical Center – the major hospital in the north of Israel – which provides us with access to rich clinical material and collaboration with clinicians. Many of them spend active research periods in our laboratories and bring the bench closer to the patient bed and vice versa. The Center is in an active phase of growth, and offers excellent research opportunities, space and facilities for students, post-doctoral fellows, and physicians.

Research Groups The Ubiquitin System and Cellular Protein Turnover and Interactions Immunity and Host Defense Cardiovascular Biology The Central Nervous System in Health and Disease Developmental Biology and Cancer Research Genetics

SOURCE 

http://www.rappaport.org.il/Rappaport/Templates/ShowPage.asp?DBID=1&TMID=842&FID=76

The cancer and vascular biology research center was established in 2003 to promote an in-depth interdisciplinary basic and clinical research on the control of cellular and molecular processes that are involved in cancer development and progression. Our goal is to advance knowledge in fundamental biological questions that are highly relevant for cancer.

	The cancer and vascular biology research center was established in 2003 to promote an in-depth interdisciplinary basic and clinical research on the control of cellular and molecular processes that are involved in cancer development and progression. Our goal is to advance knowledge in fundamental biological questions that are highly relevant for cancer.

SOURCE

http://www.technioncancer.co.il/index.php

Home  >>  Research Groups

Aaron Ciechanover Protein Turnover Intracellular protein degradation and mechanisms of cancer Israel Vlodavsky Cancer Biology Impact of heparanase and the tumor microenvironment on cancer progression: Basic aspects and clinical implications Gera Neufeld Tumor Progression & Angiogenesis Blood vessels and tumor progression: The neuropilin connection Amir Orian Genetic Networks Genetic networks in development and cancer

Home About the Cancer Centers Research Groups Administration / Contact Join – Us Seminars and Events Links Beyond Science Friends and supporters Ms. Sigal Alfasi – Izrael, Center’s coordinator e-mail: gsigal@tx.technion.ac.il Tel: +972-4-829-5424 Fax: +972-4-852-3947

SOURCE

http://www.technioncancer.co.il/ResearchGroups.php

Yuval Shaked, PhD

Publications by Yuval Shaked, PhD

Assistant Professor of Molecular Pharmacology

PhD, 2004 – Hebrew University, Israel

Understanding host – tumor interactions during cancer therapy

Personalized medicine holds promise of better cures with fewer side effects for many diseases. Individualized cancer therapy is sometimes utilized after multiple attempts of standard therapies and is based on several considerations, such as tumor type, acquired resistance to a specific therapy, previous treatment protocols, and other tumor-related factors. We have recently demonstrated that many cancer therapies can induce pro-tumorigenic or metastatic effects that derive not only from the tumor cells themselves, but also from host cells within the tumor microenvironment. The focus of research in my laboratory is to identify, characterize, and seek ways to block such pro-tumorigenic host effects observed after anti-cancer therapy, and thus potentially improve the outcome of current cancer therapies. Our findings may foster a paradigm shift in cancer therapy by minimizing the gap between preclinical findings and the clinical setting, laying the foundation for development of entirely new strategies for improving cancer therapy.

SOURCE

http://www.rappaport.org.il/Rappaport/Templates/ShowPage.asp?DBID=1&TMID=610&FID=77&PID=0&IID=1268

 

Other Related articled published on this Open Access Online Scientific Journal included the following:

D&D NT’s Solution: Galectin Proteins for Therapy and Diagnosis of Autoimmune Inflammatory and Cancer Diseases, Dr. Itshak Golan, CEO

http://pharmaceuticalintelligence.com/2014/05/28/dd-nts-solution-galectin-proteins-for-therapy-and-diagnosis-of-autoimmune-inflammatory-and-cancer-diseases-dr-itshak-golan-ceo/

MaimoniDex RA:  Monoclonal Antibodies for Therapy and Diagnosis of Cancer and Autoimmune Inflammatory Diseases – Dr. Itshak Golan, CEO

http://pharmaceuticalintelligence.com/2014/05/28/maimonidex-ra-monoclonal-antibodies-for-therapy-and-diagnosis-of-cancer-and-autoimmune-inflammatory-diseases-dr-itshak-golan-ceo/

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Immunity and Host Defense – A Bibliography of Research @Technion

Posted in Biological Networks, Gene Regulation and Evolution, Biomarkers & Medical Diagnostics, Biomedical Measurement Science, CANCER BIOLOGY & Innovations in Cancer Therapy, Cancer Prevention: Research & Programs, Cell Biology, Signaling & Cell Circuits, Chemical Biology and its relations to Metabolic Disease, Chemical Genetics, Diagnostic Immunology, Drug Delivery Platform Technology, Drug Toxicity, FDA Regulatory Affairs, Genome Biology, Genomic Testing: Methodology for Diagnosis, Human Immune System in Health and in Disease, Immunodiagnostics, Innovation in Immunology Diagnostics, Intellectual Property, Innovations, Commercialization, Investment in technological breakthrough, Interviews with Scientific Leaders, Medical and Population Genetics, Molecular Genetics & Pharmaceutical, Personalized and Precision Medicine & Genomic Research, Pharmaceutical Analytics, Pharmaceutical R&D Investment, Pharmacogenomics, Pharmacologic toxicities, Population Health Management, Genetics & Pharmaceutical, Proteomics, Regulated Clinical Trials: Design, Methods, Components and IRB related issues, Scientist: Career considerations, Signaling, Technology Transfer: Biotech and Pharmaceutical, Translational Science on May 27, 2014| Leave a Comment »

Immunity and Host Defense – A Bibliography of Research @Technion

Reporter: Aviva Lev-Ari, PhD, RN

Article ID #138: Immunity and Host Defense – A Bibliography of Research @Technion. Published on 5/27/2014

WordCloud Image Produced by Adam Tubman

 

 

 

Antigen-Dependent Integration of Opposing Proximal TCR-Signaling Cascades Determines the Functional Fate of T Lymphocytes 2014 Shai Shen-Orr, PhD Authors : Wolchinsky R, Hod-Marco M, Oved K, Shen-Orr SS, Bendall SC, Nolan GP, Reiter Y. J Immunol. 2014 Mar 1;192(5):2109-19.

Identification of functionally important conserved trans-membrane residues of bacterial P(IB) -type ATPases 2013 Oded Lewinson, PhD Authors : Zhitnitsky D, Lewinson O. Mol Microbiol. 2013 Dec 19. doi: 10.1111/mmi.12495. [Epub ahead of print] PubMed PMID: 24350798.

Variability in the immune system: of vaccine responses and immune states 2013 Shai Shen-Orr, PhD Authors : Shen-Orr SS, Furman D. Curr Opin Immunol. 2013 Aug;25(4):542-7.

Computational deconvolution: extracting cell type-specific information from heterogeneous samples. 2013 Shai Shen-Orr, PhD Authors : Shen-Orr SS, Gaujoux R. Curr Opin Immunol. 2013 Oct 19. [Epub ahead of print] PubMed PMID: 24148234.

Challenges and promise for the development of human immune monitoring. 2013 Shai Shen-Orr, PhD Authors : Shen-Orr S. Rambam Maimonides Med J. 2012 Oct 31;3(4):e0023.

Homeostatic regulation of aging and rejuvenation in the B lineage cells 2013 Doron Melamed, PhD Authors : Melamed D. Crit Rev Immunol. 2013;33(1):41-56.

Variability in the immune system: of vaccine responses and immune states 2013 Shai Shen-Orr, PhD Authors : Shen-Orr S, Furman D. Curr Opin Immunol. 2013 Aug 13. doi:pii: S0952-7915(13)00113-1.

A single intact ATPase site of the ABC transporter BtuCD drives 5% transport activity yet supports full in-vivo vitamin B12 utilization. 2013 Oded Lewinson, PhD Authors : Tal N, Ovcharenko E, Lewinson O. Proc Natl Acad Sci U S A. (March 19 Epub ahead of print)

Apoptosis and other immune biomarkers predict influenza vaccine responsiveness. 2013 Shai Shen-Orr, PhD Authors : Furman D, Jojic V, Kidd B, Shen-Orr S, Price J, Jarrell J, Tse T, Huang H, Lund P, Maecker HT, Utz PJ, Dekker CL, Koller D, Davis MM. Molecular Systems Biology. 9, 659

The dual roles of inflammatory cytokines and chemokines in the regulation of autoimmune diseases and their clinical implications. 2013 Nathan Karin, PhD Authors : Shachar, I., and N. Karin. J Leukoc Biol 93:51-61.

Two molybdate/tungstate ABC transporters that interact very differently with their substrate binding proteins. 2013 Oded Lewinson, PhD Authors : Vigonsky, Ovcharenko E, Lewinson O. Proc Natl Acad Sci U S A. (March 19 Epub ahead of print)

Dissecting the Autocrine and Paracrine Roles of the CCR2-CCL2 Axis in Tumor Survival and Angiogenesis. 2012 Nathan Karin, PhD Authors : Izhak, L., G. Wildbaum, S. Jung, A. Stein, Y. Shaked, and N. Karin. PloS one 7:e28305

Dose-related effects of hyperoxia on the lung inflammatory response in septic rats 2012 Nitza Lahat, PhD Authors : Waisman D, Brod V, Rahat MA, Amit-Cohen BC, Lahat N, Rimar D, Menn-Josephy H, David M, Lavon O, Cavari Y, Bitterman H. Shock. 2012 Jan;37(1):95-102.

Robust and sensitive analysis of xMap bead arrays using SAxCyB. 2012 Shai Shen-Orr, PhD Authors : Won JH, Goldberger O, Shen-Orr SS, David MM, Olshen RA. Proc Natl Acad Sci U S A. 109, 2848-53.

The Entamoeba histolytica methylated LINE-binding protein EhMLBP provides protection against heat shock 2012 Serge Ankri, PhD Authors : Katz S, Kushnir O, Tovy A, Siman Tov R, Ankri S. Cell Microbiol. 2012 Jan;14(1):58-70

Hypoxia increases membranal and secreted HLA-DR in endothelial cells, rendering them T-cell activators. 2011 Nitza Lahat, PhD Authors : Lahat N, Bitterman H, Weiss-Cerem L, Rahat MA. Transpl Int. 2011 Oct;24(10):1018-26.

The Entamoeba histolytica methylated LINE-binding protein EhMLBP provides protection against heat shock. 2011 Serge Ankri, PhD Authors : Katz S, Kushnir O, Tovy A, Siman Tov R, Ankri S. Cell Microbiol. 2011 Sep 8. [Epub ahead of print]

Dose-Related Effects of Hyperoxia on the Lung Inflammatory Response in Septic Rats. Shoc 2011 Nitza Lahat, PhD Authors : Waisman D, Brod V, Rahat MA, Amit-Cohen BC, Lahat N, Rimar D, Menn-Josephy H, David M, Lavon O, Cavari Y, Bitterman H. 2011 Sep 3. [Epub ahead of print]

Glucose starvation boosts Entamoeba histolytica virulence. 2011 Serge Ankri, PhD Authors : Tovy A, Hertz R, Siman-Tov R, Syan S, Faust D, Guillen N, Ankri S. PLoS Negl Trop Dis. 2011 Aug;5(8):e1247.

The binding activity of Mel-18 at the Il17a promoter is regulated by the integrated signals of the TCR and polarizing cytokines. 2011 Eur J Immunol. 2011 Aug;41(8):2424-35.

phosphorylation of SLP-76 at tyrosine 173 is required for activation of T and mast cells. 2011 Deborah Yablonski, PhD Authors : Sela M, Bogin Y, Beach D, Oellerich T, Lehne J, Smith-Garvin JE, Okumura M, Starosvetsky E, Kosoff R, Libman E, Koretzky G, Kambayashi T, Urlaub H, Wienands J, Chernoff J, Yablonski D. Sequential EMBO J. 2011 Jul 1;30(15):3160-72.

The binding activity of Mel-18 at the Il17a promoter is regulated by the integrated signals of the TCR and polarizing cytokines. 2011 Orly Avni, PhD Authors : Hod-Dvorai R, Jacob E, Boyko Y, Avni O. Eur J Immunol. 2011 Jun 15. [Epub ahead of print]

MMP expression in leaking filtering blebs and tears after glaucoma filtering surgery. 2011 Nitza Lahat, PhD Authors : Mathalone N, Marmor S, Rahat MA, Lahat N, Oron Y, Geyer O. Graefes Arch Clin Exp Ophthalmol. 2011 Mar 31. [Epub ahead of print]

B cell depletion reactivates B lymphopoiesis in the BM and rejuvenates the B lineage in aging. 2011 Doron Melamed, PhD Authors : Keren Z, Naor S, Nussbaum S Golan K, Itkin T, Sasaki Y, Schmidt-Supprian M, Lapidot T, Melamed D. Blood 117, 3104 – 3112.

Chronic B cell deficiency from birth prevents age-related alterations in the B lineage J. 2011 Doron Melamed, PhD Authors : Keren Z, Averbuch D, Shahaf G, Zisman-Rozen S, Golan K, Itkin T, Lapidot T, Mehr R, Melamed D. Immunol 187, 2140 – 2147.

Epigenetics in the unicellular parasite Entamoeba histolytica. 2010 Serge Ankri, PhD Authors : Tovy A, Ankri S. Future Microbiol. 2010 Dec;5:1875-84.

The MAPK/ERK and PI3K pathways additively coordinate the transcription of recombination-activating genes in B lineage cells 2010 Orly Avni, PhD Authors : Novak R, Jacob E, Haimovich J, Avni O, Melamed D. J Immunol. 2010 Sep 15;185(6):3239-47

A fusion protein encoding the second extracellular domain of CCR5 arrests chemokine-induced cosignaling and effectively suppresses ongoing experimental autoimmune encephalomyelitis 2010 Nathan Karin, PhD Authors : Sapir Y, Vitenshtein A, Barsheshet Y, Zohar Y, Wildbaum G, Karin N. J Immunol. 2010 Aug 15;185(4):2589-99.

Antigen-specific CD25- Foxp3- IFN-gamma(high) CD4+ T cells restrain the development of experimental allergic encephalomyelitis by suppressing Th17 2010 Nathan Karin, PhD Authors : Wildbaum G, Zohar Y, Karin N. Am J Pathol. 2010 Jun; 176(6):2764-75.

Circulating interleukin-10: association with higher mortality in systolic heart failure patients with elevated tumor necrosis factor-alpha 2010 Nitza Lahat, PhD Authors : Amir O, Rogowski O, David M, Lahat N, Wolff R, Lewis BS. Isr Med Assoc J. 2010 Mar;12(3):158-62.

In vitro tRNA Methylation Assay with the Entamoeba histolytica DNA and tRNA Methyltransferase Dnmt2 (Ehmeth) Enzyme 2010 Serge Ankri, PhD Authors : Tovy A, Hofmann B, Helm M, Ankri S. J Vis Exp. 2010 Oct 19;(44). pii: 2390. doi: 10.3791/2390.

Circulating interleukin-10: association with higher mortality in systolic heart failure patients with elevated tumor necrosis factor-alpha 2010 Nitza Lahat, PhD Authors : Amir O, Rogowski O, David M, Lahat N, Wolff R, Lewis BS Isr Med Assoc J. 2010 Mar;12(3):158-62

A distinct mechanism for the ABC transporter BtuCD-BtuF revealed by the dynamics of complex formation. 2010 Oded Lewinson, PhD Authors : Lewinson O, Lee AT, Locher KP, Rees DC. Nat Struct Mol Biol. 17, 332-8.

Extracting Cell-Type-Specific Gene Expression Differences from Complex Tissues. 2010 Shai Shen-Orr, PhD Authors : Shen-Orr SS*, Tibshirani R*, Khatri P, Bodian DL, Staedtler F, Perry NM, Hastie T, Sarwal MM, Davis MM*, Butte AJ*. Nature Methods 7, 287-9.

The MAPK/ERK and PI(3)K Pathways Additively Coordinate the Transcription of Recombination-Activating Genes in B Lineage Cells. 2010 Doron Melamed, PhD Authors : Novak R, Jacob E, Haimovich J, Avni O, Melamed D. Immunol 185, 3239 – 3247.

Protein denitrosylation: enzymatic mechanisms and cellular functions 2009 Moran Benhar, PhD Authors : Benhar, M., Forrester, M.T., Stamler, J.S. Nat. Rev. Mol. Cell Biol. 10:721-32.

Psoriasis patients generate increased serum levels of autoantibodies to tumor necrosis factor-alpha and interferon-alpha 2009 Nathan Karin, PhD Authors : Bergman R, Ramon M, Wildbaum G, Avitan-Hersh E, Mayer E, Shemer A, Karin N. J Dermatol Sci. 2009 Oct 1. Epub

The role of macrophage-derived IL-1 in induction and maintenance of angiogenesis 2009 Nitza Lahat, PhD Authors : Carmi Y, Voronov E, Dotan S, Lahat N, Rahat MA, Fogel M, Huszar M, White MR, Dinarello CA, Apte RN. J Immunol. 2009 Oct 1;183(7):4705-14.

Insights into the mechanism of DNA recognition by the methylated LINE binding protein EhMLBP of Entamoeba histolytica 2009 Serge Ankri, PhD Authors : Lavi T, Siman-Tov R, Ankri S. Mol Biochem Parasitol. 2009 Aug;166(2):117-25. Epub 2009 Mar 20.

A novel recombinant fusion protein encoding a 20-amino acid residue of the third extracellular (E3) domain of CCR2 neutralizes the biological activity of CCL2 2009 Nathan Karin, PhD Authors : Izhak L, Wildbaum G, Zohar Y, Anunu R, Klapper L, Elkeles A, Seagal J, Yefenof E, Ayalon-Soffer M, Karin N J Immunol. 2009 Jul 1;183(1):732-9

Selective autoantibody production against CCL3‭ ‬is associated with human type 1‭ ‬diabetes mellitus and serves as a novel biomarker for its diagnosis 2009 Nathan Karin, PhD Authors : Shehadeh N‭, ‬Pollack S‭, ‬Wildbaum G‭, ‬Zohar Y‭, ‬Shafat I‭, ‬Makhoul R‭, ‬Daod E‭,‬ J Immunol‭. ‬2009‭ ‬Jun 15‭;‬182‭(‬12‭):‬8104-9

The effect of 100% oxygen on intestinal preservation and recovery following ischemia-reperfusion injury in rats 2009 Nitza Lahat, PhD Authors : Sukhotnik I, Brod V, Lurie M, Rahat MA, Shnizer S, Lahat N, Mogilner JG, Bitterman H. Crit Care Med. 2009 Mar;37(3):1054-61.

Transcriptional regulation of GATA3 in T helper cells by the integrated activities of transcription factors downstream of the interleukin-4 receptor and T cell receptor 2009 Orly Avni, PhD Authors : Scheinman EJ, Avni O. J Biol Chem. 2009 30;284(5):3037-48.

TOLL-like receptor ligands stimulate aberrant class switch recombination in early B cell precursors 2008 Doron Melamed, PhD Authors : Edry E, Azulay-Debby H, Melamed D. Int Immunol. 2008 Dec;20(12):1575-85. Epub 2008 Oct 29.

EhMLBP is an essential constituent of the Entamoeba histolytica epigenetic machinery and a potential drug target 2008 Serge Ankri, PhD Authors : Lavi T, Siman-Tov R, Ankri S. Mol Microbiol. 2008 Jul;69(1):55-66. Epub 2008 May 12

Hypoxia enhances lysosomal TNF-α degradation in mouse peritoneal macrophages 2008 Nitza Lahat, PhD Authors : Lahat, N., Rahat, M. A., Kinarty, A., Weiss-Cerem, L., Pinchevski, S., Bitterman, H. Am J Physiol Cell Physiol 295, C2-12.

What do unicellular organisms teach us about DNA methylation? 2008 Serge Ankri, PhD Authors : Harony H Trends Parasitol. 2008 May;24(5):205-9. Epub 2008 Apr 9. PMID: 18403268 [PubMed – in process]

Regulated protein denitrosylation by cytosolic and mitochondrial thioredoxins 2008 Moran Benhar, PhD Authors : Benhar, M., Forrester, M.T., Hess, D.T., Stamler, J.S. Science 320:1050-4

Trichostatin A regulates peroxiredoxin expression and virulence of the parasite Entamoeba histolytica. 2008 Serge Ankri, PhD Authors : Isakov E, Siman-Tov R, Weber C, Guillen N Mol Biochem Parasitol. 2008 Mar;158(1):82-94.

Progress and prospects of gene inactivation in Entamoeba histolytica. 2008 Serge Ankri, PhD Authors : Abed M Exp Parasitol. 2008 Feb;118(2):151-5

Class switch recombination: a friend and a foe. 2007 Doron Melamed, PhD Authors : Edry E. Clin Immunol. 2007 Jun;123(3):244-51.

Native and fragmented fibronectin oppositely modulate monocyte secretion of MMP-9 2007 Nitza Lahat, PhD Authors : Marom, B., Rahat, M. A., Lahat, N., Weiss-Cerem, L., Kinarty, A., Bitterman, H. J Leukoc Biol 81, 1466-1476.

SLP-76 mediates and maintains activation of the Tec family kinase ITK via the T cell antigen receptor-induced association between SLP-76 and ITK. 2007 Deborah Yablonski, PhD Authors : Bogin Y, Ainey C, Beach D Proc Natl Acad Sci U S A. 2007 Apr 17;104(16):6638-43.

Dual role of SLP-76 in mediating T cell receptor-induced activation of phospholipase C-gamma1. 2007 Deborah Yablonski, PhD Authors : Beach D, Gonen R, Bogin Y, Reischl IG J Biol Chem. 2007 Feb 2;282(5):2937-46. Epub 2006 Dec 4. Read the Article

B cell receptor editing in tolerance and autoimmunity. 2007 Doron Melamed, PhD Authors : Azulay-Debby H. Front Biosci. 2007 Jan 1;12:2136-47.

Genome-wide analysis of mRNA polysomal profiles with spotted DNA microarrays. 2007 Doron Melamed, PhD Authors : Arava Y. Methods Enzymol. 2007;431:177-201

Coadministration of plasmid DNA constructs encoding an encephalitogenic determinant and IL-10 elicits regulatory T cell-mediated protective immunity in the central nervous system. 2006 Nathan Karin, PhD Authors : Schif-Zuck S, Wildbaum G, Karin N. J Immunol. 2006 Dec 1;177(11):8241-7.

Sensing DNA methylation in the protozoan parasite Entamoeba histolytica. 2006 Serge Ankri, PhD Authors : Lavi T, Isakov E, Harony H, Fisher O, Siman-Tov R. Mol Microbiol. 2006 Dec;62(5):1373-86. Read the Article:

Modulation of matrix metalloproteinase-9 (MMP-9) secretion in B lymphopoiesis. 2006 Doron Melamed, PhD Authors : Melamed D, Messika O, Glass-Marmor L, Miller A. Int Immunol. 2006 Sep;18(9):1355-62.

A Pak- and Pix-dependent branch of the SDF-1alpha signalling pathway mediates T cell chemotaxis across restrictive barriers. 2006 Deborah Yablonski, PhD Authors : Volinsky N, Gantman A, Yablonski D. Biochem J. 2006 Jul 1;397(1):213-22. PMID: 16515536 [PubMed – in process] Read more

DNA methylation and targeting of LINE retrotransposons in Entamoeba histolytica and Entamoeba invadens. 2006 Serge Ankri, PhD Authors : Harony H, Bernes S, Siman-Tov R, Ankri S. Mol Biochem Parasitol. 2006 May;147(1):55-63. Epub 2006 Feb 23. PMID: 16530279 [PubMed � in process] Read more

Pleiotropic phenotype in Entamoeba histolytica overexpressing DNA methyltransferase (Ehmeth). 2006 Serge Ankri, PhD Authors : Fisher O, Siman-Tov R, Ankri S. Mol Biochem Parasitol. 2006 May;147(1):48-54. Epub 2006 Feb 9. PMID: 16497397 [PubMed � in process] Read more

Hypoxia reduces the output of matrix metalloproteinase-9 (MMP-9) in monocytes by inhibiting its secretion and elevating membranal association 2006 Nitza Lahat, PhD Authors : Rahat, M. A., Marom, B., Bitterman, H., Weiss-Cerem, L., Kinarty, A., Lahat, N. J Leukoc Biol 79, 706-718.

Antisense inhibition of Entamoeba histolytica cysteine proteases inhibits colonic mucus degradation 2006 Serge Ankri, PhD Authors : Moncada D, Keller K, Ankri S, Mirelman D, Chadee K. Gastroenterology. 2006 Mar;130(3):721-30. PMID: 16530514 [PubMed � indexed for MEDLINE] Read more

Beneficial autoimmunity participates in the regulation of rheumatoid arthritis. 2006 Nathan Karin, PhD Authors : Zohar Y, Wildbaum G, Karin N. Front Biosci. 2006 Jan 1;11:368-79. Review. PMID: 16146738 [PubMed – indexed for MEDLINE] Read more

The RNA polymerase II subunit Rpb4p mediates decay of a specific class of mRNAs. 2005 Doron Melamed, PhD Authors : Lotan R, Bar-On VG, Harel-Sharvit L, Duek L, Melamed D, Choder M. Genes Dev. 2005 Dec 15;19(24):3004-16. PMID: 16357218 [PubMed – indexed for MEDLINE] Read more

Single point mutations in the zinc finger motifs of the human immunodeficiency virus type 1 nucleocapsid alter RNA binding specificities of the gag protein and enhance packaging and infectivity. 2005 Doron Melamed, PhD Authors : Mark-Danieli M, Laham N, Kenan-Eichler M, Castiel A, Melamed D, Landau M, Bouvier NM, Evans MJ, Bacharach E. J Virol. 2005 Jun;79(12):7756-67. PMID: 15919928 [PubMed – indexed for MEDLINE] Read more

Molecular characterization of Entamoeba histolytica Rnase III and AGO2, two RNA interference hallmark proteins. 2005 Serge Ankri, PhD Authors : Abed M, Ankri S. Exp Parasitol. 2005 Jul;110(3):265-9. Epub 2005 Apr 7. PMID: 15955322 [PubMed � indexed for MEDLINE] Read more

Targeted overexpression of IL-18 binding protein at the central nervous system overrides flexibility in functional polarization of antigen-specific Th2 cells. 2005 Nathan Karin, PhD Authors : Schif-Zuck S, Westermann J, Netzer N, Zohar Y, Meiron M, Wildbaum G, Karin N. Immunol. 2005 Apr 1;174(7):4307-15. PMID: 15778395 [PubMed – indexed for MEDLINE] Read more

T cell receptor-induced activation of phospholipase C-gamma1 depends on a sequence-independent function of the P-I region of SLP-76. 2005 Deborah Yablonski, PhD Authors : Gonen R, Beach D, Ainey C, Yablonski D. J Biol Chem. 2005 Mar 4;280(9):8364-70. Epub 2004 Dec 28. PMID: 15623534 [PubMed – indexed for MEDLINE] Read more

Naive, effector, and memory T lymphocytes efficiently scan dendritic cells in vivo: contact frequency in T cell zones of secondary lymphoid organs does not depend on LFA-1 expression and facilitates 2005 Nathan Karin, PhD Authors : Westermann J, Bode U, Sahle A, Speck U, Karin N, Bell EB, Kalies K, Gebert A. J Immunol. 2005 Mar 1;174(5):2517-24. PMID: 15728457 [PubMed – indexed for MEDLINE] Read more

Antigen receptor signaling competence and the determination of B cell fate in B-lymphopoiesis. 2005 Doron Melamed, PhD Authors : Keren Z, Melamed D. Histol Histopathol. 2005 Jan;20(1):187-96. Review. PMID: 15578437 [PubMed – indexed for MEDLINE] Read more

CD19 regulates positive selection and maturation in B lymphopoiesis: lack of CD19 imposes developmental arrest of immature B cells and consequential stimulation of receptor editing. 2005 Doron Melamed, PhD Authors : Diamant E, Keren Z, Melamed D. Blood ;105:3247-3254.

Entamoeba histolytica DNA methyltransferase (Ehmeth) is a nuclear matrix protein that binds EhMRS2, a DNA that includes a scaffold/matrix attachment region (S/MAR). 2005 Serge Ankri, PhD Authors : Banerjee S, Fisher O, Lohia A, Ankri S. Mol Biochem Parasitol. 2005 Jan;139(1):91-7. PMID: 15610823 [PubMed � indexed for MEDLINE] Read more

Epigenetic and classical activation of Entamoeba histolytica heat shock protein 100 (EHsp100) expression. 2005 Serge Ankri, PhD Authors : Bernes S, Siman-Tov R, Ankri S. FEBS Lett;579:6395-6402.

T cell receptor-induced activation of phospholipase C-γ1 depends on a sequence-independent function of the P-I region of SLP-76. 2005 Deborah Yablonski, PhD Authors : Gonen R, Beach D, Ainey C, Yablonski D. J Biol Chem ;280:8364-8370.

Characterization of cytosine methylated regions and 5-cytosine DNA methyltransferase (Ehmeth) in the protozoan parasite Entamoeba histolytica. 2004 Serge Ankri, PhD Authors : Fisher O, Siman-Tov R, Ankri S. Nucleic Acids Res ;1:287-297.

Modification of ligandindependent B cell receptor tonic signals activates receptor editing in immature B lymphocytes. 2004 Doron Melamed, PhD Authors : Keren Z, Diamant E, Ostrovsky O, Bengal E, Melamed D. J Biol Chem ;279:13418-13424.

A failsafe mechanism for negative selection of isotype-switched B cell precursors is regulated by the Fas/FasL pathway 2003 Doron Melamed, PhD Authors : Seagal J, Edry E, Keren Z, Leider N, Benny O, Machluf M, Melamed D. J Exp Med ;198:1609-1619.

Beneficial autoimmunity to proinflammatory mediators restrains the consequences of self-destructive immunity. 2003 Nathan Karin, PhD Authors : Wildbaum G, Nahir MA, Karin N. Immunity;19:679-688.

T(H) cell differentiation is accompanied by dynamic changes in histone acetylation of cytokine genes. 2002 Orly Avni, PhD Authors : Avni O, Lee D, Macian F, Szabo SJ, Glimcher LH, Rao A. Nat Immunol ;3:643-651.

Tr1 cell-dependent active tolerance blunts the pathogenic effects of determinant spreading. 2002 Nathan Karin, PhD Authors : Wildbaum G, Netzer N, Karin N. J Clin Invest ;110:701-710.

A PAK1-PIX-PKL complex is activated by the T-cell receptor independent of Nck, Slp-76 and LAT. 2001 Deborah Yablonski, PhD Authors : Ku GM, Yablonski D, Manser E, Lim L, Weiss A. EMBO Journal ;20:457-465.

Identification of a phospholipase C-γ1 (PLC- γ1) SH3 domain-binding site in SLP-76 required for T-cell receptor-mediated activation of PLC-γ1 and NFAT 2001 Deborah Yablonski, PhD Authors : Yablonski D, Kadlecek T, Weiss A. Mol Cell Biol ;21:4208-4218.

C-C chemokineencoding DNA vaccines enhance breakdown of tolerance to their gene products and treat ongoing adjuvant arthritis. 2000 Nathan Karin, PhD Authors : Youssef S, Maor G, Wildbaum G, Grabie N, Gour-Lavie A, Karin N. J Clin Invest ;106:361-371.

Cell-type-restricted binding of the transcription factor NFAT to a distal IL-4 enhancer in vivo. 2000 Orly Avni, PhD Authors : Agarwal S, Avni O, Rao A. Immunity ;12:643-652.

T cell differentiation: a mechanistic view. 2000 Orly Avni, PhD Authors : Avni O, Rao A. Curr Opin Immunol; 12:654-659.

A systemic cytokine response defect stratifies older adults into distinct immune profiles. 1900 Shai Shen-Orr, PhD Authors : Shen-Orr SS*, Furman D*, Kidd BA, Morgan A, Lovelace P, Rosenberg-Hasson Y, Maecker H, Mackey S, Dekker C, Butte AJ, Davis MM. Submitted.

 

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Pfizer Abandons Bid for AstraZeneca Regardless of Valuation of its Future Financials: The Destiny of Drug R&D Pipelines – The Case of AstraZeneca

Posted in FDA Regulatory Affairs, Health Economics and Outcomes Research, Pharmaceutical Analytics, Pharmaceutical Industry Competitive Intelligence, Pharmaceutical R&D Investment, Pharmacologic toxicities, Regulated Clinical Trials: Design, Methods, Components and IRB related issues, Statistical Methods for Research Evaluation on May 20, 2014| Leave a Comment »

Pfizer Abandons Bid for AstraZeneca Regardless of Valuation of its Future Financials: The Destiny of Drug R&D Pipelines – The Case of AstraZeneca

Reporter: Aviva Lev-Ari, PhD, RN

UPDATED on 9/3/2014

‘Back to normal’ for AstraZeneca CEO, despite Pfizer rumors

BY BEN HIRSCHLER

BARCELONA Tue Sep 2, 2014 8:59am EDT

 

(Reuters) – Though speculation is rife of a new Pfizer bid, AstraZeneca’s chief executive is not holed up with advisers in London or New York. Instead, he has spent the last three days immersed in heart science in Barcelona.

“The only thing I can tell you is I am here – and imagine where I would be if something was happening!” Pascal Soriot told Reuters on the sidelines of the European Society of Cardiology congress, the world’s largest heart meeting.

Strict British takeover rules limit what Soriot and other players can say about Pfizer’s abortive attempt to buy AstraZeneca and the possibility of a resumption of talks.

But chatter among investors that Pfizer will come back has boosted shares in Britain’s second biggest drugmaker more than 10 percent since the middle of last month, and the ending of the first of a two-stage cooling-off period on Aug. 26.

While Pfizer cannot launch another public bid until late November, AstraZeneca can now invite it back for talks and Pfizer also has one shot at making a private approach.

Although the saga may not be over, Soriot remains adamant AstraZeneca has a strong independent future.

“We are making good progress with the pipeline and everything so far – touch wood – is going in the right direction,” he said. “We’re back to normal.”

Soriot has spent his time in Barcelona focused on the heart drug Brilinta, which AstraZeneca flagged as worth a potential $3.5 billion-a-year in a strategy update that formed a central plank of its defense against Pfizer.

Sales of the drug have disappointed investors so far, totaling only $216 million in the first half of 2014, but they should pick up following the closure of a U.S. probe into a big clinical trial that had worried some doctors, Soriot said.

“It’s very clear that Brilinta will, actually, in the end make it,” Soriot said, adding he had been encouraged by feedback from key opinion leaders in Barcelona, as well a new study showing the drug was safe to use in ambulances.

SOURCE

http://www.reuters.com/article/2014/09/02/us-astrazeneca-pfizer-exclusive-idUSKBN0GX1C720140902

UPDATED on 5/27/2014

Pfizer Abandons Bid for AstraZeneca

 

By JENNY ANDERSON MAY 26, 2014 10:39 AM

Phil Noble/ReutersPfizer’s final offer valued AstraZeneca at nearly 70 billion pounds. AstraZeneca demanded an offer of more than £74 billion.

Updated, 9:36 p.m. | On the final day for Pfizer to decide whether to abandon the plan, it said it did not intend to make an offer for AstraZeneca. Last week, the British company rejected what Pfizer had called its final offer. The cash-and-stock bid, which valued AstraZeneca at about $119 billion, would have created the world’s largest drug company.

Pfizer had indicated that it would not pursue a hostile bid, which would have allowed AstraZeneca’s shareholders to vote on the deal without the approval of AstraZeneca’s board. Under British takeover rules, Pfizer is not permitted to make another offer for AstraZeneca for six months. If AstraZeneca’s board were to agree to talks, the earliest Pfizer could offer a higher price would be in three months.

“We continue to believe that our final proposal was compelling and represented full value for AstraZeneca based on the information that was available to us,” Ian C. Read, Pfizer’s chairman and chief, said in a statement. “As we said from the start, the pursuit of this transaction was a potential enhancement to our existing strategy.”

SOURCE

 

<a href="http://dealbook.nytimes.com/2014/05/26/pfizers-says-its-bid-for-astrazeneca-is-dead/?_php=true&_type=blogs&emc=edit_dlbkam_20140527&nl=business&nlid=40094405&_r=0[/embed]%20">http://dealbook.nytimes.com/2014/05/26/pfizers-says-its-bid-for-astrazeneca-is-dead/?_php=true&_type=blogs&emc=edit_dlbkam_20140527&nl=business&nlid=40094405&_r=0 

The Destiny of Drug R&D Pipelines: The Case of AstraZeneca – Valuation of its Future Financials 

Reporter: Aviva Lev-Ari, PhD, RN

May 21 (Reuters) – AstraZeneca ‘s shareholders remain split over the UK pharmaceuticals giant’s decision to reject a $118 billion offer from U.S. rival Pfizer, with AXA coming out against it while Threadneedle supported it.

“It is the view of AXA IM UK that the board of AstraZeneca should not prevent an offer from Pfizer of 55 pounds ($92.67) per share from being put to the shareholders of the company,” Jim Stride, head of UK equities at AXA Investment Managers <AXAF,PA>, said on Wednesday.

AXA is the third biggest shareholder in AstraZeneca, with a 4.51 percent stake.

“Many shareholders – but not necessarily all – will find this an attractive offer. Accordingly we believe that the board was arguably wrong and acted too hastily to dismiss the latest proposal from Pfizer,” Stride added.

Meanwhile Threadneedle, which is the fifteenth biggest shareholder with a 1.39 percent stake, said it supported AstraZeneca’s decision to reject Pfizer’s proposal.

“As long-term investors in AstraZeneca, we continue to support the board’s stance on the Pfizer offer. We feel the full implications of the proposed acquisition have not been sufficiently understood and addressed by Pfizer,” a spokeswoman for Threadneedle said.

“The company has made notable progress under (Chief Excecutive) Pascal Soriot and is a strong, stand-alone UK business with a good product pipeline.” ($1 = 0.5935 British Pounds) (Reporting By Jemima Kelly; Editing by Chris Vellacott)

 

SOURCE 

http://www.reuters.com/article/2014/05/21/idUSL6N0O73S520140521

 

5/19 3:23AM – Chairman of AstraZeneca REJECTS the FINAL Offer of Pfizer explaining the Progress in Pipeline of defense Immunotherapy in Cancer, the NEW SCIENCE will bring good value to shareholders.

VIEW VIDEO

http://www.reuters.com/video/2014/05/19/so-why-did-astrazeneca-reject-pfizer?videoId=312996516

On Sunday, Pfizer made what it called its “final” $119 billion offer for AstraZeneca, which is based in London. Pfizer also stated that while it wanted a deal, it was only making a soft “nonbinding” offer at this time.

Pfizer said it would not start a full-fledged hostile offer for AstraZeneca. A hostile bid would have involved offering terms that AstraZeneca’s shareholders could accept without the approval of AstraZeneca’s board. Given the price Pfizer offered, such a maneuver had a real chance of success.

SOURCE

http://dealbook.nytimes.com/2014/05/19/the-curious-incident-of-pfizers-final-offer-for-astrazeneca/

Schroders, Fidelity reveal investor split as Astra rejects Pfizer

BY CHRIS VELLACOTT

LONDON Tue May 20, 2014 3:50pm EDT

(Reuters) – Some leading AstraZeneca Plc shareholders were at odds over whether the British drugmaker made the right decision in rejecting Pfizer Inc’s final $118 billion bid to buy the company.

Schroder Investment Management Ltd (SDR.L), AstraZeneca’s (AZN.L) 12th-biggest shareholder, urged the drugmaker on Tuesday to restart takeover talks with Pfizer (PFE.N) while Fidelity Worldwide Investment (UK) Ltd, holder of the 18th largest stake in Astra, backed the British company’s stance.

The division highlighted a split among investors following the collapse of a potential transaction, leaving many shareholders frustrated at missing out on a big windfall.

Schroders said it was disappointed with “the quick rejection by the AstraZeneca board” of an improved 55 pounds-a-share offer and the decision by Pfizer to “draw a premature end to these negotiations by calling their latest proposal final.”

“Given the increase in the offer we would encourage the AstraZeneca management to recommence their engagement with Pfizer, and subsequently their shareholders,” the fund manager, which owns 2 percent of AstraZeneca, said.

SOURCE

http://www.reuters.com/article/2014/05/20/us-astrazeneca-pfizer-shareholders-idUSBREA4J09520140520

Pfizer failed in its takeover bid for AstraZeneca because of overconfidence

AstraZeneca’s directors played their hand well, while Pfizer’s bid was largely driven by cost savings and tax minimisation

Nils Pratley, financial editor

• The Guardian, Monday 19 May 2014 16.41 EDT

SOURCE

http://www.theguardian.com/business/2014/may/19/pfizer-failed-takeover-bid-astrazeneca

AstraZeneca Snubs Pfizer Once More

By CHAD BRAY

MAY 19, 2014, 3:23 AM 16 Comments

VIEW CNBC VIDEO

http://dealbook.nytimes.com/2014/05/19/astrazeneca-rejects-final-offer-by-pfizer/?_php=true&_type=blogs&_r=0

Updated, 10:36 p.m. | LONDON — AstraZeneca has to hope it can deliver on its vaunted drug pipeline.

On Monday, AstraZeneca, the Anglo-Swedish drug maker, rejectedPfizer’s latest — and what it described as its “final” — bid to buy AstraZeneca, which would create the world’s largest pharmaceutical company.

Barring a last-minute change of heart by AstraZeneca’s board or another sweetened bid by Pfizer later this week, the likelihood of a potential deal looks bleak. Under British takeover rules, Pfizer has until May 26 — a holiday this year in both Britain and the United States — to decide whether to walk away.

The latest offer, made Sunday evening, was worth about $119 billion. On Monday, AstraZeneca responded that the increased bid “undervalues the company and its attractive prospects.”

In making its final offer on Sunday, Pfizer said that it did not believe that AstraZeneca’s board was prepared to recommend a deal “at a reasonable price” and it encouraged AstraZeneca’s shareholders to urge the company to engage in “meaningful dialogue” about a potential combination.

Pfizer, which began its pursuit of a merger last year, has said it will not make a hostile bid.

The news sent AstraZeneca’s shares down 11.1 percent, to 42.875 pounds, in trading on Monday in London. The company’s stock had been trading higher in recent weeks as shareholders anticipated an increased offer from Pfizer.

A Pfizer spokesman said on Monday that the company was evaluating its options after the latest rejection.

Leif Johansson, the AstraZeneca chairman, said in a statement that Pfizer’s pursuit all along “appears to have been fundamentally driven by the corporate financial benefits to its shareholders of cost savings and tax minimization.” He was referring to Pfizer’s plan to reincorporate in Britain through the transaction to substantially reduce its United States tax bill.

“From our first meeting in January to our latest discussion yesterday, and in the numerous phone calls in between, Pfizer has failed to make a compelling strategic, business or value case,” Mr. Johansson said. “The board is firm in its conviction as to the appropriate terms to recommend to shareholders.”

AstraZeneca has raised a number of concerns about the potential tie-up, but the main sticking point appears to be what constitutes an appropriate price for AstraZeneca and its stable of drugs in development.

The latest proposal would have given AstraZeneca shareholders 1.747 shares of the combined company, and £24.76 in cash for each of their shares. The offer valued each share of AstraZeneca at about £55, or about $92.50.

Christopher Furlong/Getty ImagesPfizer’s bid would have combined the makers of Crestor and Viagra.

Analysts had predicted that AstraZeneca’s board would be willing to engage in meaningful discussions about a merger at that price. Yet AstraZeneca said on Monday that it was looking, at a minimum, for a price closer to £58 a share.

Sunday’s offer represented a 45 percent premium over AstraZeneca’s share price before news of Pfizer’s interest became public in April and came after a previous offer by Pfizer late on Friday.

Is AstraZeneca “realistic in what it believes ‘fair value’ is?” Timothy Anderson, a pharmaceutical analyst at Sanford C. Bernstein, said in a research note Monday. “Projecting the worth of new drug pipelines is notoriously difficult, and drug companies and financial analysts alike are often wrong to the tune of billions of dollars, especially when going out five to 10 years. Drug development is just not that predictable.”

AstraZeneca said this month that it expected to achieve annual revenue of $45 billion by 2023 as an independent company.

The company, which has an attractive portfolio of cancer drugs, has repeatedly trumpeted the strength of its drugs in development, saying it is projecting peak annual sales potential of about $23 billion for those drugs by the end of 2023.

The company’s pipeline includes potential treatments for cancer, cardiovascular disease and asthma. One promising area is its immuno-oncology drugs, which use the body’s immune system to attack tumors. MEDI4736, a cancer treatment in development, is one drug that the company is pointing to as a reason to be optimistic about its pipeline. The company expects the drug could earn $6.5 billion in peak annual sales.

Pfizer, the maker of best-selling drugs like Lipitor and Viagra, has raised questions about AstraZeneca’s prospects as a stand-alone concern and vowed to keep jobs in Britain in a bid to persuade British politicians to support the transaction.

If completed, the deal would be one of the largest acquisitions in the pharmaceutical industry, surpassing Pfizer’s takeover of Warner-Lambert 14 years ago, which was valued at $90 billion at the time. Adjusted for inflation, however, that takeover would now be valued at about $124 billion.

Bob Strong/ReutersLeif Johansson, the chairman of AstraZeneca, said the board was firm in declining Pfizer’s bid.

Savvas Neophytou, an analyst at Panmure Gordon & Company in London, said a majority of AstraZeneca’s large shareholders would have preferred that the company engage in a “more robust discussion” with Pfizer and that £55 a share would have been an attractive price for many stockholders.

Now, AstraZeneca must deliver on its lofty outlook, Mr. Neophytou said.

“From AstraZeneca’s point of view, the challenge is not the next six months,” Mr. Neophytou said. “The challenge is what happens in the medium to long term, the next three to five years.”

Pfizer’s pursuit of AstraZeneca has been a contentious one, with both companies seemingly talking past each other and AstraZeneca’s board showing little desire to engage Pfizer.

On Friday, Pfizer approached AstraZeneca with another increased offer of cash and stock worth about £53.50 a share. AstraZeneca’s board again felt the offer was too low.

On a conference call between the companies on Sunday, Mr. Johansson said, even if other crucial aspects of the deal were satisfactory, the board would be prepared to recommend only an offer price that was more than 10 percent above the Friday bid, or about £58.85, according to AstraZeneca.

Pfizer reiterated that its Friday proposal was final and would not be amended, according to AstraZeneca, but then announced an increased — and again final — proposal on Sunday, without previous notice.

The potential combination has also raised concerns among British and United States lawmakers.

In Britain, the concern has centered on whether Pfizer would eliminate jobs after a merger and hurt Britain’s standing in life sciences research. AstraZeneca employs 51,500 people worldwide, including about 6,700 in Britain.

Pfizer had committed to keep at least 20 percent of its research and development work force in Britain after a deal and to complete a research-and-development center being built by AstraZeneca in Cambridge, England.

But British politicians have pointed to Pfizer’s decision in 2011 to close a facility in Sandwich, England, as a reason to be concerned about its commitment to keeping jobs in Britain. The closing led to the loss of more than 1,500 jobs.

VIEW CNBC VIDEO

http://dealbook.nytimes.com/2014/05/19/astrazeneca-rejects-final-offer-by-pfizer/?_php=true&_type=blogs&_r=0

United States politicians also have raised questions about the company’s plans to reincorporate in Britain. The strategy, known as an inversion, is increasingly popular among United States companies, especially in the pharmaceutical industry.

The opposition Labour Party, which had accused Prime Minister David Cameron of cheerleading for the Pfizer bid, welcomed the decision by AstraZeneca.

“The AstraZeneca board has remained resolute and sought to act in the best long-term interests of the company and its vital work in developing new lifesaving drugs,” said Chuka Umunna, who speaks for the Labour Party on business issues.

“Pfizer has said today that it will not seek to launch a hostile bid and must not renege on this promise,” Mr. Umunna said.

Stephen Castle contributed reporting.

A version of this article appears in print on 05/20/2014, on page B1 of the NewYork edition with the headline: AstraZeneca Snubs Pfizer Once More 

SOURCE

http://dealbook.nytimes.com/2014/05/19/astrazeneca-rejects-final-offer-by-pfizer/?_php=true&_type=blogs&_r=0

NATURE REVIEWS DRUG DISCOVERY | PERSPECTIVES | OUTLOOK

Lessons learned from the fate of AstraZeneca’s drug pipeline: a five-dimensional framework

• David Cook,
• Dearg Brown,
• Robert Alexander,
• Ruth March,
• Paul Morgan,
• Gemma Satterthwaite
• & Menelas N. Pangalos

 

1. AstraZeneca, Innovative Medicines and Early Development, Alderley Park, Macclesfield SK10 4TG, UK.

   • David Cook,
   • Dearg Brown,
   • Ruth March,
   • Paul Morgan,
   • Gemma Satterthwaite &
   • Menelas N. Pangalos

2. AstraZeneca, Innovative Medicines & Early Development, 141 Portland Street, 10th Floor Cambridge, Massachusetts 02139, USA.

   • Robert Alexander

Competing interests statement

All authors are employees and shareholders of AstraZeneca.

Corresponding author

Correspondence to:

• Menelas N. Pangalos

• David Cook is a senior scientist and safety expert in AstraZeneca’s clinical Patient Safety group.

• Dearg Brown was a Director of Chemistry in AstraZeneca’s oncology group and is now a project manager at Manchester University, UK.

• Robert Alexander is a Clinical Vice President in AstraZeneca’s neuroscience group.

• Ruth March is the Vice President of the Personalized Healthcare and Biomarkers group at AstraZeneca.

• Paul Morgan is Head of Translation Safety in Drug Safety and Metabolism at AstraZeneca.

• Gemma Satterthwaite is a Director within AstraZeneca’s global product and portfolio strategy group.

• Menelas N. Pangalos is Executive Vice President and Global Head of Innovative Medicines and Early Development at AstraZeneca.

   

Nature Reviews Drug Discovery (2014) doi:10.1038/nrd4309

Published online 16 May 2014

The portfolio review

• Abstract•
• Introduction•
• The portfolio review•
• Key factors underlying project failures•
• Conclusions: what AstraZeneca did next•
• References•
• Acknowledgements•
• Author information•
• Related links

In 2011, a comprehensive review was undertaken of 142 drug discovery and development projects at AstraZeneca. The review covered projects from all therapeutic areas that had been active during the 2005–2010 period, from the phases following the completion of preclinical research through to the end of clinical testing in Phase II. The key aims of the review were to understand the major reasons for project closure and to identify the features of projects that correlated with successful outcomes.

We did not expand the review to look at Phase III for two reasons. First, successful transition through proof of concept (Phase II) remains the area where the industry overall has the highest rate of attrition and which must be improved. Second, the number of projects in Phase III for a single company is too small to be able to draw valid conclusions, and this number becomes even smaller if looking at successful transitions to launch of a medicine.

It should be noted that this is a single assessment from a single company, based on a limited number of projects, and over a limited timeframe. Nevertheless, we think that insights from this work could help to guide future teams and improve R&D productivity.

Methods. The aim of the review was to identify key ‘lessons learned’ in projects that could be used to improve the R&D productivity of the company. As such, the review was performed by a cross-functional group of scientists and clinicians drawn from the project team community, and conducted in a peer-to-peer manner. To be as objective as possible, structured questionnaires were used when interviewing teams and, where possible, contemporaneous documents were analysed to provide supporting evidence for assessments. In addition, to further avoid any potential bias, senior leaders who had been associated with the governance decisions over the assessment period were not involved in the review.

For this analysis, the drug development process was divided into four distinct phases: preclinical, Phase I, Phase IIa and Phase IIb. The preclinical phase was defined as the phase from the first good laboratory practice (GLP) toxicology dose of a candidate drug through to an investigational new drug (IND) application or first clinical trial application (CTA) before first-in-human testing. Phase I was defined as the phase that included the first-in-human trials within a small trial population (typically <50 patients) and included safety, tolerability and dose-ranging studies. These studies were often conducted in healthy volunteers, but in some indications (for example, oncology) they could include patients. Phase II trials were defined as trials that were aimed at evaluating the candidate drug’s efficacy in a patient population, leading up to clinical proof of concept. Within our analysis, we subdivided Phase II into Phase IIa and Phase IIb. Phase IIa studies were generally smaller (typically <200 patients) and designed to mainly address early evidence of drug activity, whereas Phase IIb studies included larger numbers of patients (typically <400 patients) and were designed to demonstrate clinical proof of concept and an understanding of dose response.

For each of these phases, projects were classified as being ‘active’ (still in that phase), ‘closed’ (shut during that phase) or ‘successful’ (transitioned from this phase to the next one). Every project was analysed separately in each phase of its development path; so, for example, a project that had reached Phase III trials was analysed four times across the entire development process. Data were collected for each project, for each of the development phases that it had completed, using comprehensive surveys and questionnaires with over 200 questions covering all aspects of the project (for example, the scientific rationale, target validation and physicochemical properties of the candidate drug). Questionnaires were adapted so that they were specific to each phase of the review to allow for the retrospective understanding of the data that were available for a project at that stage, and to analyse how the project knowledge and data developed as the project passed through different phases. Written surveys were supplemented with in-depth peer-to-peer interviews with project teams. Responses to the questionnaires and interviews were subjected to rigorous peer review by a team of experienced scientists and clinicians to ensure consistent evaluation across all projects. In-depth ‘root-cause’ analysis was used to reach conclusions as to why projects had failed. Analyses that were based on answers to specific questions in the questionnaires were only performed on projects that had provided a complete set of answers to the relevant questions.

Results. Overall, we gathered data from more than 80% of the 142 AstraZeneca projects within the scope of the review, and for 95% of projects in clinical phases. Of the projects analysed, 94 closed during the period assessed; 33 closed before clinical testing and a further 61 closed during clinical testing. The remaining projects were still active at the time of this review.

We compared the success rates for our projects to pharmaceutical industry benchmarks, obtained from the Pharmaceutical Benchmarking Forum (Fig. 1a). Our success rate in the preclinical phase (defined as the percentage of projects completing this phase and moving to the next phase of development) was comparable with industry benchmarks (66% versus 63%; see the KMR Group website for further information on the Pharmaceutical Benchmarking Forum).

Our data suggested that we had a higher success rate in completing Phase I (59% versus 48%) but a markedly lower success rate in completing Phase II (15% versus 29%), compared to industry benchmarks. In addition,

Phase III success rates were lower than the industry overall (60% versus 67%), although the number of projects in this phase was very low. Therefore, AstraZeneca was allowing more projects to enter later-stage development, only to have them subsequently fail.

Overall, AstraZeneca’s success in bringing candidate drugs to market during the 2005–2010 period was significantly lower than the industry median (2% versus 6%).

 SOURCE

http://www.nature.com/nrd/journal/vaop/ncurrent/full/nrd4309.html#the-portfolio-review

 

At AstraZeneca, Occasion for Introspection By Aaron Krol May 19, 2014 | On Friday, a frank assessment of AstraZeneca’s R&D practices appeared in Nature Reviews Drug Discovery. The review, written by members of the pharmaceutical company’s Innovative Medicines and Early Development division, examined projects in preclinical, Phase I and Phase II trials from 2005-2010, and reached some stark conclusions about the corporate culture’s influence on which compounds advanced through successive stages of testing. At the same time, the review offers new reasons for optimism, and may be seen to bolster AstraZeneca in its ongoing battle to resist acquisition by Pfizer. While the top-line figures are glaring – in particular, the observation that AstraZeneca was letting an exceptional number of compounds through Phase I trials, compared to the industry as a whole, only to see disproportionate failures in Phase II – the authors’ substantive look at the causes of failure is enlightening. A lack of confidence in the underlying biology of therapies seems to have been a frequent reason for failure, even in later stages of a project. In 40% of cases where lack of efficacy led to a project’s shutdown, teams reported that they “lacked data demonstrating a clear linkage of the target to the disease or access to a well-validated animal model of the disease,” and as late as Phase IIb trials, over 40% of teams reported “low confidence” in their molecular targets. In these cases, weak evidence of efficacy in preclinical models may have been enough to move projects forward, despite no strong hypothesis linking a lead drug to the disease pathology. The authors also noted that a more well-rounded view of the biology was a powerful predictor of success. At the time of the review, only 27% of Phase II trials had failed where teams reported that their drug target had a known genetic link to the disease in humans, and only 18% of Phase IIb trials had failed if teams reported that they began testing with a biomarker for efficacy in mind. “Overall,” the authors write, “these data highlight that, throughout every phase of early R&D, it is crucial for scientists and clinicians to gain an understanding of, and confidence in, the disease biology, the relationship of the target to the disease indication, and the proposed mechanism of action of a potential drug.” While the problems identified in this review will look familiar to many working in the pharmaceutical industry, they seem to have grown particularly entrenched at AstraZeneca. The authors note that projects were frequently advanced because teams were evaluated by volume of compounds in active testing, creating a perverse incentive to promote any candidate drug that could meet minimal standards of evidence. One indicator of this culture is the lack of diversity in back-up molecules, meant as potential replacements for a lead candidate in certain key projects. The authors found that back-up molecules were often only minor tweaks of the lead candidate, advanced with no reason to believe they would differ in activity or outperform the lead drug on any metric. “In one extreme case,” they write, “we identified a project with seven back-up molecules in the family… [which] all failed owing to the same preclinical toxicology finding.” Although the review was completed in 2011, it has been published at a fortuitous time for AstraZeneca, which has fought off repeated takeover attempts by Pfizer, including an offer of $117 billion over the weekend. There has been frequent speculation that AstraZeneca’s shareholders may rebel against the wishes of the board and accept a high bid by Pfizer, which is offering a high premium over the market value of AstraZeneca shares. While AstraZeneca’s board members insist that Pfizer is still undervaluing their drug portfolio, skeptics note that AstraZeneca has struggled to bring new drugs to market in recent years. This report offers reasons to believe that the company’s R&D practices may have changed since 2011, with a new emphasis on biological understanding over volume. The authors note that the company’s early development portfolio is significantly smaller than it was three years ago, and that teams are now expected to articulate their hypotheses relating drugs to disease targets, and more encouraged to seek out relevant biomarkers, companion diagnostics, and patient subpopulations. While acknowledging that “it is too early to see tangible benefits to the AstraZeneca pipeline,” they also observe that both preclinical and Phase II success rates have risen since the new R&D philosophy was implemented, while inflated Phase I success rates have fallen. While the timing may be coincidence, for AstraZeneca boosters looking for evidence to point to when arguing that Pfizer’s takeover bids undervalue the flagging company, this review will be a welcome addition to the public record. For everyone else, it is an instructive glimpse into misguided incentives at the root level of the drug industry. SOURCE http://www.bio-itworld.com/2014/5/19/astrazeneca-occasion-introspection.html

 

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Bristol-Myers Squibb: A global BioPharma leader – Tracing the innovative biotech core of $3.7 billion R&D Investment and $16.4 billion in Net Sales

Posted in Pharmaceutical Analytics, Pharmaceutical Industry Competitive Intelligence, Pharmaceutical R&D Investment, Pharmacogenomics, Population Health Management, Genetics & Pharmaceutical, Population Health Management, Nutrition and Phytochemistry, Regulated Clinical Trials: Design, Methods, Components and IRB related issues, Technology Transfer: Biotech and Pharmaceutical, Translational Science on May 12, 2014| Leave a Comment »

Bristol-Myers Squibb (BMS): A global BioPharma leader – Tracing the innovative biotech core of $3.7 billion R&D Investment and $16.4 billion in Net Sales

Reporter: Aviva Lev-Ari, PhD, RN

 

BMS’s  innovative biotech core represents +150 years of American leadership in Life Sciences and Pharmaceutics.

History

Our company has a strong legacy of innovation that began in New York in 1858 when Edward R. Squibb, M.D., founded a pharmaceutical company in Brooklyn, and in 1887 when two friends, William McLaren Bristol and John Ripley Myers purchased a struggling drug manufacturing firm in Clinton. Together, they laid the foundation for our company today — a global BioPharma leader that continues this legacy of innovation.

• 1858
• 1878
• 1898
• 1918
• 1938
• 1958
• 1978
• 1998
• 2009

As a young U.S. Navy doctor, Edward Robinson Squibb (1819-1900) was so unimpressed by the quality of medicines available on ships during the Mexican War that he pitched the unfit drugs overboard. In 1858, he founded his own pharmaceutical laboratory in Brooklyn, New York. E.R. Squibb, M.D. was dedicated to the production of consistently pure medicines.

1858

Squibb became the source of medicines for the Union Army during the Civil War. He invented the Squibb pannier—a compact wooden medicine chest used on the battlefield—filled with some 50 medicines to treat casualties. The chest sold for about $100, and included ether and chloroform for use as an anesthetic during amputations, quinine and whiskey to treat symptoms of malaria, and herbal treatments for dysentery and other diseases that ravaged the unsanitary military camps.

1860

August 2012

Bristol-Myers purchased Clairol, a company founded by the husband-and-wife team of Lawrence Gelb and Joan Clair. Clairol transformed hair coloring from a difficult-to-use specialty item into a highly successful mainstream consumer product.

1959

E.R. Squibb & Sons marketed the world’s first electronic toothbrush in 1961. By 1990 more than 150 other brands of automatic toothbrushes were introduced, most of which essentially imitated the original Squibb model invented by Professor Philippe G. Woog.

1961

1967

Bristol-Myers acquired Mead Johnson & Company, a leader in science-based infant and children’s nutrition. Mead Johnson introduced its first baby formula in 1910 and over the decades expanded into vitamins, pharmaceutical products and prenatal nutrition. The Enfamil® brand grew to be recognized worldwide for its leadership in pediatric nutrition.

1967

Squibb delved into cancer research, discovering and developing hydroxyurea for leukemia and advanced ovarian cancer.

For a time, Bristol-Myers was in show biz. In 1970, the company formed Palomar Pictures, which produced “The Taking of the Pelham One, Two, Three,” starring Walter Matthau and Robert Shaw, and “The Stepford Wives,” starring Katharine Ross and Paula Prentiss. Palomar was terminated in 1974.

1970

Squibb established worldwide headquarters in Princeton, New Jersey. It also expanded facilities for the Squibb Institute in Princeton, New Jersey. This expansion allowed Squibb to make more groundbreaking discoveries and advancements in medical research.

1971

In the 1970s Bristol-Myers introduced several early medicines, beginning in 1973 with BLENOXANE® (bleomycin sulfate) for squamous cell cancers, head and neck cancers, and non-Hodgkins lymphomas; followed in 1974 with MUTAMYCIN® (mitomycin) for bone cancer and stomach and pancreas tumors; in 1976 with CEENU® (lomustine), a chemotherapy product for brain cancer and Hodgkins lymphoma; in 1977 with BICNU (carmustine), for treatment of brain and lymphatic cancers; and in 1978 with anticancer agents PLATINOL and LYSODREN (mitotane).

1973

Squibb researchers Miguel A. Ondetti (on left) and David W. Cushman created CAPOTEN (captopril)®; the first in a new class of high blood pressure agents called ACE (angiotensin-converting enzyme) inhibitors. CAPOTEN was an important new medical discovery for the treatment of patients with high blood pressure.

1975

Squibb sold a dental bandage in the 1970s that maintained its stickiness on warm, moist surfaces. At the time, ostomy patients were forced to use irritating substances such as rubber cement and adhesive tape to secure their ostomy pouches to their bodies. Squibb formed ConvaTec as a separate division in 1978 to develop adhesive skin barriers and products that could give people with an ostomy new freedom. Headquartered in Skillman, New Jersey, ConvaTec grew into a global company with 3,000 employees in 100 countries.

1978

Bristol-Myers marketed VEPESID® (etoposide) for cancer.

1983

Bristol-Myers opened a state-of-the-art research complex in Wallingford, Connecticut, designed to house more than 800 scientists and support staff. In 1995, this facility was named the Richard L. Gelb Center for Pharmaceutical Research and Development after the former Bristol-Myers chairman and CEO.

1986

Bristol-Myers merged with Squibb, creating a global leader in the health care industry. The merger created Bristol-Myers Squibb company, which was then the world’s second-largest pharmaceutical enterprise.

1989

PARAPLATIN® (carboplatin) was approved for the treatment of recurrent ovarian cancer.

The U.S. Food and Drug Administration approved VIDEX® (didanosine).

VIDEX® (didanosine)
Prescribing Information including Boxed WARNINGS
Medication Guide

1991

Approvals in 1991 included two cardiovascular medicines, PRAVACHOL® (pravastin sodium) and MONOPRIL® (fosinopril sodium).

PRAVACHOL® (pravastatin sodium)
Prescribing Information

Bristol-Myers Squibb developed a new compound, TAXOL® (paclitaxel). The company invested hundreds of millions of dollars to supply TAXOL for clinical trials, prepare data for regulatory submission and develop alternative sources of TAXOL (which originally derived from the bark of the endangered Pacific Yew tree). TAXOL launched in 1993.

An antibiotic, CEFZIL® (cefprozil) was approved in 1992.

1992

The company completed its acquisition of Union Pharmacologique Scientifique Appliquee (UPSA), a leading manufacturer of pharmaceutical and consumer medicines, based in France. It acquired GLUCOPHAGE® (metformin hydroxchloride), from Lipha Pharmaceuticals, Inc. and received FDA approval of ZERIT® (stavudine).

GLUCOPHAGE® (metformin hydrochloride)
Prescribing Information

ZERIT® (stavudine)
Prescribing Information including Boxed WARNINGS
Medication Guide

1994

The company had more than 60 product lines with $50 million or more in annual sales worldwide. PRAVACHOL® (pravastatin sodium) granted expanded usage from the FDA.

PRAVACHOL® (pravastin sodium)
Prescribing Information including Boxed WARNINGS

1995

The company opened a 433-acre research campus in Hopewell, New Jersey. Two important new medicines codeveloped with Sanofi-Sythelabo received approvals: AVAPRO® (irbesartan) and PLAVIX® (clopidogrel bisulfate).PLAVIX® would become the company’s leading product.PLAVIX® (clopidogrel bisulfate)
Prescribing Information including Boxed WARNING Medication Guide
Product Website

1997

 

The FDA granted clearance to market EXCEDRIN® Migraine for the relief of migraine headache pain and associated symptoms. Excedrin became the first migraine headache medication available to consumers without a prescription.

1998

President Bill Clinton awarded the National Medal of Technology to Bristol-Myers Squibb —America’s highest honor for technological innovation—“for extending and enhancing human life through innovative pharmaceutical research and development, and for redefining the science of clinical study through groundbreaking and hugely complex clinical trials that are recognized models in the industry.”

Bristol-Myers Squibb announced SECURE THE FUTURE®, a $100 million commitment to advance HIV/AIDS research and community outreach programs in seven African countries: Botswana, Namibia, Lesotho, Swaziland, Uganda, Burkina Faso and Tanzania.

1999

Bristol-Myers Squibb, together with four other pharmaceutical companies and international agencies, joined the UNAIDS Drug ACCESS Initiative. The ACCESS program aimed to make antiretroviral medicines and therapies more widely available in African countries by reducing prices. The company offered to lower the prices of HIV/AIDS medicines in those countries by 90 percent.

2000

Bristol-Myers Squibb committed $15 million for extending SECURE THE FUTURE® to four Western African countries—Burkina Faso, Côte d’Ivoire, Mali and Senegal.

Bristol-Myers Squibb announced a new strategy that included a sharpened focus on medicines and an aggressive external development program. As part of this new strategy, the company sold its Clairol business.

The company launched GLUCOVANCE® (glyburide and metformin hydrochloride), a single-pill combination of metformin and glyburide. It also launched GLUCOPHAGE XR (metformin hydrochloride), a once-daily formulation of GLUCOPHAGE.

GLUCOVANCE® (glyburide and metformin hydrochloride)
Prescribing Information 

GLUCOPHAGE® (metformin hydrochloride)
Prescribing Information

GLUCOPHAGE® XR EXTENDED RELEASE (metformin hydrochloride)
Prescribing Information

Bristol-Myers Squibb was chosen “America’s Most Admired Pharmaceutical Company” by FORTUNE Magazine.

2001

The Bristol-Myers Squibb Children’s Hospital opened in March 2001 as part of the Robert Wood Johnson University Hospital in New Brunswick, New Jersey. The first freestanding children’s hospital in the state, the hospital offered care without regard to the family’s ability to pay and offered more than 45 pediatric specialties.

The company announced the purchase of DuPont Pharmaceuticals Company for $7.8 billion with the intention to further strengthen Bristol-Myers Squibb’s medicines business. With the DuPont acquisition, Bristol-Myers Squibb added SUSTIVA® (efavirenz) and COUMADIN® (warfarin sodium) to its portfolio. The company also acquired Bristol-Myers Squibb Medical Imaging.

SUSTIVA® (efavirenz)
Prescribing Information 
Product Website

COUMADIN® (warfarin sodium)
Prescribing Information including Boxed WARNING Medication Guide
Product Website

The U.S. FDA approved ABILIFY® (aripiprazole) in November. It was jointly marketed in the U.S. by Bristol-Myers Squibb and Otsuka America Pharmaceutical.

ABILIFY® (aripiprazole)
Prescribing Information including Boxed WARNINGS
Medication Guide
Product Website

2002

The company sponsored the Bristol-Myers Squibb TOUR OF HOPE™, an unprecedented week-long coast-to-coast cycling event. En route, the 26-member team of cancer survivors, caregivers, physicians, nurses and researchers raised awareness of cancer research and the importance of clinical trials in developing new treatments. Building on the success of the 2003 event, Bristol-Myers Squibb again to sponsored the 2004 Tour of Hope coast-to-coast cycling event.

2003

In July, REYATAZ® (atazanavir sulfate) was introduced in the U.S.

REYATAZ® (atazanavir sulfate)
Prescribing Information
Product Website

In February, the U.S. FDA approved ERBITUX® (cetuximab), co-developed and co-marketed with ImClone Systems Incorporated.

ERBITUX® (cetuximab)
Prescribing Information including Boxed WARNINGS
Product Website

2004

in March, the U.S. FDA approved BARACLUDE® (entecavir). In late December, the U.S. FDA approved ORENCIA® (abatacept).

BARACLUDE® (entecavir)
Prescribing Information including Boxed WARNINGS
Product Website

ORENCIA® (abatacept)
Prescribing Information 
Product Website

2005

The U.S. FDA approved SPRYCEL®(dasatinib) in June.

SPRYCEL®(dasatinib)
Prescribing Information
Product Website

2006

In July, Bristol-Myers Squibb and Gilead Sciences announced the U.S. FDA approval of ATRIPLA® (efavirenz 600 mg/emtricitabine 200 mg/tenofovir disoproxil fumarate 300 mg).

ATRIPLA® (efavirenz/emtricitabine/tenofovir disoproxil fumarate)
Prescribing Information including Boxed WARNINGS
Product Website

Bristol-Myers Squibb announced a new strategy to transform itself from a midcap pharmaceutical company to a next-generation BioPharma company focused on the discovery and development of innovative medicines to fight serious diseases. To accelerate this transformation, the company introduced the String of Pearlsapproach to complement and enhance its internal capabilities with a suite of innovative alliances, partnerships and acquisitions with small and large companies.

2007

In October, Bristol-Myers Squibb announced U.S. FDA approval of IXEMPRA™(ixabepilone).

IXEMPRA™(ixabepilone)
Prescribing Information including Boxed WARNING
Product Website

Bristol-Myers Squibb acquired Adnexus Therapeutics, developer of a new class of biologics called Adnectins™. The acquisition helped advance Bristol-Myers Squibb’s biologics strategy across multiple therapeutic areas and included a Phase I oncology biologic, CT-322. Adnexus was the first acquisition in the company’s String of Pearls strategy, which aims to accelerate the discovery and development of new therapies with innovative alliances, partnerships and acquisitions.

Underscoring its worldwide commitment to children with HIV/AIDS, Bristol-Myers Squibb opened a new clinical center at the Bristol-Myers Squibb Children’s Hospital at Robert Wood Johnson University Hospital in New Brunswick, New Jersey. Dedicated to the research and treatment of children’s immune system disorders and infectious diseases, the Bristol-Myers Squibb Pediatric Infectious Disease and Immunology Center was made possible by a $5 million gift from the Bristol-Myers Squibb Foundation.

Bristol-Myers Squibb sold its Medical Imaging business to the private equity firm Avista Capital Partners for $525 million, as part of its effort to focus on its core pharmaceutical pipeline. Bristol-Myers Squibb also sold its ConvaTec business unit to Nordic Capital Fund VII and Avista Capital Partners for $4.1 billion. ConvaTec was a world leader in the development and marketing of innovative wound therapeutics and ostomy care products.

2008

Bristol-Myers Squibb announced in April 2008 its plan to sell approximately 10-20 percent of Mead Johnson Nutrition Company stock to the public through an IPO and to retain at least an 80 percent equity interest for the foreseeable future. This announcement, in addition to the Medical Imaging and ConvaTec sales, was part of the BioPharma transformation to better focus Bristol-Myers Squibb on its biopharmaceutical business.

Bristol-Myers Squibb entered into an exclusive agreement with KAI Pharmaceuticals, Inc., a privately held biotechnology company, to globally develop and commercialize a therapy for cardiovascular diseases.

Bristol-Myers Squibb purchased Kosan Biosciences, a cancer therapeutics company based in California, for approximately $190 million. This acquisition enhanced the company’s pipeline with compounds in two important classes of anticancer agents.

Bristol-Myers Squibb entered into an exclusive agreement with PDL BioPharma of Redwood City, California to develop and globally commercialize a therapy for multiple myeloma.

Bristol-Myers Squibb entered into a global collaboration with Exelixis, a biotechnology company based in San Francisco, California, to develop and commercialize two novel therapies: one for medullary thyroid cancer and the other as a treatment for advanced solid tumor malignancies.

 

Bristol-Myers Squibb entered into a global collaboration with ZymoGenetics of Seattle, Washington to develop and commercialize PEG-Interferon lambda, a new treatment for hepatitis C.

2009

Bristol-Myers Squibb entered into a global collaboration with Nissan Chemical Industries and Teijin Pharma for the development and commercialization of an oral atrial-selective antiarrhythmic medication.

In late July, Bristol-Myers Squibb announced the FDA approval of ONGLYZA™ (saxagliptin).

ONGLYZA™ (saxagliptin)
Prescribing Information
Product Website

Bristol-Myers Squibb acquired Medarex Inc., a biotech company and a partner since 2005. This acquisition was the largest String of Pearls transaction to date, and significantly expanded Bristol-Myers Squibb’s oncology and immunology pipeline, positioned the company for long-term leadership in biologics and allowed it to gain full rights for ipilimumab.

Bristol-Myers Squibb entered into a global collaboration with Alder Biopharmaceuticals Inc. of Bothell, Washington, to develop and commercialize a novel investigational biologic for the treatment of rheumatoid arthritis.

On December 23, the company completed its strategic split-off of its shares of Mead Johnson. The split-off focuses Bristol-Myers Squibb completely on its biopharmaceutical business, and completed the company’s transformation to a BioPharma leader.

Bristol-Myers Squibb and Allergan, Inc. announced a global agreement for the development and commercialization of an oral medication for the treatment of neuropathic pain.

2010

In November, KOMBIGLYZE™ XR (saxagliptin and metformin HCL extended release) approved in the U.S.

KOMBIGLYZE™ XR (saxagliptin and metformin HCL extended release)
Prescribing Information including Boxed WARNINGS

In December, Bristol-Myers Squibb acquired the worldwide rights from Oncolys BioPharma Inc. to manufacture, develop and commercialize festinavir, a once-a-day, orally available nucleoside reverse transcriptase inhibitor.

In March, YERVOY™ (ipilimumab) was approved by the U.S. FDA.

YERVOY™ (ipilimumab)
Prescribing Information including Boxed WARNING
Medication Guide
REMS Materials
Product Website

2011

In June, NULOJIX® (belatacept) was approved by the U.S. FDA.

NULOJIX® (belatacept)
Prescribing Information including Boxed WARNINGS 
Medication Guide
REMS Materials
Product Website

In July, Bristol-Myers Squibb and Innate Pharma announced a global agreement for the development and commercialization of an investigational immuno-oncology biologic.

In September, Bristol-Myers Squibb acquired Amira Pharmaceuticals, a small-molecule pharmaceutical company focused on the discovery and early development of new drugs to treat inflammatory and fibrotic diseases.

In September, Bristol-Myers Squibb and Ono Pharmaceutical Co., Ltd., entered into a strategic agreement to expand Bristol-Myers Squibb’s territorial rights to an investigational cancer immunotherapy, an anti-PD-1 antibody, and for the co-development and co-commercialization of Orencia in Japan.

ORENCIA® (abatacept)
Prescribing Information 
Product Website

In September, Bristol-Myers Squibb and Ambrx, Inc., announced a collaboration to research, develop and commercialize novel biologics programs in diabetes and heart failure.

In October, Bristol-Myers Squibb and Gilead Sciences, announced licensing agreement for development and commercialization of new fixed-dose combination pill for people living with HIV.

In November, Bristol-Myers Squibb and ASLAN Pharmaceuticals announced an innovative partnership to license and develop an investigational oncology compound.

In February 2012, Bristol-Myers Squibb acquired Inhibitex, Inc.

2012

In August 2012, Bristol-Myers Squibb acquired Amylin Pharmaceuticals, a biopharmaceutical company focused on the research, development and commercialization of a franchise of GLP-1 agonists for the treatment of type 2 diabetes.

In December, ELIQUIS® (apixaban) was approved by the U.S. FDA.

ELIQUIS® (apixaban)
Prescribing Information including Boxed WARNING
Medication Guide
REMS Materials
Product Website

In February 2014, Bristol-Myers Squibb sold its global diabetes business to AstraZeneca. The transaction includes the rights to Bristol-Myers Squibb’s global diabetes business that was part of its collaboration with AstraZeneca, the former Amylin manufacturing facility in West Chester, Ohio, and also covers the future purchase by AstraZeneca of Bristol-Myers Squibb’s Mount Vernon, Indiana, manufacturing facility approximately 18 months following the close of the deal.

2014

SOURCE

http://www.bms.com/ourcompany/Pages/history.aspx

 

Key Facts

Chief Executive Officer:	Lamberto Andreotti
Headquarters:	New York City
Business:	Biopharmaceuticals
Web Address:	www.bms.com
NYSE Listing:	BMY
Net Sales:	$16.4 billion in 2013
R&D Investment:	$3.7 billion in 2013
2013 Largest-Selling Products:	ABILIFY®, $2.3 billion SUSTIVA® franchise, $1.6 billion REYATAZ®, $1.6 billion BARACLUDE®, $1.5 billion ORENCIA® $1.4 billion SPRYCEL® $1.3 billion YERVOY® $960 million
Selected Key Products:	ABILIFY® (aripiprazole) ATRIPLA® (efavirenz / emtricitabine / tenofovir disoproxil fumarate) BARACLUDE® (entecavir) ELIQUIS® (apixaban) ERBITUX® (cetuximab) NULOJIX® (belatacept) ORENCIA® (abatacept) REYATAZ® (atazanavir sulfate) SPRYCEL® (dasatinib) SUSTIVA® (efavirenz) YERVOY® (ipilimumab)
Principal Locations:	Worldwide Facilities

 

Please click on the product links to see the Full Prescribing Information for ABILIFY®, ATRIPLA®,BARACLUDE®, ELIQUIS®, ERBITUX®, NULOJIX®, ORENCIA®, PLAVIX®, REYATAZ®, SPRYCEL®,SUSTIVA®, and YERVOY®, including Boxed WARNINGS for ABILIFY®, ATRIPLA®, BARACLUDE®,ELIQUIS®, NULOJIX®, and Boxed WARNINGS for YERVOY® regarding immune-mediated adverse reaction and Boxed WARNINGS for ERBITUX® regarding infusion reactions and cardiopulmonary arrest.

 

February, 2014

SOURCE

http://www.bms.com/ourcompany/Pages/keyfacts.aspx

Achievements What sets Bristol-Myers Squibb apart? It’s our commitment to patients with serious diseases, and our focus on finding innovative medicines to combat those diseases.Over the years, Bristol-Myers Squibb and its employees have received numerous distinguished awards and recognitions, including the National Medal of Technology, the Lasker Award for Medical Research and the Prix Galien Award. Also, we’ve been hailed year after year as one of the best companies for working mothers, a great place to work for scientists and an acknowledged industry leader in environment, health and safety. Below is a selection of awards and recognitions we have received. In April 2014, Bristol-Myers Squibb ranked first among health care companies on Corporate Responsibility magazine’s 2014 list of the 100 Best Corporate Citizens. Bristol-Myers Squibb is the only company to achieve the No. 1 ranking three times, including 2009 and 2012, and has ranked among the top 10 each of the last six years. In September 2013, Bristol-Myers Squibb was recognized as one of the 2013 Working Mother 100 Best Companies – marking the 16th consecutive year that our company has made the list. The company was recognized for its commitment to progressive workplace programs, such as child care, flexibility and paid family leave. In May, Bristol-Myers Squibb received a 2013 Environmental Tracking (ET) Carbon Ranking Leader Award as a result of being named a top 10 company in the 2013 ET North America 300 Carbon Ranking report, issued by the Environmental Investment Organization. Our company ranked in the top 30 in the 2013 ET Global 800 Carbon Ranking. In April, Bristol-Myers Squibb was chosen as one of the 2013 Top 50 Companies for Diversity by Diversity Inc. The ranking is based on a company’s answers to a detailed survey divided into four equally weighted areas: CEO Commitment, Human Capital, Corporate and Organizational Communications and Supplier Diversity. This year, 893 companies participated in the survey. For the eighth year in a row, Bristol-Myers Squibb received the top rating of 100 percent in the Corporate Equality Index. The report, released annually by theHuman Rights Campaign Foundation — the nation’s largest lesbian, gay, bisexual and transgender civil rights organization — provides an in-depth analysis and rating of large U.S. employers and their policies and practices. This year’s index rated 688 businesses. In February 2013, the National Association for Female Executives selected Bristol-Myers Squibb as one of the Top 50 Company for Executive Women, for the 11th consecutive year. Companies on this year’s list of 50 companies must have at least two women on the board of directors, a significant number of women in senior ranks and programs and policies that support women’s advancement. In July 2012, Ethisphere Institute, a leading international think-tank dedicated to the research and promotion of best practices in corporate ethics and compliance, awarded Bristol-Myers Squibb the Compliance Leader Verification Award. The award recognizes companies with best-in-industry ethics and compliance programs — those organizations that have made the decision to proactively invest resources in compliance, sending a clear signal to key stakeholders that compliance and ethics are an absolute organizational priority. In 2011, Bristol-Myers Squibb received a Prime Company rating for the fourth time in a row from oekom research, a leading European sustainability rating firm. Using social and environmental criteria, Prime Status is awarded to companies that are among the leaders in their industry. Bristol-Myers Squibb was recognized as 78th among 500 of America’s largest corporations in Newsweek’s 2012 Green Rankings. In January 2011, Bristol-Myers Squibb was recognized by R&D Directions magazine as having the “Most Innovative Pipeline” within the pharmaceutical industry. According to a report released by the Roberts Environmental Center at Claremont McKenna College, Bristol-Myers Squibb earned the highest score in the pharmaceutical sector for sustainability reporting. The report compiled Pacific Sustainability Index scores evaluating the environmental and social reporting of the 26 largest pharmaceutical companies worldwide. Bristol-Myers Squibb was recognized as the 2009 Trailblazer Company of the Yearby PM360 magazine. Among the criteria for selection were civic involvement, patient access, environmental consciousness, employee development and innovation. Our corporate website was recognized with the Best in Class award for a pharmaceutical company in 2009 by the Interactive Media Awards. Bristol-Myers Squibb was recognized in the 2009 Dow Jones Sustainability North America Index of leading sustainability-driven companies. Bristol-Myers Squibb’s Investor Relations department was rated the best in the pharmaceutical business by investors polled by Institutional Investor magazine, a leading international business-to-business publisher focused primarily on international finance. Bristol-Myers Squibb awarded the Allicense 2009 Breakthrough Alliance Award for collaboration with Exelixis. This is the second year in a row that the company has been presented with this prestigious recognition, which honors the world’s best and most innovative partnerships between biotechnology and pharmaceutical companies. FORTUNE China named Bristol-Myers Squibb China a Top Ten Green Company for 2009 in recognition of Bristol-Myers Squibb’s hepatitis awareness, prevention and care efforts in Asia. Since 2002, Bristol-Myers Squibb China has partnered with the Bristol-Myers Squibb Foundation and local non-profit organizations on 11 hepatitis prevention and control projects that have directly benefited seven million people. Barron’s 2009 Most Respected Companies Survey includes Bristol-Myers Squibb as theworld’s 40th most respected company. The survey reflects opinions of money managers for the 100 largest public companies in the world based on stock market capitalization. A variety of attributes contribute to the overall score, including strong management, sound business strategy, ethical practices and financial performance. Calvert, a leader in socially responsible investing, has created the Calvert Social Index®, a broad-based, rigorously constructed benchmark for measuring the performance of socially responsible companies. Calvert’s Social Research Department analyzes the top 1,000 largest U.S. companies annually. Bristol-Myers Squibb has been on its Social Index of companies since 2003. The Asian American Legal Defense and Education Fund honored Sandra Leung, senior vice president, general counsel and corporate secretary, as a recipient of its 2009 Justice in Action Award. The award, which recognizes exceptional individuals for their outstanding achievements and contributions in advancing justice and equality, was presented in March in New York. The Division of Medicinal Chemistry of the American Chemical Society will present John E. Macor, executive director, Neuroscience Discovery Chemistry, Research and Development, with the 2009 Robert M. Scarborough Memorial Award. This prestigious achievement recognizes scientists under the age of 50 who have documented success in the discovery of pharmaceutical compounds and who have made significant research contributions in medicinal chemistry. Macor was cited for the discovery of an anti-migraine medicine as well as a number of other clinical discoveries. The society will bestow the award at its annual meeting later this year.

SOURCE

http://www.bms.com/responsibility/Pages/achievements.aspx

Other related articles published in this Open Access Online Scientific Journal include the following:

 

Coagulation Therapy: Leading New Drugs – Efficacy Comparison

Curator: Aviva Lev-Ari, PhD, RN

http://pharmaceuticalintelligence.com/2014/05/10/coagulation-therapy-leading-new-drugs-efficacy-comparison/

 

Apixaban (Eliquis): Mechanism of Action, Drug Comparison and Additional Indications

Curator: Aviva Lev-Ari, PhD, RN

http://pharmaceuticalintelligence.com/2014/05/10/apixaban-eliquis-mechanism-of-action-drug-comparison-and-additional-indications/

 

 

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Epilogue: Volume 4 – Translational, Post-Translational and Regenerative Medicine in Cardiology

Posted in Acute Myocardial Infarction, Bone marrow derived cells, Cardiac & Vascular Repair Tools Subsegment, Cell Biology, Signaling & Cell Circuits, Computational Biology/Systems and Bioinformatics, Curation, Disease Biology, Small Molecules in Development of Therapeutic Drugs, Drug Delivery Platform Technology, Experimental validation, Frontiers in Cardiology and Cardiovascular Disorders, Genome Biology, Hematopoiesis, Mechanical Assist Devices: LVAD, RVAD, BiVAD, Artificial Heart, Molecular Genetics & Pharmaceutical, Origins of Cardiovascular Disease, PCI, Regenerative Biology and Medicine, Regulated Clinical Trials: Design, Methods, Components and IRB related issues, Stents & Tools, tagged ACS, AMI, Atrial fibrillation, cell regulatory processes, miRNA, myocardial remodelling, myocardial repair, NT-proBNP risk ratio, Omega 3 index, stem cells, ventricullar tachyarrhythmia on May 12, 2014| Leave a Comment »

Epilogue: Volume 4 – Translational, Post-Translational and Regenerative Medicine in Cardiology

• Larry H Bernstein, MD, FCAP, Author and Curator, Volume Four, Co-Editor
• Justin Pearlman, MD, PhD, FACC, Content Consultant for Series A: Cardiovascular Diseases
• Aviva Lev-Ari, PhD, RN, Co-Editor of Volume Four and Editor-in-Chief, BioMed e-Series

 

This completes Chapter 4 in two parts on the most dynamic developments in the regulatory pathways guiding cardiovascular dynamics and function in health and disease.  I have covered key features of these in two summaries, so I shall try to look further into important expected future directions and their anticipated implications.

1. Mechanisms of Disease

Signal Transduction: Akt Phosphorylates HK-II at Thr-473 and Increases Mitochondrial HK-II Association to Protect Cardiomyocytes

David J. Roberts, Valerie P. Tan-Sah, Jeffery M. Smith and Shigeki Miyamoto
J. Biol. Chem. 2013, 288:23798-23806.  http://dx.doi.org/ 10.1074/jbc.M113.482026

Backgound: Hexokinase II binds to mitochondria and promotes cell survival.
Results: Akt phosphorylates HK-II but not the threonine 473 mutant. The phosphomimetic T473D mutant decreases its dissociation from mitochondria induced by G-6P and increases cell viability against stress.
Conclusion: Akt phosphorylates HK-II at Thr-473, resulting in increased mitochondrial HK-II and cell protection.
Significance: The Akt-HK-II signaling nexus is important in cell survival.

HK-II Phosphorylation

 

 

 

 

 

 

It has been demonstrated that an increased level of HK-II at mitochondria is protective and is increased by protective interventions but decreased under stress.

It   has not  been fully determined   which  molecular  signals  regulate  the    level    of  HK-II at mitochondria.

Thr-473 in HK-II  is phosphorylated by Akt and this phosphorylation  leads to  increases  in  mitochondrial  HK-II binding  through inhibition  of  G-6P-dependent  dissociation, conferring resistance to oxidative stress  (Fig.     7).

Overexpression of  WTHK-II increases mitochondrial HK-II and confers protection against  hydrogen peroxide,  which  is enhanced significantly  in   HK-II   T473D-expressing  cells, whereas  NHK-II, lacking the ability to bind to mitochondria, does not confer protection.   Conversely,  mitochondrial  HK-II from mitochondria (Fig.6, A and B) inhibits  the  IGF-1-mediated increase in mitochondrial HK-II and cellular protection.   Similar   dose-dependent  curves were obtained in mitochondrial   HK-II     against stress    (15–25).

Gene Expression and Genetic Variation in Human Atria

Honghuang Lin PhD, Elena V. Dolmatova MD, Michael P. Morley, PhD, Kathryn L. Lunetta PhD, David D. McManus MD, ScM, et al.
Heart Rhythm  2013   http://dx.doi.org/10.1016/j.hrthm.2013.10.051

Background— The human left and right atria have different susceptibilities to develop atrialfibrillation (AF). However, the molecular events related to structural and functional changes that
enhance AF susceptibility are still poorly understood.
Objective— To characterize gene expression and genetic variation in human atria.
Results— We found that 109 genes were differentially expressed between left and right atrial tissues. A total of 187 and 259 significant cis-associations between transcript levels and genetic
variants were identified in left and right atrial tissues, respectively. We also found that a SNP at a known AF locus, rs3740293, was associated with the expression of MYOZ1 in both left and right
atrial tissues.
Conclusion— We found a distinct transcriptional profile between the right and left atrium, and extensive cis-associations between atrial transcripts and common genetic variants. Our results
implicate MYOZ1 as the causative gene at the chromosome 10q22 locus for AF.

Long-Term Caspase Inhibition Ameliorates Apoptosis, Reduces Myocardial Troponin-I Cleavage, Protects Left Ventricular Function, and Attenuates Remodeling in Rats With Myocardial Infarction

Y. Chandrashekhar,  Soma Sen, Ruth Anway,  Allan Shuros,  Inder Anand,

J Am Col  Cardiol  2004; 43(2)   http://dx.doi.org/10.1016/j.jacc.2003.09.026

This study was designed to evaluate whether in vivo caspase inhibition can prevent myocardial contractile protein degradation, improve myocardial function, and attenuate ventricular remodeling.
Apoptosis is thought to play an important role in the development and progression of heart failure (HF) after a myocardial infarction (MI). However, it is not known whether inhibiting apoptosis can attenuate left ventricular (LV) remodeling and minimize systolic dysfunction.

A 28-day infusion of caspase inhibitor was administeredimmediately after an anterior MI. In addition, five sham-operated rats given the caspase inhibitor were compared with 17 untreated sham-operated animals to study effects in non-MI rats. Left ventricular function, remodeling parameters, and hemodynamics were studied four weeks later. Myocardial caspase 3 activation and troponin-I contractile protein cleavage were studied in the non-infarct, remote LV myocardium using Western blots. Apoptosis was assessed using immunohistochemistry for activated caspase-positive cells as well as the TUNEL method. Collagen volume was estimated using morphometry.

Caspase inhibition reduced myocardial caspase 3 activation. This was accompanied by less cleavage of troponin-I, an important component of the cardiac contractile apparatus, and fewer apoptotic cardiomyocytes. Furthermore, caspase inhibition reduced LV-weight-to- body-weight ratio, decreased myocardial interstitial collagen deposition, attenuated LV remodeling, and better preserved LV systolic function after MI.

Caspase inhibition, started soon after MI and continued for four weeks, preserves myocardial contractile proteins, reduces systolic dysfunction, and attenuates ventricular remodeling.

These findings may have important therapeutic implications in post-MI HF. J Am Col Cardiol 2004;43:295–301)

Precardiac deletion of Numb and Numblike reveals renewal of cardiac progenitors

Lincoln T Shenje,  Peter P Rainer , Gun-sik Cho , Dong-ik Lee , Weimin Zhong , Richard P Harvey , David A Kass , Chulan Kwon *,  et al.
eLife 2014.    http://dx.doi.org/10.7554/eLife.02164.001

Cardiac progenitor cells (CPCs) must control their number and fate to sustain the rapid heart growth during development, yet the intrinsic factors and environment governing these processes remain unclear. Here, we show that deletion of the ancient cell-fate regulator Numb (Nb) and its homologue Numblike (Nbl) depletes CPCs in second pharyngeal arches (PA2s) and is associated with an atrophic heart. With histological, fow cytometric and functional analyses, we fnd that CPCs remain undifferentiated and expansive in the PA2, but differentiate into cardiac cells as they exit the arch. Tracing of Nb- and Nbl-defcient CPCs by lineage-specifc mosaicism reveals that the CPCs normally populate in the PA2, but lose their expansion potential in the PA2. These fndings demonstrate that Nb and Nbl are intrinsic factors crucial for the renewal of CPCs in the PA2 and
that the PA2 serves as a microenvironment for their expansion.

2. Diagnostics and Risk Assessment

Classical and Novel Biomarkers for Cardiovascular Risk Prediction in the United States

Aaron R. Folsom
J Epidemiol 2013;23(3):158-162   http://dx.doi.org/10.2188/jea.JE20120157

Cardiovascular risk prediction models based on classical risk factors identified in epidemiologic cohort studies are useful in primary prevention of cardiovascular disease in individuals. This article briefly reviews aspects of
cardiovascular risk prediction in the United States and efforts to evaluate novel risk factors. Even though many novel risk markers have been found to be associated with cardiovascular disease, few appear to improve risk prediction
beyond the powerful, classical risk factors. A recent US consensus panel concluded that clinical measurement of certain novel markers for risk prediction was reasonable, namely,

1. hemoglobin A1c (in all adults),
2. microalbuminuria (in patients with hypertension or diabetes), and
3. C-reactive protein,
4. lipoprotein-associated phospholipase,
5. coronary calcium,
6. carotid intima-media thickness, and
7. ankle/brachial index (in patients deemed to be at intermediate cardiovascular risk, based on traditional risk factors).

Diagnostic accuracy of NT-proBNP ratio (BNP-R) for early diagnosis of tachycardia-mediated cardiomyopathy: a pilot study

Amir M. Nia, Natig Gassanov, Kristina M. Dahlem, Evren Caglayan, Martin Hellmich, et al.
Clin Res Cardiol (2011) 100:887–896    http://dx.doi.org/10.1007/s00392-011-0319-y

Tachycardia-mediated cardiomyopathy (TMC) occurs as a consequence of prolonged high heart rate due to ventricular and supraventricular tachycardia. In animal models, rapid pacing induces severe biventricular remodeling with dilation and dysfunction [7]. On a cellular basis, cardiomyocytes exert fundamental morphological and functional roles.

When heart failure and tachycardia occur simultaneously, a useful diagnostic tool for early discrimination of patients with benign tachycardia-mediated  cardiomyopathy (TMC) versus major structural heart disease  (MSHD) is not available. Such a tool is required to prevent unnecessary and wearing diagnostics in patients with reversible TMC. Moreover, it could lead to early additional diagnostics and therapeutic approaches in patients with  MSHD.

A total of 387 consecutive patients with supraventricular arrhythmia underwent assessment.  Of these patients, 40 fulfilled the inclusion criteria
with a resting heart rate C100 bpm and an impaired left ventricular ejection fraction \40%. In all patients, successful electrical cardioversion was performed. At baseline, day 1 and weekly for 4 weeks, levels of NT-proBNP and echocardiographic parameters were evaluated.

NT-proBNP ratio (BNP-R) was calculated as a quotient of baseline NT-proBNP/follow-up NT-proBNP. After 4 weeks, cardiac catheterization was performed to identify patients with a final diagnosis of TMC versus MSHD.

Initial NT-proBNP concentrations were elevated and consecutively decreased after cardioversion in all patients studied. The area under the ROC curve for BNP-R to detect TMC was 0.90 (95% CI 0.79–1.00; p \ 0.001) after 1 week  and 0.995 (95% CI 0.99–1.00; p \ 0.0001) after 4 weeks. One week after cardioversion already, a BNP-R cutoff C2.3 was useful for TMC diagnosis indicated by an accuracy of 90%, sensitivity of 84% and specificity of 95%.

BNP-R was found to be highly accurate for the early diagnosis of TMC.

Omega-3 Index and Cardiovascular Health

Clemens von Schacky
Nutrients 2014; 6: 799-814;  http://dx. doi.org/10.3390/nu602099

Fish, marine oils, and their concentrates all serve as sources of the two marine omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), as do some products from algae.
To demonstrate an effect of EPA + DHA on heart health, a number of randomized, controlled intervention studies with clinical endpoints like overall mortality or a combination of adverse cardiac events were conducted in populations with elevated cardiovascular risk. One early intervention study with oily fish, rich in EPA + DHA, and some early studies with fish oil or fish oil concentrate or even purified EPA at doses ranging between 0.9 and 1.8 g/day indeed demonstrated effects in terms of fewer sudden cardiac deaths, fatal or non-fatal myocardial infarctions, or a combination of adverse cardiac events.

Recent meta-analyses found no significant benefits on total mortality, cardiovascular mortality, and other adverse cardiac or cardiovascular events [13–18]. This is in contrast to findings in epidemiologic studies, where intake of EPA + DHA had been found to correlate generally with an up to 50% lower incidence of adverse cardiac events [18,19], and in even sharper contrast to epidemiologic studies based on levels of EPA + DHA, demonstrating e.g., a 10-fold lower incidence of sudden cardiac death associated with high levels of the
fatty acids, as compared to low levels.

This seemingly contradictory evidence has led the American Heart Association to recommend “omega-3 fatty acids from fish or fish oil capsules (1 g/day) for cardiovascular disease risk reduction” for secondary prevention, whereas the European Society for Cardiology recommends “Fish at least twice a week, one of which to be oily fish”, but no supplements for cardiovascular prevention.

A similar picture emerges for atrial fibrillation: In epidemiologic studies, consumption of EPA + DHA or higher levels of EPA + DHA were associated with lower risk for developing atrial fibrillation, while intervention studies found no effect. Pertinent guidelines do not mention EPA + DHA. A similar picture also emerges for severe ventricular rhythm disturbances.

Why is it that trial results are at odds with results from epidemiology? What needs to be done to better translate the epidemiologic findings into trial results? The current review will try to shed some light on this  issue, with a special consideration of the Omega-3 Index.

Recent large trials with eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in the cardiovascular field did not demonstrate a beneficial effect in terms of reductions of clinical endpoints like

• total mortality,
• sudden cardiac arrest or
• other major adverse cardiac events.

Pertinent guidelines do not uniformly recommend EPA + DHA for cardiac patients. In contrast,

• in epidemiologic findings, higher blood levels of EPA + DHA were consistently associated with a lower risk for the endpoints mentioned.

The following points argue for the use of erythrocytes: erythrocyte fatty acid
composition has a low biological variability, erythrocyte fat consists almost exclusively of phospholipids, erythrocyte fatty acid composition reflects tissue fatty acid composition, pre-analytical stability, and other points.  In 2004, EPA + DHA in erythrocyte fatty acids were defined as the Omega-3 Index and suggested as a risk factor for sudden cardiac death [39]. Integral to the definition was a specific and standardized analytical procedure, conforming the quality management routinely implemented in the field of clinical chemistry.

The laboratories adhering to the HS-Omega-3 Index methodology perform regular proficiency testing, as mandated in routine Clinical Chemistry labs. So far, the HS-Omega-3 Index is the only analytical procedure used in several laboratories. A standardized analytical procedure is a prerequisite to generate the data base necessary to transport a laboratory parameter from research into clinical routine. Moreover, standardization of the analytical procedure is the first important criterion for establishing a new biomarker for cardiovascular risk set forth by the American Heart Association and the US Preventive Services Task Force.

Because of low biological and analytical variability, a standardized analytical procedure, a large database and for other reasons,

• blood levels of EPA + DHA are frequently assessed in erythrocytes, using the HS-Omega-3 Index methodology.

Table 1. Mean HS-Omega-3 Index values in various populations, Mean (±standard deviation (SD)). Please note that in every population studied, a lower value was found to be associated with a worse condition than a higher value. References are given, if not, unpublished, n = number of individuals measured.

All levels of fatty acids are determined by the balance of substance entering the body and those leaving the body. Neither a recent meal, even if rich in EPA + DHA, nor severe cardiac events altered the HS-Omega-3 Index. However, while long-term intake of EPA + DHA, e.g., as assessed with food questionnaires, was the main predictor of the HS-Omega-3 Index, long-term intake explained only 12%–25% of its variability. A hereditary component of 24% exists. A number of other factors correlated positively (+) or negatively (−), like age (+), body mass index (−), socioeconomic status (+), smoking (−), but no other conventional cardiac risk factors. More factors determining the level of the HS-Omega-3 Index, especially regarding efflux remain to be  defined. Therefore, it is impossible to predict the HS-Omega-3 Index in an individual, as it is impossible to predict the increase in the HS-Omega-3 Index in an individual in response to a given dose of EPA + DHA. In Table 2, current evidence is presented on the relation of the HS-Omega-3 Index to CV events.

The HS-Omega-3 Index has made it possible to reclassify individuals from intermediate cardiovascular risk into the respective high risk and low risk strata, the third criterion for establishing a new biomarker for CV  risk.

A low Omega-3 Index fulfills the current criteria for a novel cardiovascular risk factor.

Increasing the HS-Omega-3 Index by increased intake of EPA + DHA in randomized controlled trials improved a number of surrogate parameters for cardiovascular risk:

1. heart rate was reduced,
2. heart rate variability was increased,
3. blood pressure was reduced,
4. platelet reactivity was reduced,
5. triglycerides were reduced,
6. large buoyant low-density lipoprotein (LDL)-particles were increased and
7. small dense LDL-particles were reduced,
8. large buoyant high-density lipoproteins (HDL)2 were increased,
9. very low-density lipoprotein (VLDL1) + 2 was reduced,
10. pro-inflammatory cytokines (e.g., tumor necrosis factor alpha, interleukin-1β, interleukins-6,8,10 and monocyte chemoattractant protein-1) were reduced,
11. anti-inflammatory oxylipins were increased.

Importantly, in a two-year randomized double-blind angiographic intervention trial, increased erythrocyte EPA + DHA

• reduced progression and increased regression of coronary lesions, an intermediate parameter.

Taken together, increasing the HS-Omega-3 Index improved surrogate and intermediate parameters for cardiovascular events. A large intervention trial with clinical endpoints based on the HS-Omega-3 Index remains to be conducted. Therefore, the fourth criterion, proof of therapeutic consequence of determining the HS-Omega- Index, is only partially fulfilled.

 

Neutral results of intervention trials can be explained by issues of bioavailability and trial design that surfaced after the trials were initiated.

In the future, incorporating the Omega-3 Index into trial designs by

1. recruiting participants with a low Omega-3 Index and
2. treating them within a pre-specified target range (e.g., 8%–11%),
3. will make more efficient trials possible and
   • provide clearer answers to the questions asked than previously possible.

 

3. Stem Cells and Regenerative Biology

Adult Stem Cells Reverse Muscle Atrophy In Elderly Mice   http://www.science20.com/profile/news_staff

Bioengineers at the University of California, Berkeley in a new study published in Nature say they have identified two key regulatory pathways that control how well adult stem cells repair and replace damaged tissue. They then tweaked how those stem cells reacted to those biochemical signals to revive the ability of muscle tissue in old mice to repair itself nearly as well as the muscle in the mice’s much younger counterparts. Irina Conboy, an assistant professor of bioengineering and an investigator at the Berkeley Stem Cell Center and at the California Institute for Quantitative Biosciences (QB3), led the research team conducting this study. Because the findings relate to adult stem cells that reside in existing tissue, this approach to rejuvenating degenerating muscle eliminates the ethical and medical complications associated with transplanting tissues grown from embryonic stem cells. The researchers focused on

• the interplay of two competing molecular pathways that control the stem cells,

which sit next to the mature, differentiated cells that make up our working body parts. When the mature cells are damaged or wear out, the stem cells are called into action to begin the process of rebuilding.

old muscle tissue is left with

 

 

 

 

 

 

 

 

 

 

 

 

“We don’t realize it, but as we grow our bodies are constantly being remodeled,” said Conboy. “We are constantly falling apart, but we don’t notice it much when we’re young because we’re always being restored. As we age, our stem cells are prevented, through chemical signals, from doing their jobs.” The good news, the researchers said, is that

• the stem cells in old tissue are still ready and able to perform their regenerative function
• if they receive the appropriate chemical signals.

Studies have shown that when old tissue is placed in an environment of young blood, the stem cells behave as if they are young again. “Conversely, we have found in a study published last year that even young stem cells rapidly age when placed among blood and tissue from old mice,” said Carlson, who will stay on at UC Berkeley to expand his work on stem cell engineering.

• Adult stem cells have a receptor called Notch that, when activated,
• tells them that it is time to grow and divide
• stem cells also have a receptor for the protein TGF-beta
• that sets off a chain reaction activatingthemoleculepSmad3 and
  • ultimately producing cyclin-dependent kinase (CDK) inhibitors, which regulate the cell’s ability to divide.
• activated Notch competeswithactivatedpSmad3 for
  • binding to the regulatory regions of the same CDK inhibitors in the stem cell

“We found that Notch is capable of physically kicking off pSmad3 from the promoters for the CDK inhibitors within the stem cell’s nucleus, which tells us that a precise manipulation of the balance of these pathways would allow the ability to control stem cell responses.” Notch and TGF-beta are well known in molecular biology, but Conboy’s lab is the first to connect them to the process of aging, and the first to show that they act in opposition to each other within the nucleus of the adult stem cell. Aging and the inevitable march towards death are, in part, due to the progressive decline of Notch and the increased levels of TGF-beta , producing a one-two punch to the stem cell’s capacity to effectively rebuild the body, the researchers said.

The researchers disabled the “aging pathway” that tells stem cells to stop dividing by using an established method of RNA interference that reduced levels of pSmad3. The researchers then examined the muscle of the different groups of mice one to five days after injury to compare how well the tissue repaired itself. As expected,

•  muscle tissue in the young mice easily replaced damaged cells with new, healthy cells. In contrast,
• the areas of damaged muscle in the control group of old mice were characterized by fibroblasts and scar tissue. However,
• muscles in the old mice whose stem cell “aging pathway”had been dampened showed levels of cellular regeneration that were
  • comparable to their much younger peers, and that were 3 to 4 times greater than those of the group of “untreated” old mice.

Adult Stem Cells To Repair Damaged Heart Muscle

http://www.science20.com/profile/news_staff

In the first trial of its kind in the world, 60 patients who have recently suffered a major heart attack will be injected with selected stem cells from their own bone marrow during routine coronary bypass surgery. The Bristol trial will test

• whether the stem cells will repair heart muscle cells damaged by the heart attack,
• by preventing late scar formation and hence impaired heart contraction.

“ Cardiac stem cell therapy aims to repair the damaged heart as it has the potential to replace the damaged tissue.” We have elected to use a very promising stem cell type selected from the patient’s own bone marrow. This approach ensures no risk of rejection or infection. It also gets around the ethical issues that would result from use of stem cells from embryonic or foetal tissue.

In this trial (known as TransACT), all patients will have bone marrow harvested before their heart operation. Then either stem cells from their own bone marrow or a placebo will be injected into the patients’ damaged hearts during routine coronary bypass surgery. The feasibility and safety of this technique has already been demonstrated. As a result of the chosen double blind placebo-controlled design, neither the patients nor the surgeon knows whether the patient is going to be injected with stem cells or placebo. This ensures that results are not biased in any way, and is the most powerful way to prove whether or not the new treatment is effective.

Research of Stem Cells Repair Damaged Heart

By Kelvinlew Minhan | March 26th 2008

Under highly specific growth conditions in laboratory culture dishes, stem cells

• can be coaxed into developing as new cardiomyocytes and vascular endothelial cells (Kirschstein and Skirboll, 2001).

Discoveries that have triggered the interest in the application of adult stem cells to heart muscle repair in animal models have been made by researchers in the past few years (Kirschstein and Skirboll, 2001). One  study demonstrated that cardiac tissue can be regenerated in the mouse heart attack model through the introduction of adult stem cells from mouse bone marrow (Kirschstein and Skirboll, 2001). These cells were transplanted into the marrow of irradiated mice approximately 10 weeks before the recipient mice were subjected to heart attack thru tying off different major heart blood vessel, the left anterior descending (LAD) coronary artery. The survival rate was 26 percent at two to four weeks after the induced cardiac injury (Kirschstein and Skirboll, 2001). Another study of the region surrounding the damaged tissue in surviving mice showed the presence of donor-derived cardiomyocytes and endothelial cells (Kirschstein and Skirboll, 2001).

• the mouse hematopoietic stem cells transplanted into the bone marrow had migrated to the border part of the damaged area, and differentiated into several types of tissue for cardiac repair.

Regenerating heart tissue through stem cell therapy

http://www.mayo.edu/research/discoverys-edge/regenerating-heart-tissue-stem-cell-therapy

Summary

A groundbreaking study on repairing damaged heart tissue through stem cell therapy has given patients hope that they may again live active lives. An international team of Mayo Clinic researchers and collaborators has done it by discovering a way to regenerate heart tissue.

“It’s a paradigm shift,” says Andre Terzic, M.D., Ph.D., director of Mayo Clinic’s Center for Regenerative Medicine and senior investigator of the stem cell trial. “We are moving from traditional medicine, which addresses the symptoms of disease to cure disease.” Treating patients with cardiac disease has typically involved managing heart damage with medication.  In collaboration with European researchers, Mayo Clinic researchers have discovered a novel way to repair a damaged heart. In Mayo Clinic’s breakthrough process,

• stem cells are harvested from a patient’s bone marrow.
•  undergo a laboratory treatment that guides them into becoming cardiac cells,
• which are then injected into the patient’s heart in an effort to grow healthy heart tissue.

The study is the first successful demonstration in people of the feasibility and safety of transforming adult stem cells into cardiac cells. Beyond heart failure, the Mayo Clinic research also is a milestone in the emerging field of regenerative medicine, which seeks to fully heal damaged tissue and organs.

Creating a heart repair kit

This image shows the process used in the clinical trials to repair damaged hearts. Cardioprogenitor cells is another term for cardiopoietic cells, those that were transformed into cardiac cells.

Transformation: The cardiopoietic cells on the left react to the cardiac environment, cluster together with like cells and form tissue.

 Mayo Clinic researchers pursued this research, inspired by an intriguing discovery. In the early 2000s, they analyzed stem cells from 11 patients undergoing heart bypass surgery. The stem cells from two of the patients had an unusually high expression of certain transcription factors — the proteins that control the flow of genetic information between cells. Clinically, the two patients appeared no different from the others, yet their stem cells seemed to show unique capacity for heart repair.

That observation drove them to  determine how to convert  nonreparative stem cells to become reparative. Doing so required determining precisely how the human heart naturally develops, at a subcellular level. That painstaking work was led by Atta Behfar, M.D., Ph.D., a cardiovascular researcher at Mayo Clinic in Rochester, Minn. With other members of the Terzic research team, Dr. Behfar identified hundreds of proteins involved in the process of heart development (cardiogenesis). The researchers then set out to identify which of these proteins are essential in driving a stem cell to become a cardiac cell. Using computer models,

• they simulated the effects of eliminating proteins one by one from the process of heart development.
• That method yielded about 25 proteins.
  • The team then pared that number down to 8 proteins that their data indicated were essential.

The research team was then able to develop the lab procedure that guides stem cells to become heart cells.

The treated stem cells were dubbed cardiopoietic, or heart creative. A proof of principle study about guided cardiopoiesis, whose results were published in the Journal of the American College of Cardiology in 2010, demonstrated that animal models with heart disease that had been injected with caridiopoietic cells had improved heart function compared with animals injected with untreated stem cells. Hailed as “landmark work,” by the journal’s editorial writer, the study showed it was indeed possible to teach stem cells to become cardiac cells. Stem cells from each patient in the cardiopoiesis group were successfully guided to become cardiac cells. The treated cells were injected into the heart wall of each of those patients without apparent complications.
“Ihis newprocessofcardiopoiesiswas achieved in 100 percent of cases, with a very good safety profile,” Dr.Terzic says. “We are enabling the heart toregainitsinitial structure and function,” Dr.Terzic says, “and we will not stop here.” The clinicaltrialfindingsareexpectedto be published in the Journal of the American College of Cardiology in 2013.  Meanwhile, research to improve the injection process and effectiveness is underway.

Stem Cells from Humans Repair Heart Damage in Monkeys

• Kevin Mayer

GEN News Highlights  May1, 2014

implanted graft of cardiac cells derived from human stem cells (green)

Regeneration of the heart by 4 different classes of proteins

Stem cells have shown promise in small-animal models, that is, in mice and rats. Still, it was unclear whether human embryonic-stem-cell-derived cardiomyocytes (hESC-CMs) could be produced in adequate numbers, and cryopreserved with sufficient viability, to even approach human application In a step up from small-animal models, scientists at the University of Washington used a monkey model of myocardial infarction to test how well hESC-CMs could replace damaged tissue with new heart cells and restore failing hearts to normal function. The scientists injected 1 billion heart muscle cells derived from hESC-CMs into the infarcted muscle of pigtail macaques (Macaca nemestrina). This was 10 times more of these types of cells than researchers have ever been able to generate before.

The researchers found that over subsequent weeks, the stem-cell derived heart muscle cells infiltrated into the damaged heart tissue, then matured, assembled into muscle fibers, and began to beat in synchrony with the macaque heart cells. After three months, the cells appeared to have fully integrated into the macaque heart muscle. The research team published its results April 30 in Nature, in an article entitled “Human embryonic-stem-cell-derived cardiomyocytes regenerate non-human primate hearts.” In this article, the authors indicated that their work demonstrated that

• hESCs can be grown,
• differentiated into cardiomyocytes, and
• cryopreserved at a scale sufficient to treat a large-animal model of myocardial infarction.

“With further refinements in manufacturing, the scale up to trials in humanpatientsseemsfeasible,” the researchers wrote. “Large-animal models are important forerunners to human trials, because they impart real-world rigor to issues such as cell production, delivery, and end-point analyses, while permitting mechanistic studies not possible in patients.”

Molecule Implicated In Leukemia Also Important In Muscle Repair

http://www.science20.com/profile/news_staff

The study shows that immature muscle cells require the molecule, called miR-29, to become mature, and that

• the molecule is nearly missing in cells from rhabdomyosarcoma, a cancer caused by the proliferation of immature muscle cells.

Cells from human rhabdomyosarcoma tumors showed levels of the molecule that were

• 10 percent or less of those in normal muscle cells.
• Artificially raising the level of the molecule in the cancer cells
  • cut their growth by half and caused them
  • to begin maturing, slowing down tumor growth.

MiR-29 is a type of microRNA, a family of molecules that helps regulate the proteins cells produce. Researchers say this study is unusual because
it also sheds light on the how a microRNA itself is regulated.

• The gene for miR-29 is silenced by the action of a protein, called NF kappa B.
•  this protein is present at highlevelsinrhabdomyosarcoma cells, and
  • this keeps miR-29 shut off,
  • preventing muscle progenitor cells from maturing.

When they raised the level of the microRNA molecule in the cells,

• or lowered the level of the NF kappa B protein,
  • the cells’ growth rate dropped two fold, and

they began taking on the appearance of mature muscle cells.

4. Drug Discovery

GPCR Insights Brighten Drug Discovery Outlook

Ken Doyle, Ph.D.

GEN Apr 15, 2014 (Vol. 34, No. 8)

Recent years have seen major advances in understanding the structure-function relationships of G protein-coupled receptors (GPCRs). This large superfamily of transmembrane receptors comprises over 800 members in humans.

GPCRs regulate a wide variety of physiological processes including

• sensation (vision, taste, and smell),
• growth,
• hormone responses, and
• regulation of the immune and
• autonomic nervous systems.

Their involvement in multiple disease pathways makes GPCRs attractive targets for drug discovery efforts.

These multifaceted proteins will be the subject of “GPCR Structure, Function and Drug Discovery,” a Global Technology Community conference scheduled to take place May 22–23 in Boston. The conference is expected to cover a broad range of topics including biased signaling, membrane protein structures, GPCR signaling dynamics, computational approaches to disease.

According to Bryan Roth, M.D., Ph.D., Michael Hooker Distinguished Professor at the University of North Carolina, Chapel Hill,

• drugs that can selectively target various downstream GPCR pathways hold the most promise.

Dr. Roth’s laboratory studies approximately 360 different GPCRs with therapeutic potential using massively parallel screening methods. His research focuses on “functional selectivity,” which he describes as

• “the ligand-dependent selectivity for certain signal transduction pathways in one and the same receptor.”

Dr. Roth notes that structural data have demonstrated that GPCRs exist in multiple conformations: “The structures of the 5-hydroxytryptamine 2B receptor and the recent high-resolution delta-opioid receptor structure have provided evidence for conformational rearrangements that contribute to functional selectivity.” Drugs that take advantage of this selectivity by preferentially stabilizing certain conformations may have unique therapeutic utility.

“Generally, we look at G protein versus arrestin-based signaling, although it’s also possible to examine how drugs activate one G protein-mediated signaling pathway versus another.

 

fluorescently tagged Arrestin and GPRC of interest

 

 

 

 

 

 

 

• β-Arrestins constitute a major class of intracellular scaffolding proteins that regulate GPCR signaling by preventing or enhancing the binding of GPCRs to intracellular signaling molecules. Laura Bohn, Ph.D., associate professor at Scripps Florida,  studies the roles that β-arrestins play in GPCR-mediated signaling.
• a particular β-arrestin can play multiple, tissue-specific roles—shutting down the signaling of a receptor in one tissue while activating signaling in another.
• different ligands can direct GPCR signaling to different effectors, which could result in different physiological effects,” comments Dr. Bohn. “Our challenge is in determining what signaling pathways to harness to promote certain effects, while avoiding others.”

Arrestin binding to active GPCR kinase (GRK)-phosphorylated GPCRs blocks G protein coupling

 

 

 

 

 

 

 

 

 

 

 

Using Designer Proteins

The multifunctional signaling abilities of β-arrestins has prompted large-scale study of their properties. Vsevolod Gurevich, Ph.D., professor of pharmacology at Vanderbilt University, studies

1. the structure,
2. function, and
3. biology of arrestin proteins.

β-arrestins have three main functions.

1. First, they prevent the coupling of GPCRs to G proteins, thereby blocking further G protein-mediated signaling (a process known as desensitization).
2. Second, the binding of a GCPR releases the β-arrestin’s carboxy-terminal “tail” and promotes internalization of the receptor.
3. Third, receptor-bound β-arrestins bind other signaling proteins, resulting in a second wave of arrestin-mediated signaling.

Dr. Gurevich’s laboratory studies β-arrestin biology through the use of three types of specially designed mutants—

1. enhanced phosphorylation-dependent,
2. receptor-specific, and
3. signaling-biased mutants.

an enhanced mutant of visual β-arrestin-1 partially compensates for defects of rhodopsin phosphorylation in vivo,

“Several congenital disorders are caused by mutant GPCRs that cannot be normally phosphorylated because they have lost GPCR kinase (GRK) sites. Enhanced super-active arrestins have the potential to compensate for these defects, bringing the signaling closer to normal.”

• Dr. Gurevich explains the strategy involved in creating designer β-arrestins: “We identify residues critical for individual β-arrestin functions by mutagenesis, using limited structural information as a guide.
• We also work on getting more structural information. In collaboration with different crystallographers, we solved the crystal structures of all four vertebrate β-arrestin subtypes in the basal state, as well as the structure of the arrestin-1-rhodopsin complex.”
• Dr. Gurevich believes that designer β-arrestins “are the next step in research and therapy, moving way beyond what small molecules can achieve.
• The difference in capabilities between redesigned signaling proteins, including β-arrestins, and conventional small molecule drugs is about the same as that between airplanes and horse-driven carriages.”
• Dr. Gurevich observes that redesigned signaling proteins face considerable obstacles in terms of gene delivery, but that the efforts are worth it. “Using designer signaling proteins, we can tell the cell what to do in a language it cannot disobey,” asserts Dr. Gurevich.

Synthesis and Antihypertensive Screening of Novel Substituted 1,2- Pyrazoline Sulfonamide Derivatives

Avinash M. Bhagwat , Anilchandra R. Bha , Mahesh S. Palled , Anand P. Khadke , Anuradha M. Patil, et al.

Am. J. PharmTech Res. 2014; 4(2).    http://www.ajptr.com/ 

Angiotensin II receptor antagonists, also known as angiotensin receptor blockers , AT1-receptor antagonists or sartans, are a group of pharmaceuticals which modulate the renin-angiotensin-aldosterone system. Their main use is in hypertension, diabetic nephropathy and congestiveheart failure. These substances are AT1-receptor antagonists which

• block the activationof angiotensin II AT1 receptors.

Blockade of AT1 receptors directly causes

1 vasodilation,

2 reduces secretion of vasopressin,

3 reduces production and secretion of aldosterone, amongst other actions –

4 the combined effect of which is reduction of blood pressure.

Irbesartan is a safe and effectiveangiotensin II receptor antagonist with an affinity for the AT1 receptor that is more than 8,500times greater than its affinity for AT2 receptor. This agent has a higher bioavailability (60-80%) than other drugs in its class . In both Losartan and Irbesartan structures imidazole moiety is being present. A structure analog of losartan and Irbesartan are designed by incorporating the heterocycles like pyrazoline group. We felt it would be interesting to explore the possibilities of 1,2-pyrazoline derivatives for Angiotensin II receptor antagonistic activity.

The Irbesartan structure was a modified Losartan structure, which had all the identity of a Losartan molecule but with groups that would fit the hydrophobic cavity with a tetramethylene group and an alkyl side chain that would fit in the pocket in the AT1 receptor. The hydroxyl methyl group of Losartan being replaced with carbonyl group of Irbesartan. With a view to introduce a hydrogen bonding interaction with AT1 receptor, these structures were further modified with a view of retaining both hydrogen bonding characteristics and as well as lipophilic groups. Losartan and Irbesartan structure contains a diphenyl molecule & imidazole ring.

In Losartan and Irbesartan diphenyl molecule is attached to the nitrogen of the imidazole ring. It is interesting to to see the activity of compounds containing two phenyl rings attached at two different positions namely3,5 position of 1, 2-pyrazoline ring. The sulphonamide derivatives known for its diuretics activity which reduces renal hypertension. We use to synthesize sulphonamide and pyrazoline in one molecule to check its possible Angiotensin II receptor antagonist property. For this reason chalcones were synthesized reacted with hydrazine hydrate to yield the corresponding 1,2-pyrazoline derivatives which further condensed with sulphanilamide and formaldehyde by mannich condensation reaction.

Acute Toxicity Study (LD50)

This study was carried out in order to establish the therapeutic and toxic doses of the newly synthesized 1,2 pyrazoline derivatives. To establish LD50 of these compounds the method described by Miller & Tainter was employed.

We report new 1,2 pyrazolines which defined combination of substituents confers appropriate polarity and charge distribution for good activity. The spectral data of compounds confirms the structures.

We also report various derivatives of 1,2 pyrazolines from Chalcones to achieve the promising and selective inhibition. The synthesized 1,2 pyrazoline derivatives have resemblance to some of Angiotensin II blocking agents like Irbesartan and Losartan. Hence it was thought of carrying out Angiotensin II blocking screening by 1K-1C Goldblatt noninvasive blood pressure measurement method. As a result, the screened compounds have shown significant Angiotensin II blocking activity. Irbesartan was used as the standard drug for Angiotensin II blocking activity.
Compounds synthesized have shown the significant Angiotensin II blocking activity when compared with the control but however are not comparable to the standard Irbesartan. The results were calculated by taking mean SE and finding the ‘P’ values. Hence from the SAR studies the chloro substituted compounds PH-2 and PH-7 exhibit better Angiotensin II blocking activityamongst the synthesized compounds. The structures of all the synthesized compounds were established on the basis of M.P., TLC, IR, NMR (PMR) . The compounds synthesized were found to be non-toxic and could be synthesized in good yields. The active compounds could be taken as lead for structural and molecular modification was thought of in future.

The present work, which was undertaken is a bonafide and novel work on the synthesis of 1,2 pyrazoline derivatives. We have made an attempt in reviewing the literature on 1,2 pyrazoline derivatives for their medicinal uses with the help of chemical abstract, journals and internet surfing. For the synthesis of 1,2 pyrazoline derivatives scheme were established. Around eight derivatives were synthesized. The synthesized compounds were tested for their purity, preliminary tests, physical constants and TLC. The structure of the final compound were confirmed by IR, H-NMR spectra and GCMS. The compounds synthesized were found to be non-toxic and could be synthesized in good yields.

5. Synthetic Biology

Artists and biologists team up to ush boundaries of synthetic biology

Kenrick Vezina | May 1, 2014 | Genetic Literacy Project

Synthetic biologists are often accused of “playing God,” of tampering with his Creation. Well, if you’re going to Create then you might as well do so with the help of some creative individuals? That’s just what the biologists in the pages of the new book Synthetic Aesthetics, from MIT Press, aims to do. Its arrival is well-timed, with the

first synthetic yeast chromosome having been created last month amid a flurry of scientific milestones in biotechnology.

Alun Anderson has reviewed the new book for New Scientist. Unlike the typically defensive posture found in biotech broadly, he writes, the spirit captured by this book is “freewheeling” and collaborative, with 20 authors ranging from the arts and sciences putting their minds together to generate original ideas. Anderson notes that parts of the book “may irritate conventional scientists – some of the ideas were dreamed up while ‘performing a dance based on the myth of the Golem’, for example. But it certainly explains the key ideas of the field and leads you to many lateral conversations about what it may become.” The book is itself an offshoot of a larger project, which you can check out at its official page. It describes itself as an “experimental, international research project between synthetic biology, art, design and social science” It has roots at the University of Edinburgh, Scotland, and Stanford University, California. And the main project team is comprised of bioengineers Drew Endy (Stanford) and Alistair Elfick (Edinburgh), social scientists Jane Calvert (Edinburgh) and Pablo Schyfter (Edinburgh), and designer/artist Alexandra Daisy Ginsberg.

In the book Synthetic Aesthetics, Ginsberg provides a thought-provoking counterpoint to the engineering definition of “design”.  Anderson explains in his review: An engineer might think of designing a bridge to a particular specification; a synthetic biologist of designing a microorganism with a new commercial application, pumping out green gasoline for example; but a real designer, a fashion designer, for example, is doing something else. As artist Daisy Ginsberg puts it, design “is about possibility”, the unimagined things that life could be.

Synthetic biology, she writes, has been addressing “humanity’s needs” – limitless fuel, for example – rather than “our needs as individual, diverse and complex humans”.  This is refreshing: worries about the separation between the top-down design of the future and those who must live with the results are quite rare in science. These words ring true, given the intensely “problem oriented” approach to most synthetic biology research. This approach extends to the coverage of this research in the media, where even a research achievement with sweeping potential like the synthetic yeast chromosome ends up broken down into pragmatic chunks. (Yeast could mass-produce medicines! Help process fuels!) Alistair Elfick, one of the leads on the Synthetics Aesthetics project, has written a fascinating opinion piece at The Conversation to accompany the release of his book. In it, he puts forth the idea it’s time for synthetic biologists to stop thinking “like scientists,” lest they hamstring themselves.

Kenrick Vezina is Gene-ius Editor for the Genetic Literacy Project and a freelance science writer, educator, and naturalist based in the Greater Boston area. Sources:

•  ”Synthetic biology gets reborn as an aesthetic dream,” Alun Anderson | New Scientist
• “If synthetic biologists think like scientists, they may miss their eureka moment,” Alistair Elfick | The Conversation
• Synthetic Aesthetics project

• “Breakthrough biology: First synthetic chromosome for yeast created, capping month of biotech innovations,” Kenrick Vezina | Genetic Literacy Project

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