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GSK Partners With SG3 Ventures to Add $100 Million to the Pittsburgh Biotech Scene

From Biospace News: Backed by GlaxoSmithKline (GSK), New VC Firm SG3 Ventures Has $100 Million to Bet on Pittsburg Startups

Reporter: Stephen J. Williams, Ph.D.

Source: http://www.biospace.com/News/backed-by-glaxosmithkline-new-vc-firm-sg3-ventures/412039/source=TopBreaking?intcid=homepage-seekernewssection-tabtopbreakingnews

 

Pittsburgh-area entrepreneurs will soon have another funding option for growing early phase startup companies.

Pharmaceutical giant GlaxoSmithKline has thrown its support behind the creation of a $100 million venture capital fund, which will help meet a need for early stage business startup capital in the Pittsburgh area. Philadelphia-based SG3 Ventures anticipates awarding its first round of funding in about a year, according to Brian McVeigh, vice president of worldwide business development transactions and investment management at GSK.

From Pittsburgh Post Gazette: http://www.post-gazette.com/business/healthcare-business/2016/03/11/New-early-stage-venture-fund-forming-with-eye-on-Pittsburgh-startups/stories/201603090016

New early-stage venture fund forming with eye on Pittsburgh startups

Pittsburgh-area entrepreneurs will soon have another funding option for growing early phase startup companies.

Pharmaceutical giant GlaxoSmithKline has thrown its support behind the creation of a $100 million venture capital fund, which will help meet a need for early stage business startup capital in the Pittsburgh area. Philadelphia-based SG3 Ventures anticipates awarding its first round of funding in about a year, according to Brian McVeigh, vice president of worldwide business development transactions and investment management at GSK.

“There is a huge untapped opportunity,” Mr. McVeigh said. “Let’s bring the money here.”

New prescription drug treatments will be a priority for fund investments, but a balanced portfolio including life science technologies is planned.

In the venture ecosystem, insurers, pension funds and other institutions use such funds to invest in promising startup companies — both to balance their portfolios and to get a shot at investment returns that would not otherwise be possible. The venture funds oversee allotting capital to a portfolio of startup companies.

The investment money enables startups to mature and eventually bring in other investors through a public offering or acquisition by a larger company, generating money to repay the initial investors.

GSK and other big pharmaceutical companies are making similar investments to maximize returns and keep their product pipelines full, but GSK has been focusing on earlier stage companies, shifting its focus to pre-clinical technologies about five years ago, Mr. McVeigh said.

In addition, Big Pharma is increasingly relying on outsourced research and development operations, often in collaboration with universities, to fill industry product pipelines. GSK has funded a number of these initiatives, including a cancer collaboration with the University of California, San Diego School of Medicine and Moores Cancer Center.

SG3 Managing Director Keith Marmer said the new venture fund will be committed to technologies developed outside the better known tech hubs of Silicon Valley and Boston-Cambridge.

“We’re here, we’re from here, and we want to be here,” he told a group of entrepreneurs at a recent breakfast meeting in Oakland. “Sustaining technology through research funding isn’t happening anywhere.”

Parsippany N.J.-based GSK closed its consumer health care operations in Moon in 2015, eliminating 274 jobs a year after the company’s merger with Swiss vaccine maker Novartis. Mr. McVeigh works at the company’s offices in King of Prussia, Pa.

With federal research dollars flat in recent years, universities nationwide have been turning to commercialization of intellectual property as a new source of revenue.

At the same time, Pittsburgh’s startup community is showing signs of new life.

Among the signs: Patrick Gallagher’s commitment to the commercialization of faculty research since becoming University of Pittsburgh chancellor 18 months ago, awakening a sleeping giant of economic development and innovation and hospital system UPMC’s creation of a commercial enterprises arm to fund promising technologies.

The timing couldn’t be better for venture capital funds like SG3.

Nationwide, early stage funding has been chasing fewer deals, according to a report by Money Tree, which was compiled by PricewaterhouseCoopers and the National Venture Capital Association based on data provided by Thomson Reuters.

Early stage investments nationally last year totaled $19.8 billion, a 23 percent increase from $16.1 billion in 2014. But the number of deals were essentially flat from the previous year, suggesting that some companies were left out in the cold.

What’s more, the amount of money available to Pittsburgh-area entrepreneurs after the earliest rounds of investment isn’t keeping pace with the innovations coming out of the city’s universities, said Dietrich Stephan, a serial entrepreneur who also chairs the human genetics department at Pitt.

“There’s real substance here,” he said. “Without money, we can’t build.”

Seed investment funding — the earliest level of funding — is not a problem in Pittsburgh, said Buchanan Ingersoll Rooney PC lawyer Jeremy Garvey, who also chairs the Bridgeville-based Pittsburgh Venture Capital Association.

“The predominance of funding in this market comes in the earliest stages,” he said. “Institutional funding is much harder to get in this market.”

Early stage venture funding began drying up with the stock market crash of 2008, which also chilled the financial markets for initial public offerings for biotech companies, Mr. McVeigh said. Eventually, conditions thawed for IPOs, but the lower valuations for new companies than before 2008 made that less attractive than before.

“We’re really energized by the energy there” in Pittsburgh, Mr. McVeigh said. “We’re looking to bring venture capital to the region.”

Kris B. Mamula: kmamula@post-gazette.com

About SG3 Ventures

SG3 Ventures is an early stage life science venture capital firm. Our primary focus in on therapeutics and digital health; however, we will invest opportunistically when presented with a potential vehicle to drive superior returns for our limited partners. We are active in company formation, deploying financial and human resources to help deliver value. In addition, we access deep industry networks to ensure a path to market with strong commercial partnerships built into our companies from the beginning. SG3 prefers to invest in the greater Philadelphia Region (Princeton to the north, Baltimore to the south and Pittsburgh to the west). We prefer to make initial investments at the formation or seed stage with a focus on providing financing through mature rounds of investment.

  • Website

    http://sg3ventures.com

  • Industry

    Financial Services

  • Type

    Partnership

  • Headquarters

    3711 Market Street Suite 800Philadelphia, PA 19104 United States

  • Company Size

    1-10 employees

More articles on the Open Access Journal on Biotech Investing Include

J.P. Morgan 34th Annual Healthcare Conference & Biotech Showcase™ January 11 – 15, 2016 in San Francisco

New Values for Capital Investment in Technology Disruption: Life Sciences Group @Google and the Future of the Rest of the Biotech Industry

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

 

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From Biospace News: GlaxoSmithKline (GSK) and Johnson & Johnson (JNJ)-Backed VC Firm Medicxi Launches $250 Million Fund For Life Science Startups

Reporter: Stephen J. Williams, PhD

original article: http://www.biospace.com/News/glaxosmithkline-and-johnson-johnson-backed-vc-firm/407338/source=TopBreaking


Press release

Medicxi Ventures, Formerly Index Ventures Life Sciences, Launches as an Independent Venture Capital Firm and Announces Closing of a €210m Fund including GSK and Johnson & Johnson Innovation

LONDON, GENEVA and JERSEY, February 2, 2016 /PRNewswire/ —

  • Medicxi Ventures comprises all of the existing life sciences team, portfolio company investments and life sciences funds of Index Ventures
  • GSK and Johnson & Johnson Innovation expand their commitment to the asset-centric approach
  • Index Ventures technology practice remains unchanged

Medicxi Ventures, a new venture capital firm comprising all of the existing life sciences portfolio companies, funds and team from Index Ventures, today announces the close of Medicxi Ventures 1 (MV1), a new €210 million ($250 million) fund that will focus on early-stage life sciences investments. MV1 will predominantly invest in Europe and principally follow the “asset-centric” strategy pioneered by its partners at Index.

By investing in MV1, GlaxoSmithKline (GSK) and Johnson & Johnson Innovation – JJDC, Inc. (JJDC) have renewed and expanded their commitment to the asset-centric approach, following the prior investment in Index Life 6 (IL-6) alongside other financial investors.

Medicxi Ventures starts its operations as one of the largest independent European life sciences focused investment firms. The Company’s mission is to focus on strengthening R&D innovation by providing solutions to unmet medical needs. Collaboration with pharmaceutical companies will continue to be a key strategy helping the firm to deliver on this mission.

Medicxi Ventures will be managed by four General Partners, Francesco De Rubertis, David Grainger, Kevin Johnson and Michèle Ollier, all of whom previously led the life sciences practice of Index Ventures. The four partners will form the executive management of the new firm.

Francesco De Rubertis, General Partner of Medicxi Ventures, said: “We are excited to take this next step in our evolution as a life sciences focused investment firm. A high percentage of the drugs approved every year by the FDA were discovered in European academic labs. By working in close partnership with academia, biotech and the pharmaceutical industry, we are committed to translating this high quality science in Europe into effective new medicines.”

He added: “It has been a privilege working with Neil Rimer, Giuseppe Zocco and the other tech partners at Index Ventures for the last 20 years and we have benefitted from their expertise in investing in and building high growth entrepreneurial companies.”

Dr Moncef Slaoui, Chairman Global Vaccines and GSKs representative on Medicxis Scientific Advisory Board, commented on the announcement: “We are delighted to support the Medicxi team and this early stage investment fund. We believe in the potential to create an exciting pipeline of new medicine candidates by collaborating and investing with an asset-centric model. The team at Medicxi has a proven track record in partnering with world-class entrepreneurs and scientists to translate disruptive science from academia and industry into new medicines with demonstrable patient benefits.”

Dr Richard Mason, Head, Johnson & Johnson Innovation, London, commented: “Johnson & Johnson Innovation is focused on enabling and advancing all stages of science and technology across the world’s most robust innovation ecosystems. We are optimistic that applying the asset-centric investment model of Medicxi across Europe and beyond will uncover the new and highly differentiated science and technology that is needed to turn early stage research into viable products and patient solutions. We are delighted to work closely with the Medicxi team to help increase the productivity and likelihood of success for the life sciences innovation community throughout the region. ”

The Scientific Advisory Board of the new fund will include some of the top R&D and business development executives from the two pharmaceutical companies as well as Medicxi-appointed executives. As in IL-6, the two pharmaceutical companies have not received any specific rights to the portfolio companies.

Neil Rimer, co-founder of Index Ventures, said: “The creation of Medicxi Ventures as a new entity is a natural evolution given that Index’ life sciences team has been operating autonomously within the firm for several years. Whilst Index and Medicxi will operate independently, we retain close ties and look forward to continuing to share ideas and expertise.”

Notes for Editors

About Medicxi Ventures

Medicxi Ventures is based in London, Geneva and Jersey. It comprises all of the legacy portfolio companies, funds and the life sciences team of Index Ventures, and a new €210 million fund (MV1) that will focus on early-stage investments in life sciences. The Company’s mission is to invest and collaborate along the full healthcare continuum focusing on drug discovery and development and pharmaceutical innovation. Leading healthcare companies, GSK and Johnson & Johnson Innovation-JJDC are investors in Medicxi Ventures’ funds.

Medicxi Ventures’ team has been investing in life sciences for over 20 years and has backed many successful companies, including Genmab (Nasdaq Copenhagen: GEN), PanGenetics (sold to AbbVie), Molecular Partners (SWX: MOLN), XO1 (sold to Janssen) Egalet (EGLT), Minerva Neurosciences (NERV) and Versartis (VSAR).

Please see http://www.medicxiventures.com for more information.

About the Medicxi Ventures Executive Team

  • Francesco De Rubertis joined Index in 1997 to lead the firm’s life sciences activity and has been involved with and overseen all of the investments that Index has made in life sciences
  • David Grainger joined Index in 2012. Prior to this, David led an internationally recognised research group in Cambridge University’s Department of Medicine, where he published more than 80 first author papers in leading journals including Nature, Science and Nature Medicine. He is an inventor on more than 150 patents and patent applications.
  • Kevin Johnson has been working with Index since 2003. He focuses on life sciences, especially drug development companies and was part of the management team that floated Cambridge Antibody Technology on the London Stock Exchange. Two of his products, Humira (Abbott Pharmaceutical) and Benlysta (Human Genome Sciences, GSK), are now on the market.
  • Michèle Ollier joined Index in 2006. She has spent more than 15 years in several development and marketing positions at Sanofi International, Bristol-Myers Squibb, RPR/Gencell/Aventis international and Serono International.

For further information, please contact:

Francesco De Rubertis
General Partner, Medicxi Ventures
francesco@medicxiventures.com
+44(0)207-154-2020

Katja Stout, Sylvie Berrebi
Citigate Dewe Rogerson
katja.stout@citigatedr.co.uk
Sylvie.berrebi@citigatedr.co.uk
+44(0)207-638-9571

Bill Douglass
Gotham Communications LLC
bill@gothamcomm.com
+1(646)504-0890

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PROGRAM ANNOUNCEMENT

Conference Program is available at

http://www.sachsforum.com/newyork14/


Event’s agenda available at:
http://www.sachsforum.com/newyork14/newyork14-agenda.html

Wednesday, 19th March 2014
Registration and coffee begins – 08.00
Program begins – 08.15
Networking reception will take place at 18.00 – 20.00

Once you arrive at 7 World Trade Center (250 Greenwich St, New York, NY10007, USA).
Please use the D Elevator Bank to the 40th floor where Sachs Team will welcome you at the registration desk.

For urgent issues, please contact:
Tomas@sachsforum.com (cell number +44 77 043 158 71)
Or Mina@sachsforum.com (cell number +44 74 636 695 04) Cells available from 15th March.

Announcement

LEADERS IN PHARMACEUTICAL BUSINESS INTELLIGENCE will cover the event for the Scientific Media

Dr. Lev-Ari will be in attendance on 3/19/2014 at 

The New York Academy of Sciences.

Editorials of event coverage via our 

Open Access Scientific Journal

http://pharmaceuticalintelligence.com

Date             Views to Date      # of articles      “NIH Clicks”  “Nature Clicks”

3/05/2014      338,958                 1,717                 1,830                   965

  • 369 Articles on Cancer
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https://pharmaceuticalintelligence.com/?s=Cancer+

  • Cancer e-Book

Series C: e-Books on Cancer & Oncology

Series C Content Consultant: Larry H. Bernstein, MD, FCAP 

VOLUME ONE 

Cancer Biology and Genomics for Disease Diagnosis

2014

Stephen J. Williams, PhD, Senior Editor

sjwilliamspa@comcast.net

Tilda Barliya, PhD, Editor

tildabarliya@gmail.com

Ritu Saxena, PhD, Editor

ritu.uab@gmail.com

https://pharmaceuticalintelligence.com/biomed-e-books/series-c-e-books-on-cancer-oncology/cancer-biology-and-genomics-for-disease-diagnosis/

SIX SOURCES of INVESTMENT for BioMed INVENTIONS

Curator: Aviva Lev-Ari, PhD, RN

Investing and inventing: Is the Tango of Mars and Venus Still on

MEDIA COVERAGE

The Event will be broadcasted via our distributions channels on the Internet and all Search Engines featuring WordPress.com

  • Scientific Journal

http://pharmaceuticalintelligence.com

https://pharmaceuticalintelligence.com/2014/03/05/milestone-for-our-venture-we-celebrate-our-top-authors-by-number-of-articles-in-the-journal-to-date-1000-301-58-49-46-43-40-28-20/

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http://twitter.com/pharma_BI

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  • Dr. Lev-Ari’s BioMed Group launched by and managed by on LinkedIn.com – LEADERS IN PHARMACEUTICAL BUSINESS INTELLIGENCE

http://www.linkedin.com/groups?gid=4346921&trk=hb_side_g

2nd ANNUAL

Sachs Cancer Bio Partnering &
Investment Forum

Promoting Public & Private Sector Collaboration & Investment

in Drug Development

19th March 2014 • New York Academy of Sciences • USA  
spi2012

http://www.sachsforum.com/newyork14/

 

The 2nd Annual Sachs Cancer Bio Partnering & Investment Forum is designed to bring together thought leaders from cancer research institutes, patient advocacy groups, pharma and biotech to facilitate partnering and funding/investment. We expect around 200 delegates and there is an online meeting system and meeting facilities to make the event transactional. There will also be a track of about 30 presentations by listed and private biotechnology companies seeking licensing/investment.

divider

The 2nd Annual Sachs Cancer Bio Partnering & Investment Forum will cover the following topics in the program:

  • Advances in Translational Research
  • Strategies for Small Molecule and Biologicals Drug Development
  • Deal Making
  • Public & Private Partnerships
  • Diagnostics
  • Immunotherapies and Cancer Vaccines
  • Case Study

Confirmed Speakers & Chairs include:
Anne Altmeyer, Executive Director Business Development & LicensingNovartis Pharmaceuticals
Ariel Jasie, Executive Director of Business DevelopmentCelgene
Beth Jacobs, Managing PartnerExcellentia Global Partners
Boris Peaker, Executive Director, Biotechnology Equity ResearchOppenheimer & Co. Inc.
Carole Nuechterlein, Head Roche Venture FundF.Hoffmann-La Roche AG Roche Venture Fund
Dan Snyder, President and COOMolecularMD
Daryl Mitteldorf, Executive DirectorGlobal Prostate Cancer Alliance
Dennis Purcell, Senior Managing PartnerAisling Capital
Doug Plessinger, Vice President of Clinical and Medical AffairsArgos Therapeutics, Inc.
Elizabeth Bachert, Senior Director Worldwide Business DevelopmentPfizer
Esteban Pombo-Villar, COOOxford BioTherapeutics AG
Florian Schodel, CEO, Philimmune LLC
Frederick Cope, President and CSONavidea Biopharmaceuticals
Guillaume Vignon, Director of Global BD Oncology, Merck Serono SA
Harren Jhoti, PresidentAstex Pharmaceuticals Inc.
Harry Glorikan, Managing DirectorPrecision for Medicine
James Mulé, Executive Vice President and Associate Center Director for Translational Research,
H Lee Moffit Cancer Center
Keith Knutson, Program Director and Principal Investigator of the Cancer Vaccines and immune Therapies ProgramVaccine and Gene Therapy Institute of Florida
Kevin DeGeeter, AnalystLadenburg Thalmann & Co, Inc.
Klaus Urbahns, Head, Discovery TechnologiesMerck Serono
Kristina Khodova, Project Manager, OncologySkolkovo Foundation
Lorenza Castellon, Business Development ConsultantSuda Ltd.
Louis DeGennaro, Executive VP, CMO, The Leukemia and Lymphoma Society
Louise Perkins, Chief Science OfficerMelanoma Research Alliance
Mara Goldstein, Managing Director, Senior Healthcare AnalystCantor Fitzgerald
Michael Goldberg, Managing PartnerMontaur Capital
Nathan Tinker, Executive DirectorNewYorkBIO
Nicholas Dracopoli, Vice President and Head of OncologyJanssen Research & Development
Peter Hoang, Managing Director, Office of Innovations, Technology Based VenturesThe University of Texas MD Anderson Cancer Center
Philip Gotwals, Executive Director, Oncology Research CollaborationsNovartis Institutes for BioMedical Research
Robert Petit, CSOAdvaxis Inc.
Stephen Brozak, Managing Partner and PresidentWBB Securities, LLC
Steven Tregay, CEOForma Therapeutics
Steven W. Young, PresidentAddario lung Cancer Medical Institute
Stuart Barich, Managing Director, Healthcare Investment BankingOppenheimer & Company
Tariq Kassum MD, Vice President, Business Development and StrategyMillennium Pharmaceuticals
TBC, Cardinal Health
TBC, UCSD
Timothy Herpin, Vice President, Head of Transactions (UK), Business DevelopmentAstraZeneca
Vikas Sharma, Director, Business DevelopmentRexahn Pharmaceuticals, Inc.
Walter Capone, PresidentThe Multiple Myeloma Research Foundation

View the full list of 2013 Forum Speakers & Chairs >>

divider

Presenting Opportunities for Biotech, Pharmaceutical companies  and Patient Advocacy Groups

Presenting at the forum offers excellent opportunities to showcase activities and highlight investment and partnership opportunities. Biotech companies will be able to communicate investment and licensing opportunities. These are for both public and private companies. The audience is comprised of financial and industry investors. These are streamed 15 minute presentations. The patient advocacy presentations are 30 minutes.

Sachs forums are recognised as the leading international stage for those interested in investing in the biotech and life science industry and are highly transactional. They draw together an exciting cross-section of early-stage/pre-IPO, late-stage and public companies with leading investors, analysts, money managers and pharmas. The Boston forum provides the additional interaction with the academic/scientific and patient advocacy communities.

Sponsorship and Exhibition

Sachs Associates has developed an extensive knowledge of the key individuals operating within the European and global biotech industry. This together with a growing reputation for excellence puts Sachs Associates at the forefront of the industry and provides a powerful tool by which to increase the position of your company in this market.

Raise your company’s profile directly with your potential clients. All of our sponsorship packages are tailor made to each client, allowing your organisation to gain the most out of attending our industry driven events.

To learn more about presenting, exhibition or sponsorship opportunities, please contact
Mina Orda + 44 (0)203 463 4890 or by email: Mina Orda.

 

spi2012
Register Now
Register
To Exhibit
Register
To Present
OVERVIEW sachs Speakers sachs Presenting Companies sachs Attendees sachs Program sachs Sponsors / Supporters sachs Venue sachs Accommodation
Biotech i Europe Investor Forum
sachs sachs
Companies Who Presented at the 2013 Forum Included:
Aileron Therapeutics, Inc.
AnaptysBio, Inc
Argos Therpeutics, Inc
Atossa Genetics
BioCancell Ltd.
BioLineRx Ltd.
Cellectis
CENTROSE
Churchill Pharmaceuticals
Constellation Pharmaceuticals
CureVac GmbH
Dicerna Pharmaceuticals
Etubics Corporation
Genisphere
immatics biotechnologies GmbH
ImmunoGen, Inc
Life Science Nation
MacroGenics, Inc
Melanovus Oncology
MiNA Therapeutics
MolecularMD
Oncolix, Inc.
OncoSec Medical Incorporated
Oxford BioTherapeutics
RAMOT at Tel Aviv University
Rescue Therapeutics, Inc.
Sialix, Inc.
Sorrento Therapeutics
to-BBB technologies BV
TVAX Biomedical, Inc.
The 2nd Annual Sachs Cancer Bio Partnering & Investment Forum is designed to bring together thought leaders from cancer research institutes, patient advocacy groups, pharma and biotech to facilitate partnering and funding/investment. We expect around 200 delegates and there is an online meeting system and meeting facilities to make the event transactional. There will also be a track of about 30 presentations by listed and private biotechnology companies seeking licensing/investment.dividerThe 2nd Annual Sachs Cancer Bio Partnering & Investment Forum will cover the following topics in the program:

  • Advances in Translational Research
  • Strategies for Small Molecule and Biologicals Drug Development
  • Deal Making
  • Public & Private Partnerships

Confirmed Speakers & Chairs include:

The 2nd Annual Sachs Cancer Bio Partnering & Investment Forum will cover the following topics in the program:

  • Advances in Translational Research
  • Strategies for Small Molecule and Biologicals Drug Development
  • Deal Making
  • Public & Private Partnerships
  • Diagnostics
  • Immunotherapies and Cancer Vaccines

Confirmed Speakers & Chairs include:
Anne Altmeyer, Executive Director Business Development & LicensingNovartis Pharmaceuticals
Ariel Jasie, Executive Director of Business DevelopmentCelgene
Beth Jacobs, Managing PartnerExcellentia Global Partners
Boris Peaker, Executive Director, Biotechnology Equity ResearchOppenheimer & Co. Inc.
Carole Nuechterlein, Head Roche Venture FundF.Hoffmann-La Roche AG Roche Venture Fund
Daryl Mitteldorf, Executive DirectorGlobal Prostate Cancer Alliance
Dennis Purcell, Senior Managing PartnerAisling Capital
Doug Plessinger, Vice President of Clinical and Medical AffairsArgos Therapeutics, Inc.
Elizabeth Bachert, Senior Director Worldwide Business DevelopmentPfizer
Esteban Pombo-Villar, COOOxford BioTherapeutics AG
Florian Schodel, CEO, Philimmune LLC
Guillaume Vignon, Director of Global BD Oncology, Merck Serono SA
Harren Jhoti, PresidentAstex Pharmaceuticals Inc.
Harry Glorikan, Managing DirectorPrecision for Medicine
James Mulé, Executive Vice President and Associate Center Director for Translational Research,
H Lee Moffit Cancer Center
Keith Knutson, Program Director and Principal Investigator of the Cancer Vaccines and immune Therapies ProgramVaccine and Gene Therapy Institute of Florida
Klaus Urbahns, Head, Discovery TechnologiesMerck Serono
Kristina Khodova, Project Manager, OncologySkolkovo Foundation
Lorenza Castellon, Business Development ConsultantSuda Ltd.
Louis DeGennaro, Executive VP, CMO, The Leukemia and Lymphoma Society
Louise Perkins, Chief Science OfficerMelanoma Research Alliance
Mara Goldstein, Managing Director, Senior Healthcare AnalystCantor Fitzgerald
Nathan Tinker, Executive DirectorNewYorkBIO
Nicholas Dracopoli, Vice President and Head of OncologyJanssen Research & Development
Peter Hoang, Managing Director, Office of Innovations, Technology Based VenturesThe University of Texas MD Anderson Cancer Center
Philip Gotwals, Executive Director, Oncology Research CollaborationsNovartis Institutes for BioMedical Research
Robert Petit, CSOAdvaxis Inc.
Steven Tregay, CEOForma Therapeutics
Steven W. Young, PresidentAddario lung Cancer Medical Institute
Stuart Barich, Managing Director, Healthcare Investment BankingOppenheimer & Company
Tariq Kassum MD, Vice President, Business Development and StrategyMillennium Pharmaceuticals
Timothy Herpin, Vice President, Head of Transactions (UK), Business DevelopmentAstraZeneca
Walter Capone, PresidentThe Multiple Myeloma Research Foundation

_______

View the full list of 2013 Forum Speakers & Chairs >>

dividerPresenting Opportunities for Biotech, Pharmaceutical companies  and Patient Advocacy Groups

Presenting at the forum offers excellent opportunities to showcase activities and highlight investment and partnership opportunities. Biotech companies will be able to communicate investment and licensing opportunities. These are for both public and private companies. The audience is comprised of financial and industry investors. These are streamed 15 minute presentations. The patient advocacy presentations are 30 minutes.

Sachs forums are recognised as the leading international stage for those interested in investing in the biotech and life science industry and are highly transactional. They draw together an exciting cross-section of early-stage/pre-IPO, late-stage and public companies with leading investors, analysts, money managers and pharmas. The Boston forum provides the additional interaction with the academic/scientific and patient advocacy communities.

Sponsorship and Exhibition

Sachs Associates has developed an extensive knowledge of the key individuals operating within the European and global biotech industry. This together with a growing reputation for excellence puts Sachs Associates at the forefront of the industry and provides a powerful tool by which to increase the position of your company in this market.

Raise your company’s profile directly with your potential clients. All of our sponsorship packages are tailor made to each client, allowing your organisation to gain the most out of attending our industry driven events.

To learn more about presenting, exhibition or sponsorship opportunities, please contact
Mina Orda + 44 (0)203 463 4890 or by email: Mina Orda.

SOURCE

http://www.sachsforum.com/newyork14/index.html

From: Mina@sachsforum.com
To: AvivaLev-Ari@alum.berkeley.edu
Sent: Mon Dec 16 12:01:21 UTC 2013

From: Tomas Andrulionis <Tomas@sachsforum.com>
Date: Tue, 10 Dec 2013 16:13:53 +0000
To: “avivalev-ari@alum.berkeley.edu” <avivalev-ari@alum.berkeley.edu>
Conversation: Complimentary Invitation for the 2nd Annual Sachs Cancer Bio Partnering & Investment Forum, 19th March 2014, New York Academy of Sciences

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Myocardial Infarction: The New Definition After Revascularization

Reporter: Aviva Lev-Ari, PhD, RN

 

UPDATED on 7/31/2014

Myocardial Ischemia Symptoms

Reporter: Aviva Lev-Ari, PhD, RN

https://pharmaceuticalintelligence.com/2014/07/29/myocardial-ischemia-symptoms/

 

VIEW VIDEO

Gregg Stone, MD

Co-DIrector, Medical Research & Education Division Cardiovascular Research Foundation

http://www.medpagetoday.com/Cardiology/MyocardialInfarction/42256?xid=nl_mpt_DHE_2013-10-15&goback=%2Egmr_4346921%2Egde_4346921_member_5795830612724035588#%21

Primary source: Journal of the American College of Cardiology
Source reference: Moussa I, et al “Consideration of a new definition of clinically relevant myocardial infarction after coronary revascularization: an expert consensus document from the Society for Cardiovascular Angiography and Interventions (SCAI)” J Am Coll Cardiol2013; 62: 1563-1570.

Additional source: Journal of the American College of Cardiology
Source reference:White H “Avatar of the universal definition of periprocedural myocardial infarction” J Am Coll Cardiol 2013; 62: 1571-1574.

Moussa reported that he had no conflicts of interest.

Stone is a consultant for Boston Scientific, Eli Lilly, Daiichi Sankyo, and AstraZeneca. The other authors reported relationships with Guerbet, The Medicines Company, Bristol-Myers Squibb/Sanofi, Merck, Maya Medical, AstraZeneca, Abbott Vascular, Regado Biosciences, Janssen Pharma, Lilly/Daiichi Sankyo, St. Jude Medical, Medtronic, Terumo, Bridgepoint/Boston Scientific, Gilead, Boston Scientific, Eli Lilly, and Daiichi Sankyo.

White is co-chairman for the Task Force for the Universal Definiton of Myocardial Infarction; has received research grants from sanofi-aventis, Eli Lilly, The Medicines Company, the NIH, Pfizer, Roche, Johnson & Johnson, Schering-Plough, Merck Sharpe & Dohme, AstraZeneca, GlaxoSmithKline, Daiichi Sankyo Pharma Development, and Bristol-Myers Squibb; and has served on advisory boards for AstraZeneca, Merck Sharpe & Dohme, Roche, and Regado Biosciences.

WASHINGTON, DC — A “clinically meaningful” definition of MI following PCI or CABG is urgently needed to replace the arbitrarily chosen “universal definition” proposed in recent years that has no relevance to patients and may be muddying clinical-trial results. Those are the conclusions of a new expert consensus document released Monday by the Society of Cardiovascular Angiography and Interventions (SCAI)[1].

The notion of a “universal definition of MI” was first proposed in 2000 and updated in 2007 and 2012. The 2012 document defines a PCI-related MI as an increase in cardiac troponin (cTn) of more than five times the upper limit of normal (ULN) during the first 48 hours postprocedure plus specific clinical or ECG features. Post-CABG, the definition is a cTn increase of >10 times the ULN, plus different clinical or ECG features.

The problem, lead author Dr Issam Moussa (Mayo Clinic, Jacksonville, FL) told heartwire , is that these cutoffs were arbitrarily chosen and not based on any hard evidence that these biomarker levels spelled a poor prognosis. Moreover, “overnight, the rate of MI went from 5% following these procedures to 20% to 30%!” he said.

The SCAI committee, in its new document, focuses on post-PCI procedures and highlights the importance of acquiring baseline cardiac biomarkers and differentiating between patients with elevated baseline CK-MB (or cTn) in whom biomarker levels are stable or falling, as well as those in whom it hasn’t been established whether biomarkers are changing.

SCAI’s Proposed Clinically Meaningful MI Definitions

Group Definition
Normal baseline CK-MB CK-MB rise of >10x ULN or >5x ULN with new pathologic Q-waves in at least 2 contiguous leads or new persistent left bundle branch block
OR
In the absence of baseline CK-MB, a cTn rise of >70x ULN or a rise of>35 ULN plus new pathologic Q-waves in at least 2 contiguous leads or new persistent left bundle branch block
Elevated baseline biomarkers that are stable or falling A CK-MB or cTn rise that is equal (by an absolute increment) to the definitions described for patients with normal CK-MB at baseline.
Elevated baseline biomarkers that have not been shown to be stable or falling A CK-MB or cTn rise that is equal (by an absolute increment) to the definitions described for patients with normal CK-MB at baseline
Plus
New ST-segment elevation or depression
Plus
New-onset or worsening heart failure or sustained hypotension or other signs of a clinically relevant MI.

Moussa is quick to emphasize that these new clinically meaningful definitions have limited evidence to support them—and most of what exists supports CK-MB definitions, not cTn—but that the new document is based on the best scientific evidence available.

“We don’t want to come out with a definitive statement” saying this is the final word on MI definitions,” he stressed. “There is more science that needs to be done and there remains more uncertainty. We framed this to be inclusive and also to open the field for discussion.”

His hope is that this will lead to important changes in how patients are managed and money is spent. Currently, patients with clinically meaningless biomarker elevations may become unnecessarily panicked over news that they’ve had a “heart attack,” while hospital stays may be extended and further tests ordered on the basis of these results.

Moussa et al’s proposal also has important implications for clinical trials, he continued. Currently, for studies that include periprocedural MIs as an individual end point or as part of a composite end point, the very high number of biomarker-defined “MIs” collected in the trial could potentially overwhelm the true impact of any given therapy. “You are really using an end point that is truly not relevant to patients. . . . This could really affect the whole hypothesis.”

He’s expecting some push-back from cardiologists and academics, particularly those who championed the need for the universal definition in the first place, but believes most people will welcome a clinically meaningful definition.

“I think many in the medical community will accept this because they have not really been using the universal definition in their day-to-day practice anyhow.” What’s more, the National Cardiovascular Data Registry (NCDR) does not include the reporting of MI postangiography, in part because of concerns that the universal definition of MI overestimates the true incidence of this problem. “I think many in the community will look at this definition as more reflective of the true incidence of MI after angioplasty, and if it’s accepted, they are more likely to report it to databases like NCDR and use it to reflect quality-of-care processes.”

http://www.medscape.com/viewarticle/812533?nlid=35983_2105&src=wnl_edit_medp_card&uac=93761AJ&spon=2

  • ESC/ACCF/AHA/WHF Expert Consensus Document

Circulation.2012; 126: 2020-2035  Published online before print August 24, 2012,doi: 10.1161/​CIR.0b013e31826e1058

Third Universal Definition of Myocardial Infarction

  1. Kristian Thygesen;
  2. Joseph S. Alpert;
  3. Allan S. Jaffe;
  4. Maarten L. Simoons;
  5. Bernard R. Chaitman;
  6. Harvey D. White
  7. the Writing Group on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction
  1. *Corresponding authors/co-chairpersons: Professor Kristian Thygesen, Department of Cardiology, Aarhus University Hospital, Tage-Hansens Gade 2, DK-8000 Aarhus C, Denmark. Tel: +45 7846-7614; fax: +45 7846-7619: E-mail: kristhyg@rm.dk. Professor Joseph S. Alpert, Department of Medicine, Univ. of Arizona College of Medicine, 1501 N. Campbell Ave., P.O. Box 245037, Tucson AZ 85724, USA, Tel: +1 520 626 2763, Fax: +1 520 626 0967, E-mail: jalpert@email.arizona.edu. Professor Harvey D. White, Green Lane Cardiovascular Service, Auckland City Hospital, Private Bag 92024, 1030 Auckland, New Zealand. Tel: +64 9 630 9992, Fax: +64 9 630 9915, E-mail: harveyw@adhb.govt.nz.

Table of Contents

  • Abbreviations and Acronyms. . . . . . . . . . . . . . . . . . . .2021

  • Definition of Myocardial Infarction. . . . . . . . . . . . . . .2022

  • Criteria for Acute Myocardial Infarction. . . . . . . . . . . .2022

  • Criteria for Prior Myocardial Infarction. . . . . . . . . . . .2022

  • Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2022

  • Pathological Characteristics of Myocardial Ischaemia and Infarction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2023

  • Biomarker Detection of Myocardial Injury With Necrosis. . .2023

  • Clinical Features of Myocardial Ischaemia and Infarction. . .2024

  • Clinical Classification of Myocardial Infarction. . . .2024
    • Spontaneous Myocardial Infarction (MI Type 1). . . .2024

    • Myocardial Infarction Secondary to an Ischaemic Imbalance (MI Type 2). . . . . . . . . . . . . . . . . . . . . . . .2024

    • Cardiac Death Due to Myocardial Infarction (MI Type 3). .2025

    • Myocardial Infarction Associated With Revascularization Procedures (MI Types 4 and 5). . . . . . . . . . . . . . . . . . …

New Definition for MI After Revascularization

Published: Oct 14, 2013 | Updated: Oct 15, 2013

By Todd Neale, Senior Staff Writer, MedPage Today
Reviewed by Zalman S. Agus, MD; Emeritus Professor, Perelman School of Medicine at the University of Pennsylvania and Dorothy Caputo, MA, BSN, RN, Nurse Planner

The Society for Cardiovascular Angiography and Interventions (SCAI) has released a new definition for myocardial infarction (MI) following coronary revascularization aimed at identifying only those events likely to be related to poorer patient outcomes.

In the new criteria — published as an expert consensus document inCatheterization and Cardiovascular Interventions and the Journal of the American College of Cardiology — creatine kinase-myocardial band (CK-MB) is the preferred cardiac biomarker over troponin, and much greater elevations are required to define a clinically relevant MI compared with the universal definition of MI proposed in 2007 and revised in 2012.

Also, the new definition uses the same biomarker elevation thresholds to identify MIs following both percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG), whereas the universal definition has different thresholds for events following the two procedures.

“What we’ve really tried to emphasize in this classification scheme is the primary link between biomarker elevations and prognosis,” according to Gregg Stone, MD, of Columbia University Medical Center and the Cardiovascular Research Foundation in New York City, one of the authors of the document.

“In the universal definition of MI, they even acknowledged that their criteria were arbitrary,” Stone said in an interview. “We’ve tried to reduce the arbitrariness of the cutoff values that we selected so that the researcher, academician, clinician, hospital administrator, etc., can be confident that these levels that we’re recommending are the ones that are associated with a worse prognosis for patients suffering periprocedural complications.”

The Change

The existing universal definition for MI defines events following PCI according to an increase in cardiac troponin to greater than five times the 99th percentile upper reference limit (URL) within 48 hours when baseline levels are normal, with confirmation by electrocardiogram (ECG), imaging, or symptoms.

For CABG-related MI, the increase must be more than 10 times the 99th percentile URL within 48 hours when baseline levels are normal, with confirmation by ECG, angiography, or imaging.

But, Stone and colleagues wrote, the relationship between that degree of troponin elevation after a revascularization procedure and prognosis is not as strong as the association between a CK-MB elevation and patient outcomes.

Using a small elevation in troponin to define a post-procedure MI could find myocardial necrosis that is unlikely to be associated with poor clinical outcomes, which could have far-reaching implications, they wrote.

“Widespread adoption of an MI definition not clearly linked to subsequent adverse events such as mortality or heart failure may have serious consequences for the appropriate assessment of devices and therapies, may affect clinical care pathways, and may result in misinterpretation of physician competence,” they wrote.

To address that issue, the expert panel convened by SCAI sought to define clinically relevant MI after PCI or CABG.

A clinically relevant MI is defined in the new document based on an increase of at least 10 times the upper limit of normal in the level of CK-MB within 48 hours after a revascularization procedure when baseline levels are normal.

When the CK-MB level is not available, then an increase in troponin I or T of at least 70 times the upper limit of normal can be used to define a clinically relevant MI, according to the authors.

However, if an ECG shows new pathologic Q-waves in at least two contiguous leads or a new persistent left bundle branch block, then the thresholds can be lowered to at least five times and at least 35 times the upper limit of normal for CK-MB and troponin, respectively.

Further guidance is provided for identifying clinically relevant post-procedure MIs when the cardiac biomarker levels are elevated at baseline.

Dueling Definitions

Co-chairman of the Task Force for the Universal Definition of Myocardial Infarction, Harvey White, DSc, of Auckland City Hospital in Auckland, New Zealand, noted some limitations of the new definition, including the lack of a requirement for ischemic symptoms.

“Ischemic symptoms have always been a basic tenet of the diagnosis of MI, and it should be no different for a [PCI-related] MI,” he wrote in an accompanying editorial.

In addition, with the use of such large elevations in biomarker levels in the new definition, “there will be very few PCI-related events identified, and an opportunity to improve patient outcomes may be lost,” he wrote.

Troponin should remain the preferred biomarker over CK-MB, White argued, pointing to variability in and analytical issues with CK-MB assays, the need for sex-specific cutoffs for CK-MB levels, the need for higher thresholds of CK-MB to determine abnormalities because all individuals have circulating levels of the biomarker, and the reduced sensitivity and specificity of CK-MB.

Also, he said, CK-MB is becoming increasingly unavailable at medical centers.

“With CK-MB becoming obsolete, troponin will become the gold standard, and CK-MB will no longer have a role in defining PCI injury and infarction in clinical practice,” White wrote.

Stone admitted that troponin ultimately might be preferable to CK-MB because of its greater specificity, although the evidence does not yet support it.

“I think there’s a general desirability to move to troponins, although when you look at the data that’s out there it’s much stronger correlating CK-MB elevations to subsequent prognosis,” he said. “I think a lot of the troponin elevations are just noise or troponins are just too sensitive.”

Room for Both?

White noted in his editorial that “the rationale for the SCAI definition has been well articulated by its authors and may be appropriate in an individual trial, but it should not supplant the universal definition of MI,” he wrote.

When asked whether the new definition would replace the universal definition, Stone said there is a place for both sets of criteria.

“We would propose the clinically relevant definition be the one that is used to make most substantial decisions right now, [such as] trade-offs between efficacy and safety for new drugs and devices, in judging hospital systems and physicians, etc.,” he said. “But I do think there’s value in both, and they will both continue to evolve over time as new data becomes evident.”

http://www.medpagetoday.com/Cardiology/MyocardialInfarction/42256?xid=nl_mpt_DHE_2013-10-15&goback=%2Egmr_4346921%2Egde_4346921_member_5795830612724035588#%21 

Articles citing 

Third Universal Definition of Myocardial Infarction

  • Improved long-term clinical outcomes in patients with ST-elevation myocardial infarction undergoing remote ischaemic conditioning as an adjunct to primary percutaneous coronary interventionEur Heart J. 2013;0:eht369v1-eht369

  • The role of myeloperoxidase (MPO) for prognostic evaluation in sensitive cardiac troponin I negative chest pain patients in the emergency departmentEuropean Heart Journal: Acute Cardiovascular Care. 2013;2:203-210,
  • Coronary artery bypass grafting or percutaneous revascularization in acute myocardial infarction?Interact CardioVasc Thorac Surg. 2013;0:ivt381v1-ivt381,
  • Ischemic Conditioning as an Adjunct to Percutaneous Coronary InterventionCirc Cardiovasc Interv. 2013;6:484-492,
  • High sensitivity cardiac troponin in patients with chest painBMJ. 2013;347:f4222,
  • Chest Pain and Palpitations: Taking a Closer LookCirculation. 2013;128:271-277,
  • An Updated Definition of Stroke for the 21st Century: A Statement for Healthcare Professionals From the American Heart Association/American Stroke AssociationStroke. 2013;44:2064-2089,
  • Factors Influencing the 99th Percentile of Cardiac Troponin I Evaluated in Community-Dwelling Individuals at 70 and 75 Years of AgeClin. Chem.. 2013;59:1068-1073,
  • Detection and management of asymptomatic myocardial injury after noncardiac surgeryEuropean Journal of Preventive Cardiology.2013;0:2047487313494294v1-2047487313494294,
  • Postoperative Troponin Screening: A Cardiac Cassandra?Circulation. 2013;127:2253-2256,
  • Remote Ischemic Preconditioning Improves Outcome at 6 Years After Elective Percutaneous Coronary Intervention: The CRISP Stent Trial Long-term Follow-upCirc Cardiovasc Interv. 2013;6:246-251,
  • Outcomes for Clinical Studies Assessing Drug and Revascularization Therapies for Claudication and Critical Limb Ischemia in Peripheral Artery DiseaseCirculation. 2013;127:1241-1250,
  • Prevalence, Incidence, and Implications of Silent Myocardial Infarctions in Patients With Diabetes MellitusCirculation. 2013;127:965-967,
  • 2013 ACCF/AHA Key Data Elements and Definitions for Measuring the Clinical Management and Outcomes of Patients With Acute Coronary Syndromes and Coronary Artery Disease: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Clinical Data Standards (Writing Committee to Develop Acute Coronary Syndromes and Coronary Artery Disease Clinical Data Standards)Circulation. 2013;127:1052-1089,
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  • The curious life of the biomarkerJournal of the American Dental Association. 2013;144:126-128,
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Reporter: Aviva Lev-Ari, PhD, RN

See on Scoop.itCardiovascular Disease: PHARMACO-THERAPY

FDA Adds Antinausea, Cardiac Drugs to Watch List
Medscape
The beta blocker metoprolol succinate (Toprol-XL, AstraZeneca) also landed on the list, posted on the FDA Web site last month, because of reports that suggested therapeutic ineffectiveness.

FDA Adds Cardiac Drugs to Watch List

Jun 25, 2013

Drug & Reference Information

The other drug on the latest watch list, metoprolol succinate, is used to treat angina, heart failure, and hypertension

The US Food and Drug Administration (FDA) has put a class of antiemetic drugs, including ondansetron (Zofran, GlaxoSmithKline, and Zuplenz, Par Pharmaceutical), on its latest quarterly list of products to monitor because of potential signals of an increased risk for serotonin syndrome.

The beta blocker metoprolol succinate (Toprol-XL, AstraZeneca) also landed on the list, posted on the FDA Web site last month, because of reports that suggested therapeutic ineffectiveness.

The agency received reports of possible adverse events for these products in the FDA Adverse Event Reporting System (FAERS) database during the first 3 months of 2013. The FDA cautions that an appearance on the watch list does not mean that the agency has concluded that the drug poses the health risk reported through FAERS. What it does mean is that the FDA will investigate whether there is a causal connection. If there is one, the agency would consider a regulatory action such as collecting more data to better characterize the risk, revising the drug’s label, or requiring a risk evaluation and mitigation strategy.

Likewise, by adding a drug to the list, the FDA is not implying that clinicians should cease prescribing it or that patients should stop taking it, the agency says.

The antiemetics on the watch list belong to a subtype of serotonin blockers that bind to the 5-HT3 receptor. Clinicians prescribe them to prevent nausea and vomiting in patients undergoing chemotherapy for cancer. Serotonin syndrome, which was reported to FAERS in conjunction with these antiemetics, is caused by excessive levels of the neurotransmitter. It can be fatal. Symptoms include confusion, agitation, dilated pupils, headache, rapid heart rate, and changes in blood pressure and temperature.

The other drug on the latest watch list, metoprolol succinate, is used to treat angina, heart failure, and hypertension.

Potential Signals of Serious Risks/New Safety Information Identified by FAERS, January 2013 to March 2013

Product name: active ingredient (trade) or product class Potential signal of a serious risk/new safety information Additional information (as of May 1, 2013)
Metoprolol succinate (Toprol-XL, AstraZeneca) extended-release products Lack of therapeutic effect, possibly related to product quality issues FDA is continuing to evaluate this issue to determine the need for any regulatory action.
Serotonin-3 (5-HT3) receptor antagonist products: ondansetron(Zofran, GlaxoSmithKline, andZuplenz, Par Pharmaceutical), palonosetron (Aloxi, Helsinn Healthcare), granisetron (Kytril, Hoffmann-La Roche) Serotonin syndrome FDA is continuing to evaluate this issue to determine the need for any regulatory action.

 SOURCE

http://www.medscape.com/viewarticle/806890

More information on FAERS and its quarterly watch list is available on the FDA Web site.

Potential Signals of Serious Risks/New Safety Information Identified by FAERS, January 2013 to March 2013

http://www.medscape.com/viewarticle/806890

Carvedilol superior to Metoprolol in MADIT-CRT analysis

APRIL 2, 2013 

Rochester, NY – Treatment with carvedilol is associated with a significant 30% reduction in the risk of hospitalization for heart failure (HF) or death when compared with patients treated metoprolol, according to a new analysis of the Multicenter Automatic Defibrillator Implantation Trial with Cardiac Resynchronization Therapy (MADIT-CRT) [1].

The benefit of carvedilol over metoprolol was more pronounced in the subgroup of patients with a cardiac resynchronization therapy defibrillator (CRT-D), where carvedilol was associated with a significant 39% reduction in the risk of hospitalization for HF or death, and in those with left bundle branch block (LBBB). In the LBBB patients with a CRT-D, treatment with carvedilol was associated with a 49% reduction in risk compared with metoprolol.

“Furthermore, we found a pronounced dosage-dependent relationship between outcome and dose in carvedilol, which was not found in metoprolol-treated patients,” write Dr Martin Ruwald (University of Rochester Medical Center, New York) and colleagues in the April 1, 2013 issue of the Journal of the American College of Cardiology.

Benefit follows results observed in COMET
The MADIT-CRT study was presented and published in 2009 and included patients with mild HF or left ventricular dysfunction without symptoms. Participants in the trial had NYHA class 1 and 2 disease, systolic dysfunction, and ventricular dyssynchrony (wide QRS complexes). As reported by heartwire, the study showed that the addition of resynchronization pacing in primary-prevention patients with an implantable cardioverter defibrillator (ICD) reduced the risk of HF events by approximately one-third over 2.5 years.

Both metoprolol and carvedilol have a class IA indication in the management of patients with HF, with choice of the drug left to the discretion of the physician. In the Carvedilol or Metoprolol European Trial (COMET), there was an absolute 5.7% survival benefit with carvedilol over metoprolol. Other studies and analyses have suggested that there are differences between the two beta-blockers, say Ruwald and colleagues.

In this analysis of MADIT-CRT, which included 1515 patients with left ventricular ejection fraction (LVEF)<30%, QRS duration >130 ms, and NYHA functional class 1 or 2, the primary end point of hospitalization for HF or death from any cause occurred in 132 patients (30%) taking metoprolol and 243 patients (23%) taking carvedilol. During the 3.4-year follow-up, 48 patients (11%) taking metoprolol and 104 patients (10%) taking carvedilol died.

In multivariate analysis, the reduction in the primary end point with carvedilol translated into a 30% reduction in risk compared with metoprolol, a benefit that was driven primarily by a reduction in HF hospitalizations. There was only a trend toward a reduction in the risk of ventricular tachycardia/ventricular fibrillation (VT/VF). The reduction in the risk of hospitalization for HF/death from any cause was more pronounced in patients receiving CRT-Ds.

Reduction in HF hospitalization/death (carvedilol vs metoprolol)

Study population and subgroups Hazard ratio (95% CI)
MADIT-CRT 0.70 (0.57-0.87)
CRT-D 0.61 (0.46-0.82)
ICD 0.81 (0.59-1.11)
CRT-D and LBBB 0.51 (0.35-0.76)
CRT and non-LBBB 0.79 (0.51-1.23)
ICD and LBBB 0.96 (0.66-1.39)
ICD and non-LBBB 0.55 (0.30-1.00)
LBBB 0.73 (0.56-0.95)
Non-LBBB 0.64 (0.45-0.91)

The researchers note that mean carvedilol and metoprolol doses in MADIT-CRT were 18 mg and 64 mg, respectively. These dosages are comparable to real-life dosages administered to patients in the clinical setting, although somewhat lower than in previous randomized controlled trials, according to the researchers.

“We speculate that low baseline resting heart rates in our study indicate that the patients generally were well titrated at baseline and that the rate may have contributed to a relatively low dose in both metoprolol and carvedilol compared with the beta-blocker dosage in clinical trials,” state Ruwald et al.

http://www.theheart.org/article/1524745.do

J Am Coll Cardiol. 2013 Apr 9;61(14):1518-26. doi: 10.1016/j.jacc.2013.01.020.

Effect of metoprolol versus carvedilol on outcomes in MADIT-CRT (multicenter automatic defibrillator implantation trial with cardiac resynchronization therapy).

Ruwald MHRuwald ACJons CAlexis JMcNitt SZareba WMoss AJ.

Source

Heart Research Follow-up Program, Cardiology Division, University of Rochester Medical Center, Rochester, NY 14642, USA. mruwald@hotmail.com

Abstract

OBJECTIVES:

This study sought to compare the effects of metoprolol and carvedilol in the MADIT-CRT (Multicenter Automatic Defibrillator Implantation Trial With Cardiac Resynchronization Therapy) study.

BACKGROUND:

The impact of beta-blockers in heart failure (HF) patients with devices is uninvestigated.

METHODS:

All patients receiving either metoprolol or carvedilol in the MADIT-CRT study were identified and compared. Time-dependent Cox proportional hazard regression analyses were performed to assess differences in hospitalization for HF or death and ventricular arrhythmias.

RESULTS:

Hospitalization for HF or death occurred in 30% of the patients on metoprolol and in 23% on carvedilol. Treatment with carvedilol was associated with a significantly decreased risk of hospitalization for HF or death when compared with metoprolol (hazard ratio [HR]: 0.70, [95% confidence interval (CI): 0.57 to 0.87], p = 0.001). This reduction in risk was further attenuated in the subgroup of cardiac resynchronization therapy with implantable cardioverter-defibrillator (CRT-D) patients (HR: 0.61 [95% CI: 0.46 to 0.82], p = 0.001) and CRT-D patients with left bundle branch block (LBBB) (HR: 0.51 [95% CI: 0.35 to 0.76], p < 0.001). Ventricular arrhythmias occurred in 26% and in 22%, respectively, of the patients receiving metoprolol or carvedilol (HR: 0.80 [95% CI: 0.63 to 1.00], p = 0.050). General use of beta-blockers and adherence in this study was high, and a clear dose-dependent relationship was found in carvedilol, but not in metoprolol.

CONCLUSIONS:

In HF patients in New York Heart Association functional class I and II and with wide QRS complexes, carvedilol was associated with a 30% reduction in hospitalizations for HF or death when compared with metoprolol. A novel beneficial and synergistic effect of carvedilol was seen in patients with CRT-D and LBBB. Furthermore, we found a pronounced dose-dependent relationship in carvedilol, but not in metoprolol.

http://www.ncbi.nlm.nih.gov/pubmed/23500269?dopt=Abstract

Extended-Release Metoprolol ( Toprol-XL) Must Be Combined With Alpha-Blocker in Pheochromocytoma

On February 12, the FDA approved safety labeling revisions for metoprolol succinate (Toprol-XL extended-release tablets; AstraZeneca LP) to provide recommendations regarding its use in the setting of pheochromocytoma.

Patients diagnosed with pheochromocytoma should only receive extended-release metoprolol in combination with an alpha-blocker and only after alpha-blocker therapy has been initiated. Administration of beta-blockers alone in this setting has been linked to a paradoxic increase in blood pressure because of the attenuation of beta-mediated vasodilation in skeletal muscle.

Metoprolol is a beta 1-selective (cardioselective) adrenoceptor-blocking agent indicated for the treatment of hypertension; angina pectoris; and stable, symptomatic heart failure of ischemic, hypertensive, or cardiomyopathic origin.

http://www.medscape.com/viewarticle/591151

Study Suggests Benefit For Beta Blockers During Noncardiac Surgery
The use of perioperative beta-blockade for noncardiac surgery has been declining as a result of the controversial POISE study, which turned up evidence for harm associated with extended-release metoprolol in this setting. Now a large new observational study published in JAMA offers a contrary perspective by suggesting that perioperative beta-blockade may be beneficial in low- to intermediate-risk patients. But without better evidence the debate about this topic is unlikely to be resolved. Martin London and colleagues performed a retrospective analysis of 136,745 patients who underwent noncardiac surgery at VA hospitals, 40…
Source: CardioBrief – April 23, 2013 Category: Cardiology Authors: Larry Husten Tags: Interventional Cardiology & Surgery Prevention, Epidemiology & Outcomes beta blockers JAMA Observational study Source Type: blogs

http://www.medworm.com/rss/search.php?t=Toprol&f=drugs&blogs=1

NDA 19-962/S-038 Page 3 Rx only

TOPROL-XL® 

(metoprolol succinate) 

EXTENDED-RELEASE TABLETS TABLETS: 25 MG, 50 MG, 100 MG, AND 200 MG

DESCRIPTION 

TOPROL-XL, metoprolol succinate, is a beta1-selective (cardioselective) adrenoceptor blocking agent, for oral administration, available as extended release tablets. TOPROL-XL has been formulated to provide a controlled and predictable release of metoprolol for once-daily administration. The tablets comprise a multiple unit system containing metoprolol succinate in a multitude of controlled release pellets. Each pellet acts as a separate drug delivery unit and is designed to deliver metoprolol continuously over the dosage interval. The tablets contain 23.75, 47.5, 95 and 190 mg of metoprolol succinate equivalent to 25, 50, 100 and 200 mg of metoprolol tartrate, USP, respectively. Its chemical name is (±)1-(isopropylamino)-3-[p-(2-methoxyethyl) phenoxy]-2-propanol succinate (2:1) (salt). Its structural formula is:

Metoprolol succinate is a white crystalline powder with a molecular weight of 652.8. It is freely soluble in water; soluble in methanol; sparingly soluble in ethanol; slightly soluble in dichloromethane and 2-propanol; practically insoluble in ethyl-acetate, acetone, diethylether and heptane. Inactive ingredients: silicon dioxide, cellulose compounds, sodium stearyl fumarate, polyethylene glycol, titanium dioxide, paraffin.

CLINICAL PHARMACOLOGY General 

Metoprolol is a beta1-selective (cardioselective) adrenergic receptor blocking agent. This preferential effect is not absolute, however, and at higher plasma concentrations, metoprolol also inhibits beta2adrenoreceptors, chiefly located in the bronchial and vascular musculature. Metoprolol has no intrinsic sympathomimetic activity, and membrane-stabilizing activity is detectable only at plasma concentrations much greater than required for beta-blockade. Animal and human experiments indicate that metoprolol slows the sinus rate and decreases AV nodal conduction.

Clinical pharmacology studies have confirmed the beta-blocking activity of metoprolol in man, as shown by (1) reduction in heart rate and cardiac output at rest and upon exercise, (2) reduction of systolic blood pressure upon exercise, (3) inhibition of isoproterenol-induced tachycardia, and (4) reduction of reflex orthostatic tachycardia. NDA 19-962/S-038 Page 4

The relative beta1-selectivity of metoprolol has been confirmed by the following: (1) In normal subjects, metoprolol is unable to reverse the beta2-mediated vasodilating effects of epinephrine. This contrasts with the effect of nonselective beta-blockers, which completely reverse the vasodilating effects of epinephrine. (2) In asthmatic patients, metoprolol reduces FEV1 and FVC significantly less than a nonselective beta-blocker, propranolol, at equivalent beta1-receptor blocking doses.

In five controlled studies in normal healthy subjects, the same daily doses of TOPROL-XL and immediate release metoprolol were compared in terms of the extent and duration of beta1-blockade produced. Both formulations were given in a dose range equivalent to 100-400 mg of immediate release metoprolol per day. In these studies, TOPROL-XL was administered once a day and immediate release metoprolol was administered once to four times a day. A sixth controlled study compared the beta1-blocking effects of a 50 mg daily dose of the two formulations. In each study, beta1-blockade was expressed as the percent change from baseline in exercise heart rate following standardized submaximal exercise tolerance tests at steady state. TOPROL-XL administered once a day, and immediate release metoprolol administered once to four times a day, provided comparable total beta1blockade over 24 hours (area under the beta1-blockade versus time curve) in the dose range 100–400 mg. At a dosage of 50 mg once daily, TOPROL-XL produced significantly higher total beta1-blockade over 24 hours than immediate release metoprolol. For TOPROL-XL, the percent reduction in exercise heart rate was relatively stable throughout the entire dosage interval and the level of beta1-blockade increased with increasing doses from 50 to 300 mg daily. The effects at peak/trough (ie, at 24-hours post-dosing) were: 14/9, 16/10, 24/14, 27/22 and 27/20% reduction in exercise heart rate for doses of 50, 100, 200, 300 and 400 mg TOPROL-XL once a day, respectively. In contrast to TOPROL-XL, immediate release metoprolol given at a dose of 50–100 mg once a day produced a significantly larger peak effect on exercise tachycardia, but the effect was not evident at 24 hours. To match the peak to trough ratio obtained with TOPROL-XL over the dosing range of 200 to 400 mg, a t.i.d. to q.i.d. divided dosing regimen was required for immediate release metoprolol. A controlled cross-over study in heart failure patients compared the plasma concentrations and beta1-blocking effects of 50 mg immediate release metoprolol administered t.i.d., 100 mg and 200 mg TOPROL-XL once daily. A 50 mg dose of immediate release metoprolol t.i.d. produced a peak plasma level of metoprolol similar to the peak level observed with 200 mg of TOPROL-XL. A 200 mg dose of TOPROL-XL produced a larger effect on suppression of exercise-induced and Holter-monitored heart rate over 24 hours compared to 50 mg t.i.d. of immediate release metoprolol.

The relationship between plasma metoprolol levels and reduction in exercise heart rate is independent of the pharmaceutical formulation. Using an Emax model, the maximum effect is a 30% reduction in exercise heart rate, which is attributed to beta1-blockade. Beta1-blocking effects in the range of 30– 80% of the maximal effect (approximately 8–23% reduction in exercise heart rate) correspond to metoprolol plasma concentrations from 30-540 nmol/L. The relative beta1-selectivity of metoprolol diminishes and blockade of beta2-adrenoceptors increases at plasma concentrations above 300 nmol/L.

Although beta-adrenergic receptor blockade is useful in the treatment of angina, hypertension, and heart failure there are situations in which sympathetic stimulation is vital. In patients with severely damaged hearts, adequate ventricular function may depend on sympathetic drive. In the presence of AV block, beta-blockade may prevent the necessary facilitating effect of sympathetic activity on conduction. Beta2-adrenergic blockade results in passive bronchial constriction by interfering with endogenous adrenergic bronchodilator activity in patients subject to bronchospasm and may also interfere with exogenous bronchodilators in such patients. NDA 19-962/S-038 Page 5

In other studies, treatment with TOPROL-XL produced an improvement in left ventricular ejection fraction. TOPROL-XL was also shown to delay the increase in left ventricular end-systolic and end-diastolic volumes after 6 months of treatment.

Pharmacokinetics 

Adults In man, absorption of metoprolol is rapid and complete. Plasma levels following oral administration of conventional metoprolol tablets, however, approximate 50% of levels following intravenous administration, indicating about 50% first-pass metabolism. Metoprolol crosses the blood-brain barrier and has been reported in the CSF in a concentration 78% of the simultaneous plasma concentration.

Plasma levels achieved are highly variable after oral administration. Only a small fraction of the drug (about 12%) is bound to human serum albumin. Metoprolol is a racemic mixture of R- and S- enantiomers, and is primarily metabolized by CYP2D6. When administered orally, it exhibits stereoselective metabolism that is dependent on oxidation phenotype. Elimination is mainly by biotransformation in the liver, and the plasma half-life ranges from approximately 3 to 7 hours. Less than 5% of an oral dose of metoprolol is recovered unchanged in the urine; the rest is excreted by the kidneys as metabolites that appear to have no beta-blocking activity. Following intravenous administration of metoprolol, the urinary recovery of unchanged drug is approximately 10%. The systemic availability and half-life of metoprolol in patients with renal failure do not differ to a clinically significant degree from those in normal subjects. Consequently, no reduction in dosage is usually needed in patients with chronic renal failure.

Metoprolol is metabolized predominantly by CYP2D6, an enzyme that is absent in about 8% of Caucasians (poor metabolizers) and about 2% of most other populations. CYP2D6 can be inhibited by a number of drugs. Concomitant use of inhibiting drugs in poor metabolizers will increase blood levels of metoprolol several-fold, decreasing metoprolol’s cardioselectivity. (See PRECAUTIONS, Drug Interactions.)

In comparison to conventional metoprolol, the plasma metoprolol levels following administration of TOPROL-XL are characterized by lower peaks, longer time to peak and significantly lower peak to trough variation. The peak plasma levels following once-daily administration of TOPROL-XL average one-fourth to one-half the peak plasma levels obtained following a corresponding dose of conventional metoprolol, administered once daily or in divided doses. At steady state the average bioavailability of metoprolol following administration of TOPROL-XL, across the dosage range of 50 to 400 mg once daily, was 77% relative to the corresponding single or divided doses of conventional metoprolol. Nevertheless, over the 24-hour dosing interval, ß1-blockade is comparable and dose-related (see CLINICAL PHARMACOLOGY). The bioavailability of metoprolol shows a dose-related, although not directly proportional, increase with dose and is not significantly affected by food following TOPROL-XL administration.

Pediatrics The pharmacokinetic profile of TOPROL-XL was studied in 120 pediatric hypertensive patients (6-17 years of age) receiving doses ranging from 12.5 to 200 mg once daily. The pharmacokinetics of metoprolol were similar to those described previously in adults. Age, gender, race, and ideal body weight had no significant effects on metoprolol pharmacokinetics. Metoprolol apparent oral clearance (CL/F) increased linearly with body weight. Metoprolol pharmacokinetics have not been investigated in patients < 6 years of age. NDA 19-962/S-038 Page 6

Hypertension 

The mechanism of the antihypertensive effects of beta-blocking agents has not been elucidated. However, several possible mechanisms have been proposed: (1) competitive antagonism of catecholamines at peripheral (especially cardiac) adrenergic neuron sites, leading to decreased cardiac output; (2) a central effect leading to reduced sympathetic outflow to the periphery; and

(3) suppression of renin activity.

Clinical Trials

In a double-blind study, 1092 patients with mild-to-moderate hypertension were randomized to once daily TOPROL-XL (25, 100, or 400 mg), PLENDIL® (felodipine extended release tablets), the combination, or placebo. After 9 weeks, TOPROL-XL alone decreased sitting blood pressure by 6-8/47 mmHg (placebo-corrected change from baseline) at 24 hours post-dose. The combination of TOPROL-XL with PLENDIL has greater effects on blood pressure.

In controlled clinical studies, an immediate release dosage form of metoprolol was an effective antihypertensive agent when used alone or as concomitant therapy with thiazide-type diuretics at dosages of 100-450 mg daily. TOPROL-XL, in dosages of 100 to 400 mg once daily, produces similar ß1-blockade as conventional metoprolol tablets administered two to four times daily. In addition, TOPROL-XL administered at a dose of 50 mg once daily lowered blood pressure 24-hours post-dosing in placebo-controlled studies. In controlled, comparative, clinical studies, immediate release metoprolol appeared comparable as an antihypertensive agent to propranolol, methyldopa, and thiazide-type diuretics, and affected both supine and standing blood pressure. Because of variable plasma levels attained with a given dose and lack of a consistent relationship of antihypertensive activity to drug plasma concentration, selection of proper dosage requires individual titration.

Angina Pectoris 

By blocking catecholamine-induced increases in heart rate, in velocity and extent of myocardial contraction, and in blood pressure, metoprolol reduces the oxygen requirements of the heart at any given level of effort, thus making it useful in the long-term management of angina pectoris.

Clinical Trials

In controlled clinical trials, an immediate release formulation of metoprolol has been shown to be an effective antianginal agent, reducing the number of angina attacks and increasing exercise tolerance. The dosage used in these studies ranged from 100 to 400 mg daily. TOPROL-XL, in dosages of 100 to 400 mg once daily, has been shown to possess beta-blockade similar to conventional metoprolol tablets administered two to four times daily.

Heart Failure 

The precise mechanism for the beneficial effects of beta-blockers in heart failure has not been elucidated. NDA 19-962/S-038 Page 7

Clinical Trials

MERIT-HF was a double-blind, placebo-controlled study of TOPROL-XL conducted in 14 countries including the US. It randomized 3991 patients (1990 to TOPROL-XL) with ejection fraction ≤ 0.40 and NYHA Class II-IV heart failure attributable to ischemia, hypertension, or cardiomyopathy. The protocol excluded patients with contraindications to beta-blocker use, those expected to undergo heart surgery, and those within 28 days of myocardial infarction or unstable angina. The primary endpoints of the trial were (1) all-cause mortality plus all-cause hospitalization (time to first event) and

(2) all-cause mortality. Patients were stabilized on optimal concomitant therapy for heart failure, including diuretics, ACE inhibitors, cardiac glycosides, and nitrates. At randomization, 41% of patients were NYHA Class II, 55% NYHA Class III; 65% of patients had heart failure attributed to ischemic heart disease; 44% had a history of hypertension; 25% had diabetes mellitus; 48% had a history of myocardial infarction. Among patients in the trial, 90% were on diuretics, 89% were on ACE inhibitors, 64% were on digitalis, 27% were on a lipid-lowering agent, 37% were on an oral anticoagulant, and the mean ejection fraction was 0.28. The mean duration of follow-up was one year. At the end of the study, the mean daily dose of TOPROL-XL was 159 mg.

The trial was terminated early for a statistically significant reduction in all-cause mortality (34%, nominal p= 0.00009). The risk of all-cause mortality plus all-cause hospitalization was reduced by 19% (p= 0.00012). The trial also showed improvements in heart failure-related mortality and heart failure-related hospitalizations, and NYHA functional class.

The table below shows the principal results for the overall study population. The figure below illustrates principal results for a wide variety of subgroup comparisons, including US vs. non-US populations (the latter of which was not pre-specified). The combined endpoints of all-cause mortality plus all-cause hospitalization and of mortality plus heart failure hospitalization showed consistent effects in the overall study population and the subgroups, including women and the US population. However, in the US subgroup (n=1071) and women (n=898), overall mortality and cardiovascular mortality appeared less affected. Analyses of female and US patients were carried out because they each represented about 25% of the overall population. Nonetheless, subgroup analyses can be difficult to interpret and it is not known whether these represent true differences or chance effects.

SOURCE

http://www.accessdata.fda.gov/drugsatfda_docs/label/2009/019962s038lbl.pdf

Clinical Endpoints in the MERIT-HF Study 

CLINICAL ENDPOINT NUMBER OF PATIENTS RELATIVE RISK (95% CI) RISK REDUCTION WITH TOPROLXL NOMINAL P-VALUE
PLACEBO N=2001 TOPROLXL N=1990
ALL-CAUSE MORTALITY PLUS ALL-CAUSE HOSPITALIZATION* 767 641 0.81 (0.730.90) 19% 0.00012

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Reporter: Ziv Raviv, PhD

FDA Approves BioMerieux’s BRAF Test as CDx, www.genomeweb.com

The FDA has very recently (May 29, 2013) approved two new drugs to treat unresectable and metastatic melanoma. Both drugs are inhibitors of B-Raf which is frequently mutated in melanoma (1). The new drugs are products of GlaxoSmithKline (GSK): Dabrafenib (marked as Tafinlar), a B-Raf inhibitor aimed to treat melanoma patients harboring V600E mutation (2), and Trametinib (marked as Mekinist), a MEK inhibitor that was shown in phase III clinical trials to be efficient for treating melanoma patients with BRAF V600E or V600K mutations (3). Both drugs are given orally and approved as single agents. About 75,000 new cases of melanoma are being diagnosed in the US and above 9,000 people die from the disease, each year. Until recently metastatic melanoma was considered an incurable disease with very poor prognosis and limited survival rates. These new two drugs are now joining the first two drugs approved in 2011 to treat metastatic melanoma that are already in clinical use – vemurafenib (Zelboraf) which is also a B-Raf inhibitor (4), and ipilimumab (Yervoy). The introduction of the two drugs was co-approved in concert with the THxID BRAF test from BioMérieux. This PCR-based BRAF test is designed to determine whether a melanoma patient harbors the V600E or V600K BRAF gene mutation and will assist directing the correct treatment to be given to patients. This BRAF mutation test is the second companion diagnostic approved for BRAF mutation detection following the approval of Roche’s cobas 4800 BRAF V600 Mutation Test in August 2011. Overall, the association of diagnostics with treatments as approved in this case is another step further in the ongoing efforts invested by pharmaceutical and diagnostic companies toward establishing personalized medicine to treat cancer patients.

Resources:

FDA press release

GenomeWeb report

References

  1. Mutations of the BRAF gene in human cancer. Davies H et al. Nature. 2002 Jun 27;417(6892):949-54.
  2. Dabrafenib in BRAF-mutated metastatic melanoma: a multicentre, open-label, phase 3 randomized controlled trial. Hauschild A et al. Lancet. 2012 Jul 28;380(9839):358-65.
  3. Improved survival with MEK inhibition in BRAF-mutated melanoma. Flaherty KT et al. N Engl J Med. 2012 Jul 12;367(2):107-14
  4. Improved Survival with Vemurafenib in Melanoma with BRAF V600E Mutation. Chapman PB et al. N Engl J Med. 2011 Jun 30;364(26):2507-16

Related articles on this Open Access Online Scientific Journal

  1. Whole exome somatic mutations analysis of malignant melanoma contributes to the development of personalized cancer therapy for this disease. Author: Ziv Raviv PhD
  2. In focus: Melanoma Genetics. Curator: Ritu Saxena, PhD
  3. In focus: Melanoma therapeutics. Author and Curator: Ritu Saxena, PhD

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Curator: Aviva Lev-Ari, PhD, RN

Intellectual Property: Code of Ethics Violation – A Big Pharma Sponsor of Academic R&D bypassed A University’s Technology Transfer Office: UCLA slams the door on GlaxoSmithKline’s latest R&D competition

UCLA slams the door on GlaxoSmithKline’s latest R&D competition – FierceBiotech http://www.fiercebiotech.com/story/ucla-slams-door-glaxosmithklines-latest-rd-competition/2013-05-30#ixzz2UoFhfUlh

http://www.fiercebiotech.com/story/ucla-slams-door-glaxosmithklines-latest-rd-competition/2013-05-30?utm_medium=nl&utm_source=internal

Fast Track or End Run?

May 28, 2013
 

These days many research universities are constantly looking for new grant competitions and encouraging their faculty members to apply. On Friday, the University of California at Los Angeles took the unusual step of telling professors not to apply to a major new grant competition from a pharmaceutical company, saying that the program violated university rules.

An e-mail marked “urgent” was sent Friday to all faculty members and deans about the Discovery Fast Track Competition, which was just announced this month and for which the sponsor — GlaxoSmithKline — is approaching faculty members directly, bypassing technology transfer offices at universities.

The company announced that the program was an attempt to reward academic researchers by offering a “fast track” to financing their most creative ideas. Faculty members are invited to submit short proposals and promised a quick decision later this year, leading to funding. The news release announcing the program this month said that grants would start promptly, without contract negotiations between the company, the researchers or their universities.

“To avoid initial contract negotiations, which are often perceived as the biggest bottleneck in the pharma/academia collaborative process, the [GlaxoSmithKline] team conceived the Discovery Fast Track competition as a means to rapidly identify and screen the most promising hypotheses in academia,” it said.

Faculty members just started to receive invitations last week, and when UCLA officials saw the terms of the proposed agreement, they took a step they have not taken previously — and told the entire campus not to apply.

“Please be advised that the terms and conditions do not adhere to UC policy because faculty have prior and ongoing obligations under the patent policy to disclose all discoveries to the university and have assigned patent rights to the university. Participation in the GSK competition would violate these policies and obligations,” said the e-mail, from James S. Economou, vice chancellor for research, and Brendan J. Rauw, associate vice chancellor for research and executive director of entrepreneurship.

In an interview, Rauw said that most proposals for corporate support for faculty members are coordinated through the university, which can negotiate terms consistent with university rules. He said that there was an inherent problem in a company saying that there could be no contract negotiations. Further, Rauw said that faculty members were being asked to give away rights they didn’t necessarily have (since the university has rules both for sharing intellectual property and assuring that agreements are consistent with academic principles). He also said that the phrasing of the grant proposal suggested that “background IP” from past work might be covered — even though it was not clear the company was entitled to those rights.

“This opens up our entire portfolio to a pharma company with no guarantee that our rights will be protected,” he said.

Rauw said UCLA faculty members may be among the first to have received the invitations. When he conferred with colleagues on other UC campuses last week, they had yet to receive grant details.

He noted that there has been “a perception” that universities “have given too much away” when dealing with pharmaceutical companies. Rauw said that UCLA has approved of grant relationships between GlaxoSmithKline and faculty members in the past (without problems), and that UCLA has reached out to the company to talk about how rules might be changed so that faculty members could participate.

“This is a challenging situation for us,” he said. “We are trying as a university to be open for industry and find opportunities for increased collaboration. But there is a balance there. We had to make a decision that this went too far.”

A spokeswoman for GlaxoSmithKline Friday said via e-mail Monday that she couldn’t comment on the UCLA concerns directly, but that the program was “designed to balance the playing field and avoid early IP contract negotiations, which can be the biggest obstacle to collaborative drug discovery.” She added that “there may be situations where initial interpretation of the Discovery Fast Track terms & conditions … will preclude some technology transfer officers from allowing researchers affiliated with their institution to participate,” but that she hoped university officials would “make a determined effort to read the competition documents … in detail before coming to a conclusion as to the provisions of these documents and competition outcomes.”

http://www.insidehighered.com/news/2013/05/28/ucla-tells-professors-not-apply-major-new-pharmaceutical-grant#ixzz2UoG061ic

http://www.insidehighered.com/news/2013/05/28/ucla-tells-professors-not-apply-major-new-pharmaceutical-grant#ixzz2UcMH2G4S

Three new rules for biopharma collaborations

May 21, 2012 | By 

Last week I moderated a panel called “The New Rules of Partnerships and Collaborations” at the Convergence East conference on Cape Cod, and the experience gave me a chance to probe some of the biopharma industry’s top dealmakers about their preferences and prejudices going into talks with other companies. I’ve decided to write down three key observations or “rules” that emerged during the panel and other notes from the Convergence meeting.

1. Competition is heating up for compelling clinical-stage assets–and not just those in Phase III trials. Take Biogen Idec’s ($BIIB) recent buyout of Stromedix for its Phase II-ready antibody STX-100 for combating fibrosis. Apparently, Pfizer ($PFE) was interested in buying the asset, Jose-Carlos Gutierrez-Ramos, senior vice president of biotherapeutics R&D at the drug giant, revealed during the panel. Gutierrez-Ramos and Steven Holtzman, Biogen’s chief dealmaker (who obviously won the Stromedix deal), traded some jabs about why Biogen prevailed. The bottom line: Stromedix had options.

2. Which partners are most coveted among biotechs? At least in oncology, Celgene ($CELG) appears to be winning over collaborators. In one off-the-record conversation, two heads of business development told me that biotechs are warming up to the flexibility and creativity of the Summit, NJ-based drugmaker in deals. Celgene has been quite active with the recent buyout of Avila Therapeutics,partnership deal with Epizyme and ongoing tie-up with Agios Pharmaceuticals. Yet I wonder whether sharp biotech dealmakers in Cambridge, MA, are getting the best of Celgene at the negotiating table.

This 3-part webinar series is specifically geared toward the non-science professional who needs to better understand industry terminology, science, techniques and issues. This series provides an overview of the science and technology used to enable discovery and the processes scientists use to discover new therapeutics. Register Now!

For instance, one of my panelists, Anna Protopapas, executive vice president of global business development at Takeda Pharmaceutical, didn’t think that her company would have bought Avila Therapeutics under the terms that Celgene did early this year. Protopapas noted that the key asset in the deal, Avila’s Phase I Btk inhibitor, is a third-in-class compound, and first-in-class cancer drugs have an edge because of the difficulty that later drugs in the same class face in besting them. Did Celgene–which shelled out $350 million upfront and promised up to $575 million more in milestones–overpay for Avila?

3. Big Pharma can be your friend. Sure, we know about the monumental problems large drugmakers face from expiring patents on key drugs and assaults on their old business models. And, yes, drugmakers are entertaining all kinds of diverse deal structures with biotech companies to soften the blow. Yet every week or so we learn of another strategy drugmakers are using to efficiently develop products. Pfizer’s Gutierrez-Ramos shared one with me (though it wasn’t covered during the panel). He’s now looking for biotech partners that are interested in taking over development of drugs from Pfizer’s pipeline. He’s offering the compounds for free and willing to share in the success of the programs down the line.

Of course, Pfizer’s strategy here builds on the Center for Therapeutic Innovation, which the drug giant expanded last year through several collaborations with academic groups, which work with CTI on translational research. Like CTI, externalizing clinical development of Pfizer compounds at biotech companies, including venture-backed startups, lets the drug giant tap expertise that doesn’t reside under its own roof.

“I think the misperception is that,” outside of large buyouts and tiny deals, “Pfizer is not a great partner to work with because, due to the big acquisitions, we are product-driven [and] that the perception out there is that we just want products,” Gutierrez-Ramos said. “And what we have been trying to re-prove over the last two years is that the new Pfizer is not like that.” — Ryan McBride (Email | Twitter)

Three new rules for biopharma collaborations – FierceBiotech http://www.fiercebiotech.com/story/three-new-rules-biopharma-collaborations/2012-05-21#ixzz2UoEEjN00

http://www.fiercebiotech.com/story/three-new-rules-biopharma-collaborations/2012-05-21

20 Major Pharma-Academic Alliances in 2012

By Skye Toor and Ryan McBride

Big Pharma companies’ insatiable needs for growing their pipelines and grabbing dibs on hot new science send them running to academic labs. With some pharma groups slashing internal R&D, drugmakers have taken a shining to funding discovery and early R&D work at universities and academic medical centers.

Pharma groups have dabbled in commercializing innovations from academia for decades, but what’s happened more recently is a drive to expand the number and breadth of collaborations with academics and other external groups. Traditional pharma players such as Sanofi ($SNY), Eli Lilly ($LLY) and Pfizer ($PFE) have realized that their internal R&D groups alone aren’t enough.

Here we’ve rounded up 20 notable pharma-academic collaborations from 2012 or those that made headlines this year. Check out the list and learn where Big Pharma is placing its bets and seeding projects that could yield big-time products down the road.

Lilly backs $50M launch of public/private biotech research institute

May 30, 2013 | By 

Indiana’s biotech cluster just got a big boost. Eli Lilly ($LLY) and Roche Diagnostics ($RHHBY) have joined an industry consortium that will help launch a new research institute in Indiana that plans to hire a staff of about 100 investigators to pursue new treatments for a slate of metabolic diseases. And they’ll be joined by Notre Dame, Purdue and Indiana University, with the state chipping in the first $25 million of a $50 million startup fund.

Industry and philanthropic groups are being tapped for the second half of that start-up budget, with future bills covered by industry and government-sponsored research programs into cardiovascular disease, diabetes, obesity and nutrition. The Indiana Biosciences Research Institute has already put out feelers for a new director and staff, which will be expected to help lead teams of collaborators drawn from the industry as well as regional universities.

The new institute’s research mission fits neatly into Eli Lilly’s corporate R&D strategy, which is closely focused on diabetes as one of its key disease areas.

INDIVIDUAL SESSION: $129, FULL SERIES: $239This 3-part webinar series is specifically geared toward the non-science professional who needs to better understand industry terminology, science, techniques and issues. This series provides an overview of the science and technology used to enable discovery and the processes scientists use to discover new therapeutics. Register Now!

“The Indiana Biosciences Research Institute will attract local and national scientific leaders beginning with the CEO and the recruitment of research “Indiana Fellows,” says the group’s press release. “These research fellows will lead teams of scientists and partner with industry and universities on research projects. These teams will consist of experts across a spectrum of competencies, including bioengineering, bioinformatics, nanotechnology and agriculture. These cross-functional teams will share resources and research laboratories at the Indiana Biosciences Research Institute and will work onsite at industry and research university labs with academic and industry scientists.”

– here’s the press release
– read the story from the Indianapolis Business Journal

Special Report: 20 Major Pharma-Academic Alliances in 2012

Related Articles:
Pfizer taps UCSF for small-molecule drug discovery
Three new rules for biopharma collaborations
Roche breaks ground on $300M diagnostics expansion

Lilly backs $50M launch of public/private biotech research institute – FierceBiotech http://www.fiercebiotech.com/story/lilly-backs-50m-launch-publicprivate-biotech-research-institute/2013-05-30#ixzz2UnscEHzj

20 Major Pharma-Academic Alliances in 2012 – FierceBiotech http://www.fiercebiotech.com/slideshows/20-major-pharma-academic-alliances-2012#ixzz2UnqkaqMH

http://www.fiercebiotech.com/slideshows/20-major-pharma-academic-alliances-2012?utm_medium=nl&utm_source=internal

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