Genetic tests won’t be needed to determine whether AstraZeneca Plc’s anti-clot drug Brilinta works, according to a study that may be used to differentiate the medicine from the best-selling Plavix treatment.
Two gene variations that may change how patients respond to Plavix didn’t make Brilinta less effective, researchers said in a company-funded study presented today at the European Society of Cardiology conference in Stockholm. One of the two variations also didn’t reduce the effectiveness of Effient, another anti-clotting drug sold by Eli Lilly & Co. with partner Daiichi Sankyo Co., researchers said in a second study. Both studies were published today in The Lancet.
Plavix, which had $9.8 billion in sales last year for Sanofi-Aventis SA and Bristol-Myers Squibb Co., faces generic competition in the U.S. in 2012. Copies are already approved in Europe. While its low price may make the generic version, known chemically as clopidogrel, the treatment of choice, confirmation that newer medicines don’t require gene testing may also influence doctors, Alfred Bove, immediate past president of the American College of Cardiology, told journalists in Stockholm.
“Physicians don’t like complications,” Bove said. “If I told you there was an alternative to clopidogrel that worked the same way without the variations, they would jump on it.”
Brilinta cut the risk of heart attacks, strokes and death linked to heart disease more than Plavix, at a higher risk of spontaneous major bleeding, regardless of genetic variations, researchers said today. The international team analyzed gene variations in more than 10,000 patients who participated in the Plato study presented at last year’s European cardiovascular conference.
AstraZeneca, based in London, won the backing of a U.S. Food and Drug Administration advisory panel in July for Brilinta. An FDA decision on the drug is scheduled in September.
In the second study, funded by Lilly and Daiichi Sankyo, researchers analyzed patients from the 2007 Triton trial to find that a genetic variation that diminished the effectiveness of Plavix didn’t have the same effect on Effient’s potency.
The FDA warned in March that in certain patients, known as "poor metabolizers," a genetic variant could reduce the effectiveness of Plavix. Some 2 percent to 14 percent of the population aren’t able to metabolize the drug effectively, the agency said.
A third study funded by Paris-based Sanofi and New York-based Bristol-Myers and published today in the New England Journal of Medicine found Plavix was effective regardless of genetic variation in a group of lower-risk patients that included people with irregular heartbeat and chest pain.
Doctors should take into account a range of factors that might change the way a patient responds to blood-thinning therapy, including age, sex and body-mass index, Betti Giusti and Rosanna Abbate, of the Department of Medical and Surgical Critical Care at Careggi Hospital in Florence, Italy, said in a comment published alongside the Lancet articles.
Doctors may decide against genetic tests anyway, especially for patients who need to take a drug immediately and can’t wait weeks for test results, said David Holmes, president-elect of the American College of Cardiology.
"Everybody would like to think personalized medicine is going to be perfect," Holmes said. "We don’t have chapter and verse to make sure that’s the case. The whole field is in flux."