One of Biogen Idec’s competitors in the world of multiple sclerosis drugs reported some success today. Germany’s Merck KGaA says its experimental oral pill reached its goal of reducing the rate of MS flare-ups for patients in a two-year study.
Merck KGaA said patients on a low dose of its drug, cladribine, had a 58 percent lower rate of relapse compared with those on a placebo after two years. A high dose of the treatment was almost the same-it generated a 55 percent lower rate of flare-ups than a placebo. The results from the trial were strong enough that Merck KGaA plans to file an application in mid-2009 with U.S. and European regulators for permission to start selling the drug.
The results from Merck KGaA’s pill don’t appear to surpass the effectiveness of Biogen and Elan’s natalizumab (Tysabri), but they are significant for the field of MS treatment. That’s because all of the existing treatments have to be taken by injection, not in a more convenient oral pill form. Since MS is a chronic degenerative disease, in which the immune system damages nerve cells over a period of years, researchers have long sought a way to come up with a pill that would help patients comply with a long course of treatment. The Merck KGaA drug, along with a contender from Novartis, pose a threat to Biogen’s leadership as the world’s biggest seller of MS drugs. Biogen is attempting to fend off this competition with its own oral MS drug in development, called BG-12. If any of these make it to the marketplace, they will compete over a big potential pool of patients, with more than 400,000 in the U.S. and an estimated 2.5 million worldwide.
After the MS drug announcement, Biogen Idec (NASDAQ: [[ticker:BIIB]]) shares fell 6.2 percent, to $47.70 at 12:30 pm Eastern time. It’s possible that shares also declined because the Wall Street Journal reported today that Pfizer is in talks to acquire pharmaceutical giant Wyeth, dashing some investors’ hopes that it would make a bid for Biogen, according to Christopher Raymond, an analyst with Robert W. Baird.