Biogen Halts Aducanumab Studies When Trials Show Alzheimer’s Drug Ineffective

Shares of Biogen Inc took quite the nosedive this week after the biotechnology company reported upsetting results for its experimental Alzheimer’s drug, aducanumab.  The latest research leads that the medication is likely to be ineffective and that has caused the company to halt research in what is only the most recent setback for the drugmaker’s noble efforts to develop a therapy in this degenerative disease. 

Upon release of the news, shares of the Cambridge, MA-based company plummeted 27 percent—to $233—in premarket trading, in New York, on Thursday.  This shocking drop shaved off at least a quarter of the company’s total market value, which had reached an impressive $63 billion by close of trading day, Wednesday. 

Indeed, on Thursday, Biogen Inc—and research and development partner Eisai Co Ltd, of Japan—said that they will not continue the next two late-stage trials for the experimental drug.  These trials were designed to evaluate efficacy and safety of the drug but the latest results have, unfortunately, shown that these studies were unlikely to demonstrate efficacy.  It should be noted that they stopped the trial specifically on concerns about efficacy and not about concerns regarding safety. 

In response, Biogen chief executive officer Michel Vounatsos commented, “This disappointing news confirms the complexity of treating Alzheimer’s disease and the need to further advance knowledge in neuroscience.”

Vounatsos comment actually echoes a rather poignant truth in the medical biotech world:  that many companies have encountered major obstacles in their attempt to develop an effective Alzheimer’s drug.  As a matter of fact, several drugmakers have recently hit the mark while attempting such a feat.  Biogen, of course, is the most recent but Roche Holding AG has also persisted against many setbacks.  The Swiss company’s gantenerumab also failed to prove effective four years ago.  

More important, though, the failure of these drugs—and particularly aducanumab—comes as a disparagement to those who support the beta-amyloid hypothesis.  This is the belief that Alzheimer’s disease is the result of a build-up of beta-amyloid plaques in the brain, over decades, resulting in this specific form of dementia. Many had hoped that the aducanumab would have eliminated the beta-amyloid clumps to halt Alzheimer’s progression, thus helped to prove this theory.