A drug that was seen as a strong contender to slow the progression of Alzheimer’s disease has failed to deliver in the final stage of clinical trials.
The results, based on 2,000 patients with mild dementia, are a significant blow because there are currently no treatments to slow the effects of Alzheimer’s. Few have made it to phase 3 trials.
The drug, called solanezumab, is an injectable antibody designed to stick to amyloid plaques in the brains of Alzheimer’s patients and clear away the abnormal proteins.
Scientists had hoped that, by helping to destroy the sticky plaques in the early stages of the disease, the drug would protect patients against more severe cognitive decline later on.
However, the latest results, announced by the pharmaceutical company Eli Lilly ahead of the Clinical Trials on Alzheimer’s Disease conference in San Diego next month, show the drug has no significant benefits to memory when compared with the placebo taken by some patients.
John Lechleiter, president and chief executive of Eli Lilly, said: “The results of the solanezumab trial were not what we had hoped for and we are disappointed for the millions of people waiting for a potential disease-modifying treatment for Alzheimer’s.”
In a statement, the company said: “Lilly will not pursue regulatory submissions for solanezumab for the treatment of mild dementia due to Alzheimer’s disease.”Lilly’s shares plunged 14% on Wednesday before markets opened. The same drug failed in a large 2012 trial involving people with more advanced dementia, but the company had hoped it would be more effective if given at an earlier stage.
James Warner, a consultant psychiatrist in older people’s mental health at Imperial College London, said the results represented a failure. “To my knowledge, solanezumab is the first ‘next generation’ Alzheimer’s treatment to have concluded phase 3 trials,” he added.
“It was a potentially groundbreaking approach to treatment – regular injections of a compound designed to scavenge the protein called amyloid that is deposited in the brains of people with Alzheimer’s disease.”
Robert Howard, a professor of old-age psychiatry at University College London, said: “This is disappointing, but not a great surprise. What we have learned from several decades of research, and hundreds of failed Alzheimer’s disease trials, is that no matter how promising the basic and early-phase data, all that really matters is the results of these late-phase effectiveness trials.”
The findings also raise questions about whether pharmaceutical companies are on the right track in targeting amyloid plaques, which are one of the most visible hallmarks of Alzheimer’s in the brains of patients. Not all experts agree that the plaques are the root cause, with some arguing they are just a visible symptom of a more fundamental problem.
There are 850,000 people with dementia in Britain and this figure is expected to reach 1 million by 2025. Earlier this year, dementia overtook heart disease as the leading cause of death in England and Wales.
Between 2002 and 2012, 99.6% of drugs studies aimed at preventing, curing or improving Alzheimer’s symptoms were either halted or discontinued.
