A novel, orally administered drug candidate, TTP488, has demonstrated clinical evidence of slowing of cognitive decline over 18 months of therapy in patients with mild to moderate Alzheimer's disease. TTP488 is a small-molecule drug that is the first to show clinical benefit from research on the receptor for advanced glycation endproducts (RAGE), a new biochemical target in Alzheimer's disease treatment.
TransTech Pharma, Inc. of High Point, North Carolina discovered, developed and owns all rights to this drug candidate.
These new clinical results arise out of a trial sponsored by Pfizer, Inc., and conducted by the Alzheimer's Disease Cooperative Study, a national research consortium funded by the National Institute on Aging, a part of the National Institutes of Health. The trial involved 399 patients with mild to moderate Alzheimer's disease at over 40 of the country's leading teaching hospitals involved in Alzheimer's research.
Analysis, by TransTech Pharma and third-party experts, of the study data reveals a 26% benefit relative to placebo in cognitive decline over 18 months in the group that received a 5 mg dose of TTP488. A more pronounced effect was observed in subjects with mild Alzheimer's disease, who showed a 46% benefit over placebo.
"At present, no FDA-approved drug has been shown to stop, prevent or alter the course of cognitive decline in patients with Alzheimer's disease," said Dr. Adnan Mjalli, Chairman and Chief Executive Officer of TransTech Pharma. "We are very excited about this data, which may lead to an approvable, novel treatment for millions of patients suffering from Alzheimer's disease here in the United States and around the globe. Because demand remains high for a treatment that can preserve cognitive function in this population, TransTech Pharma will be exploring options for accelerated FDA approval of this novel Alzheimer's treatment."
Dr. Mjalli added his thoughts concerning the drug's novel target, RAGE. "Exploiting the RAGE pathway offers a completely new approach to the treatment of Alzheimer's disease. Mechanistically, TTP488 acts, in part, by restoring the normal balance of amyloid protein transport into and out of the brain. Restoring this natural balance in patients with Alzheimer's disease, who have diminished capacity to clear amyloid protein from the brain, may result in long-term disease modification and maintenance of cognitive function."