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New Study Concludes There Are No Pharmacokinetic Drug Interactions Between Memantine and Donepezil

  [ 53 votes ]   [ Discuss This Article ] • March 10, 2003

Forest Laboratories, Inc. today announced the results of a new study which show there are no pharmacokinetic interactions between memantine, an investigational drug for Alzheimer's disease, and donepezil (Aricept(R)), an approved drug for the treatment of mild-to-moderate Alzheimer's disease. Data from the pharmacokinetic study, which was designed to assess for possible drug interactions between memantine and the most commonly prescribed Alzheimer's therapy donepezil, were presented last week at the American Medical Directors Association (AMDA) annual meeting in Orlando, Florida.

Researchers presenting the findings of this trial in 24 healthy subjects reported that memantine and donepezil do not interact pharmacokinetically, indicating the drugs do not interfere with each other's absorption, metabolism, distribution or elimination. In addition, co-administering memantine with donepezil did not significantly alter the inhibition of red blood cell acetylcholinesterase activity produced by donepezil alone.

"These new data demonstrate that memantine and donepezil do not exhibit a pharmacokinetic interaction when given concomitantly," said Lawrence S.
Olanoff, M.D., Ph.D., Executive Vice President, Forest Laboratories.

Memantine is the first of a new class of medications for Alzheimer's disease with a mechanism of action distinct from currently available drugs. Memantine is a moderate-affinity NMDA (N-methyl-D-aspartate) receptor antagonist. It is thought that overexcitation of NMDA receptors by the neurotransmitter glutamate may play a role in Alzheimer's disease as glutamate plays an integral role in the neural pathways associated with learning and memory. The excitotoxicity produced by excessive amounts of glutamate is thought to be responsible for neuronal cell dysfunction and the eventual cell death observed in Alzheimer's disease. Memantine is thought to selectively block the excitotoxic effects associated with excessive transmission of glutamate, while allowing for the physiological transmission associated with normal cell functioning.

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