Memapsin 2 (beta-secretase) inhibitor drug, between fantasy and reality

Curr Alzheimer Res. 2007 Sep;4(4):418-22. doi: 10.2174/156720507781788864.

Abstract

A major strategy for the development of a disease-modifying therapy against Alzheimer's disease is pharmacological intervention designed to reduce levels of beta-amyloid in the brain. Among various ways of reducing beta-amyloid production, the inhibition of beta-secretase (memapsin 2, BACE) is particularly attractive. Not only does beta-secretase initiates the amyloid cascade, it also is an aspartic protease, a class of proteases for which successful inhibitor drugs have been developed to treat AIDS patients. Extensive efforts in research and development of a beta-secretase inhibitor drug have taken place in many laboratories during the past few years. However, no drug candidate is currently in clinical trials. In spite of the lack of obvious success, much progress has been made to incorporate the drug-like properties in the evolution of better inhibitors. The inhibitors from more recent generations are indeed similar in characteristics to other protease inhibitor drugs. This progress permits optimism that development of clinical candidates of beta-secretase inhibitor drugs is a realistic goal.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / enzymology*
  • Amyloid Precursor Protein Secretases / antagonists & inhibitors
  • Amyloid Precursor Protein Secretases / metabolism*
  • Animals
  • Aspartic Acid Endopeptidases / antagonists & inhibitors
  • Aspartic Acid Endopeptidases / metabolism*
  • Enzyme Inhibitors / chemistry
  • Enzyme Inhibitors / therapeutic use*
  • Humans
  • Models, Chemical

Substances

  • Enzyme Inhibitors
  • Amyloid Precursor Protein Secretases
  • Aspartic Acid Endopeptidases
  • BACE1 protein, human