Abstract
A dynamic target-based pharmacophoric model mapping the CD4 binding site on HIV-1 gp120 was built and used to identify new hits able to inhibit gp120-CD4 protein-protein interactions. Two compounds showed micromolar inhibition of HIV-1 replication in cells attributable to an interference with the entry step of infection, by direct interaction with gp120. Inactivity of compounds toward a M475I strain suggested specific contacts with the Phe43 cavity of gp120.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Anti-HIV Agents / chemistry*
-
Anti-HIV Agents / toxicity
-
Binding Sites
-
CD4 Antigens / chemistry
-
CD4 Antigens / metabolism*
-
Cell Line
-
Computer Simulation
-
HIV Envelope Protein gp120 / chemistry
-
HIV Envelope Protein gp120 / metabolism*
-
HIV-1 / drug effects*
-
Humans
-
Models, Chemical
-
Phenylpropionates / chemistry*
-
Phenylpropionates / toxicity
-
Phthalimides / chemistry*
-
Phthalimides / toxicity
-
Protein Interaction Domains and Motifs
-
Protein Interaction Mapping
-
Virus Replication / drug effects
Substances
-
Anti-HIV Agents
-
CD4 Antigens
-
HIV Envelope Protein gp120
-
Phenylpropionates
-
Phthalimides