Inhibition of HIV infection of H9 cells by chlorpromazine derivatives.
The binding between the HIV surface protein, gp120, and the CD4 coreceptor is known to be initiated by electrostatic interactions. Because of the ability of chlorpromazine to interact with proteins by charge transfer, we tested several derivatives for their ability to block binding of HIV to CD4+ cells. We have shown that 7,8-dioxo-chlorpromazine blocks binding of fluorescein isothiocyanate-labeled anti-Leu3a and rgp120 to peripheral human blood T4 cells and blocks syncytia formation between gp120- and CD4-expressing cells. We also found that 7,8-dioxo-chlorpromazine blocks HIV infectivity of H9 cells and acts synergistically with zidovudine.
Hewlett
I
I
FDA, Center for Biological Evaluation and Research, Bethesda, Maryland, USA.
Lee
S
S
Molnar
J
J
Foldeak
S
S
Pine
P S
PS
Weaver
J L
JL
Aszalos
A
A
D019380:Anti-HIV Agents / Q000494:pharmacology*; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism; D002460:Cell Line; D002746:Chlorpromazine / Q000031:analogs & derivatives / Q000494:pharmacology*; D006678:HIV / Q000187:drug effects*; D015699:HIV Envelope Protein gp120 / Q000378:metabolism; D006801:Humans; D016133:Polymerase Chain Reaction; D013601:T-Lymphocytes / Q000821:virology
D019380:Anti-HIV Agents; D015699:HIV Envelope Protein gp120; D002746:Chlorpromazine