V-165

V-165 potently inhibits the replication of various HIV-1, HIV-2 and SIV strains in MT-4 cells, with an EC₅₀ of 8.9 μM against HIV-1 (IIIB), and exhibits low cytotoxicity in MT-4 cells, with a CC₅₀ of 120.6 μM^[1].
V-165 remains active against HIV-1 strains resistant to entry inhibitors, non-nucleoside reverse transcriptase inhibitors, and nucleoside reverse transcriptase inhibitors in MT-4 cells, with EC₅₀ values ranging from 15.1 μM to 33.5 μM^[1].
V-165 inhibits the early replication steps (reverse transcription and/or integration) of HIV-1 in 293T cells, with an EC₅₀ of 17 μM for inhibiting transduction of VSV-G pseudotyped lentiviral vectors^[1].
V-165 inhibits HIV-1 reverse transcriptase activity in vitro, with IC₅₀ values of 4.8 μM and 24.6 μM when poly (rC).oligo (dG) and poly (rA).oligo (dT) are used as template primers, respectively, and shows weak correlation with cell-based antiviral activity^[1].
V-165 (60 min) potently inhibits HIV-1 integrase activity in vitro, with an IC₅₀ value of 0.9 μM for 3' processing, 0.3 μM for overall integration, and 16.1 μM for strand transfer. Its mechanism of action involves blocking the formation of integrase-DNA complexes^[1].
V-165 inhibits the activity of wild-type HIV-1 integrase with an IC₅₀ of 3.8 μM; among the tested mutants, the HIV-1 integrase^T206S/S230N double-mutant integrase shows the highest reduction in sensitivity (1.6-fold)^[2].
V-165 (72 μM) potently inhibits the integration process of HIV-1 in 293T cells transduced with VSV-G pseudotyped lentiviral vectors, without affecting total viral DNA synthesis or the formation of 2-LTR circles^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.