Redoxal

Redoxal potently and specifically inhibits the interaction between HIV-1 Vif and A3G peptide in a cell-free TR-FRET assay with an IC₅₀ of 0.88 μM^[1].
Redoxal (0.01-100 μM; 7 days) potently inhibits replication of diverse HIV-1 isolates in human PBMCs with confirmed IC₅₀ values from 0.59 to 2.94 μM and has a high therapeutic index^[1].
Redoxal (312.5-1250 nM; up to 9 days) inhibits HIV-1 replication in an A3G-dependent manner in CEM T cells, reduces Vif levels, increases cellular A3G levels, and enhances A3G incorporation into virions^[1].
Redoxal (1250 nM; 40 h) reduces HIV-1 production and virion infectivity in 293T producer cells, with ~50% of its antiviral activity dependent on A3G expression^[1].
Redoxal (1250 nM; 36 h) augments A3G protein stability in HIV-1 Vif-expressing 293T cells, with no impact on Vif protein stability^[1].
Redoxal (1250 nM; 40 h) augments cellular and virion-associated A3G levels and reduces HIV-1 infectivity by inhibiting de novo pyrimidine biosynthesis, as these effects are reversed by pyrimidine precursor supplementation in 293T cells^[1].
Redoxal acts as a non-competitive inhibitor of purified recombinant human dihydroorotate dehydrogenase with K_ic values ranging from 402 nM to 487 nM and K_iu values ranging from 506 nM to 507 nM^[2].
Redoxal acts as a non-competitive (mixed-type for QD) inhibitor of purified recombinant rat dihydroorotate dehydrogenase with K_ic values ranging from 116 nM to 216 nM and K_iu values ranging from 208 nM to 233 nM, and is 2-3-fold more potent against the rat enzyme than the human enzyme^[2].
Redoxal (1 nM-50 μM) can strongly inhibit the activity of dihydroorotate dehydrogenase in isolated human and rat liver mitochondria. The IC₅₀ for human was 0.43 μM and the IC₅₀ for rat was 0.91 μM, but it had no significant effect on succinate or NADH-induced mitochondrial respiration^[2].

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