Redoxal 

Redoxal is a dihydroorotate dehydrogenase (DHODH) inhibitor and anti-HIV-1 agent. Redoxal induces intracellular pyrimidine depletion by inhibiting the de novo pyrimidine biosynthesis pathway, enhances the protein stability of APOBEC3G (A3G), upregulates the abundance of A3G protein in cells and progeny viral particles, thereby strengthening the host endogenous antiviral restriction mediated by A3G. Redoxal selectively targets DHOdehase at the mitochondrial level, with an IC₅₀ of 430 nM for inhibiting DHO oxidation in human mitochondria and an IC₅₀ of 910 nM in rat mitochondria. Redoxal can be used in studies related to HIV-1 infection^[1][2].

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.

484.50

C₂₈H₂₄N₂O₆

52962-95-5

O=C(C1=C(NC2=CC=C(C3=CC(OC)=C(NC4=C(C(O)=O)C=CC=C4)C=C3)C=C2OC)C=CC=C1)O

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• [1]. Pery E, et al. Redoxal, an inhibitor of de novo pyrimidine biosynthesis, augments APOBEC3G antiviral activity against human immunodeficiency virus type 1. Virology. 2015;484:276-287.

  [2]. Knecht W, et al. Redoxal as a new lead structure for dihydroorotate dehydrogenase inhibitors: a kinetic study of the inhibition mechanism. FEBS Lett. 2000;467(1):27-30.