Valpromide is a carboxamide derivative of valproic acid with anticonvulsant properties and used in the treatment of epilepsy and some affective disorders. It is also a potent inhibitor of liver microsomal epoxide hydrolase.
Valpromide (VPM), an amide derivative of valproic acid that is not an HDAC (histone deacetylase) inhibitor, prevented expression of two EBV genes, BZLF1 and BRLF1, that mediate lytic reactivation. VPM also inhibited expression of a viral late gene, but not early genes, when BZLF1 was exogenously expressed. VPM selectively inhibits both viral and cellular gene expression[1]. Valpromide does not induce histone acetylation, does not induce demethylation or expression of CMV-GFP[2]. VPD (Valpromide) had little effect on limb morphology and no significant effect on HDAC activity or the expression of marker genes[3]. While both VPA (valproic acid) and sodium butyrate are reported to block sodium channel function as well as HDACs, regeneration was not inhibited by valpromide, an analogue of VPA that lacks HDAC inhibition but retains sodium channel blocking activity[4]. The HDAC inhibitor trichostatin A (TSA) also inhibited adipogenesis, whereas the VPA analog valpromide, which does not possess HDAC inhibitory effects, did not prevent adipogenesis[5].
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