HIV-1 latency remains a major problem for the eradication of viruses in infected individuals. We evaluated the effect of MC1293 on the epigenetic change at HIV-1 LTR and the induction of the latent viruses in the latency Jurkat T cell line. We found MC1293 can activate HIV-1 gene expression, increase the acetylation level of H3 and H4 at the nuc-1 site of HIV-1 LTR. In addition, MC1293 can synergize with prostratin to activate the HIV-1 promoter, and has relatively lower toxicity compared to Trichostatin A (TSA). The results suggest that the acetylation of histone plays an important role in regulating HIV-1 LTR gene expression, and MC1293 is potential drug candidate for antilatency therapies.