SGI-110 (S-110) is a stable and potent inhibitor for DNA methylation, inhibits DNMT1 when SGI-110 is activated by phosphorylation and incorporated into DNA.

>98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

SGI-110 sodium；S-110 sodium

DMSO

DNA Methyltransferase

After HCT116 colorectal carcinoma cells are treated for 6 days, a dose-dependent increase in p16expression is observed with S-110. In addition, T24 and HCT116 cells treated with S-110 or 5-aza-CdR for 3 days show a dose-dependent increase in the level of p16 protein, showing the competence of S-110 to inhibit DNA methylation and induce p16 at both mRNA and protein levels as well as 5-aza-CdR. Thus, S-110 is able to inhibit DNA methylation at 5′-region and induce the expression of the p16 gene in T24 and HCT116 cells at concentrations comparable to 5-aza-CdR, and the induction of p16 expression by both agents correlates with the demethylation at the 5′-end region of the gene in both cell lines. S-110 is slightly less toxic than 5-aza-CdR at the doses tested up to 1 μM concentration but displaying similar toxicity at 10 μM concentration.

S-110 at 10mg/kg is an effective dose at reducing DNA methylation and retarding tumor growth, and caused roughly the same level of toxicity as 5-Aza-CdR. S-110 is effective in vivo at reactivating the expression of the p16 gene, which is heavily methylated in the parent EJ6 cells. S-110 is effective in reducing the level of DNA methylation in vivo at the p16 promoter region. S-110 is better tolerated than 5-Aza-CdR in vivo, suggesting that it can be an attractive alternative for potential clinical use.