Guadecitabine sodium (Synonyms: SGI-110 sodium; S-110 sodium) |
| Catalog No.GC36196 |
Guadecitabine is a novel hypomethylating dinucleotide of decitabine and deoxyguanosine that is resistant to degradation by cytidine deaminase.
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Cas No.: 929904-85-8
Sample solution is provided at 25 µL, 10mM.
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Guadecitabine is a novel hypomethylating dinucleotide of decitabine and deoxyguanosine that is resistant to degradation by cytidine deaminase. Guadecitabine Sodium is the easily dissolved form of Guadecitabine[1].
Guadecitabine (0.1, 0.3, 1, 5µM, 48h) increased sensitivity to cisplatin for both the parental and the resistant A2780 cells. Although among other ovarian cancer cell lines, the parental A2780- cisplatin resistant cells is considered to be cisplatin “sensitive”, it has a relatively high IC50 for the drug[2].
Guadecitabine (50nM-2µM, 24h) pretreatment synergistically interacted with ASTX660 to induce cell death in five AML cell lines (MOLM-13, ML-2, MV4-11, PLB-985, KG-1) with various genetic backgrounds and representing different AML subtypes [3].
Tumor-bearing immune-deficient mice were exposed subcutaneously to Guadecitabine at doses of 3, 6.1, or 10 mg/kg, daily for 5 days, with tumors harvested on day 7. Most mice treated on the 5 day schedule with 10mg/kg/day Guadecitabine died; all mice treated with 6.1mg/kg/day Guadecitabine developed gastrointestinal toxicity. Minimal toxicity was observed in mice treated with 3mg/kg/day. Guadecitabine treatment caused hypomethylation of LINE-1 and NY-ESO-1 at all doses[4].
References:
[1].Issa JJ, Roboz G, et al. Safety and tolerability of guadecitabine (SGI-110) in patients with myelodysplastic syndrome and acute myeloid leukaemia: a multicentre, randomised, dose-escalation phase 1 study. Lancet Oncol. 2015 Sep;16(9):1099-1110.
[2].Fang F, Munck J, et al. The novel, small-molecule DNA methylation inhibitor SGI-110 as an ovarian cancer chemosensitizer. Clin Cancer Res. 2014 Dec 15;20(24):6504-16.
[3].Dittmann J, Haydn T, et al. Next-generation hypomethylating agent SGI-110 primes acute myeloid leukemia cells to IAP antagonist by activating extrinsic and intrinsic apoptosis pathways. Cell Death Differ. 2020 Jun;27(6):1878-1895.
[4].rivastava P, Paluch BE, et al. Immunomodulatory action of SGI-110, a hypomethylating agent, in acute myeloid leukemia cells and xenografts. Leuk Res. 2014 Nov;38(11):1332-41.
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