Decitabine, 50 mg

A DNA methyltransferase inhibitor supplied as a 50 mg small molecule research reagent by STEMCELL Technologies. The compound is a hypomethylating agent that inhibits DNA synthesis by binding to DNA methyltransferase. It is a cytosine nucleoside analog that is incorporated into DNA strands during DNA replication; when DNA methyltransferase binds to DNA, the compound traps the enzyme and prevents it from continuing DNA replication (Kantarjian et al.).

Physical and chemical properties reported on the manufacturer's product sheet include: a white powder physical appearance; purity ≥ 98%; alternative names 5-aza-2'-deoxycytidine, 5-AzadCyD, and NSC-127716; CAS Number 2353-33-5; chemical formula C8H12N4O4; molecular weight 228.2 g/mol. The product is stable for 12 months from the date of receipt when stored at -20°C, and STEMCELL recommends storing all small molecules away from direct light, with a desiccant for long-term storage. Reported solubility is ≤ 45 mM in water and ≤ 105 mM in DMSO. Stock solutions should be prepared fresh before use, aliquoted into working volumes to avoid repeated freeze-thaw cycles, and final DMSO concentration in cell culture should be kept below 0.1% due to potential cell toxicity.

Published cancer research applications listed for this product include: inhibition of proliferation in A375, SKMEL1, SKMEL3, SKMEL28, MeWo, and B16 human cutaneous melanoma cell lines (Alcazar et al.); induction of apoptosis in U937 and HL60 human leukemia cell lines via increased generation of reactive oxygen species (Shin et al., 2012); induction of cell cycle arrest at G2/M phase in AGS gastric and A549 lung carcinoma cells (Shin et al., 2013); reduction of proliferative capacity and marginal increase in apoptosis in the Kasumi-1 AML cell line (Flotho et al.); and induction of cellular senescence by upregulation of p16ink4a in oral squamous cell carcinoma and hepatocellular carcinoma cell lines (Suh et al.; Timmermann et al.), as well as cellular senescence in HepG2 and Hep3B cell lines with p53-dependent tumor cell senescence and DNA double-strand breaks (Venturelli et al.).