Chen SH, Li DL, Yang F, et al. Gemcitabine-induced pancreatic cancer cell death is associated with MST1/Cyclophilin D mitochondrial complexation. Biochimie. 2014 Apr 13. Epub ahead of print]. PMID: 24732633. Su CH, Chu WC, Lan KH, et al. Gemcitabine causes telomere attrition by stabilizing TRF2. Eur J Cancer. 2012 Dec;48(18):3465-74. PMID: 22704123. Greggs WM 3rd, Clouser CL, Patterson SE, et al. Discovery of drugs that possess activity against feline leukemia virus. J Gen Virol. 2012 Apr;93(Pt 4):900-5. PMID: 22258856. Cerqueira NM, Fernandes PA, Ramos MJ. Understanding ribonucleotide reductase inactivation by gemcitabine. Chemistry. 2007;13(30):8507-15. PMID: 17636467. Blackwood E, Epler J, Yen I, et al. Combination drug scheduling defines a “window of opportunity” for chemopotentiation of gemcitabine by an orally bioavailable, selective ChK1 inhibitor, GNE-900. Mol Cancer Ther. 2013 Oct;12(10):1968-1980. PMID: 23873850. Reconstituted gemcitabine as the hydrochloride salt in the original vials is chemically stable at room temperature for 35 days but may develop crystals when stored at 4 degrees C. The crystals do not redissolve upon warming. Gemcitabine prepared as intravenous admixtures of 0.1 and 10 mg/mL as the hydrochloride salt in 5% dextrose injection and 0.9% sodium chloride injection in PVC bags and as a solution of 38 mg/mL in 0.9% sodium chloride injection packaged in plastic syringes is physically and chemically stable for at least 35 days at 4 degrees C and 23 degrees C. Gemcitabine as the hydrochloride salt is stable for at least 7 days at concentrations of 0.1, 10, and 38 mg/mL in 5% dextrose injection and 0.9% sodium chloride injection stored at 32 degrees C during simulated ambulatory infusion.