Gemcitabine

Gemcitabine (LY 188011) is a pyrimidine nucleoside analog antimetabolite and an antineoplastic agent. Gemcitabine inhibits DNA synthesis and repair, and can modulate autophagy. Gemcitabine induces apoptosis through the activation of p38 MAPK. Gemcitabine demonstrates efficacy in mouse models of pancreatic and breast cancer. Gemcitabine can be used for cancer research, such as pancreatic cancer, non-small cell lung cancer, and breast cancer^[1][2][3][4]. IC50 & Target:DNA synthesis^[1] In Vitro:Gemcitabine (15 nM, 48 h) exerts synergistic cytotoxicity with Indole-3-carbinol (I3C) (HY-N0170) in BxPC-3 cells via enhancing the I3C-induced upregulation of hENT1 protein expression in pancreatic cancer cell lines such as BxPC-3, Mia Paca-2, and PANC-1^[1].
Gemcitabine (48 h) inhibits BxPC-3, Mia Paca-2, PANC-1, PL-45 and AsPC-1 cells with IC₅₀s of 37.6, 42.9, 92.7, 89.3 and 131.4 nM, respectively^[1].
Gemcitabine (10 μM, 24-72 h) induces apoptosis in PK-1 and PCI-43 human pancreatic cancer cells via activating p38 MAPK signaling pathway^[2]. In Vivo:Gemcitabine (50 mg/kg, i.p., twice weekly until the endpoint) increases median survival, inhibits tumor growth, reduces the incidence and multiplicity of pancreatic tumors, and decreases metastasis to the liver in LSL-Kras^G12D/+; LSL-Trp53^R172H; Pdx-1-Cre mice^[3].
Gemcitabine (10 mg/kg, i.v., every 3 days for 21 days) inhibits tumor growth in 4T1 xenograft mouse model^[4].