FTI 277 HCl是FTI 277的甲酯，是一種有效的選擇性farnesyltransferase (FTase)抑制劑，IC50為500 pM，選擇性比密切相關的GGTase I 高100倍。
FTI-277 inhibits Ras processing with an IC50 of 100 nM, but not the geranylgeranylated Rap1A processing in whole cells. FTI-277 induces accumulation of cytoplasmic non-farnesylated H-Ras, accumulates inactive Ras/Raf complexes in the cytoplasm, and blocks constitutive MAPK activation in H-RasF cells. FTI-277 causes increased apoptosis after irradiation and increases radiosensitivity in H-ras-transformed rat embryo cells. FTI-277 also inhibits cell growth and induces apoptosis in drug-resistant myeloma tumor cells. In SH-SY5Y cells, FTI-277 diminishes the toxic effects of methamphetamine on induction in cell degeneration, activation in c-Jun-N-terminal kinase cascades, and Ras activation.
In mice coinfected with hepatitis B virus (HBV) and HDV, FTI-277 (50 mg/kg/d i.p.) effectively clears HDV viremia.
FTI 277 HCl是FTI 277的甲酯，是一種有效的選擇性farnesyltransferase (FTase)抑制劑，IC50為500 pM，選擇性比密切相關的GGTase I 高100倍。FTI 277 HCl可抑制細胞生長并誘導凋亡。FTI 277 HCl可有效清除HDV病毒血癥。
| Target | Value |
FTase
(Cell-free assay)
|
500 pM
|
FTI-277抑制Ras加工，IC50 為100 nM，但不抑制全細胞中四異戊二烯化Rap1A加工。FTI-277誘導細胞質非法尼化H-Ras積累，在細胞質中積累無活性的Ras/Raf，并阻斷H-RasF細胞中組成型MAPK激活。 FTI-277引起輻射后細胞凋亡增加，并增加H-ras轉化的大鼠胚胎細胞的輻射敏感性。在耐藥骨髓瘤細胞中，F(xiàn)TI-277也會抑制細胞生長，并誘導細胞凋亡。在SH-SY5細胞中，F(xiàn)TI-277減少細胞退化，活化，c-Jun-N端激酶級聯(lián)和Ras激活過程中甲基苯丙胺誘導的毒性作用。
在感染乙型肝炎病毒(HBV) 和 HDV的小鼠體內，F(xiàn)TI-277 (50 mg/kg/d i.p.)有效清除HDV病毒血癥。
