UCF 101 是竞争性的促凋亡蛋白酶Omi/HtrA2选择性抑制剂。它对 MI/R 损伤具有明显的心脏保护作用，还具有一定的神经保护作用。它在 543 nm 处具有天然的红色荧光，可用于监视其进入哺乳动物细胞的能力。

UCF 101 is a specific inhibitor of HtrA2 and reduces apoptosis in PC12 cells.

PC12 cells treated with 60 μM 6-OHDA for 24 h had significantly decreased cell viability compared to that of controls. A low concentration (2.5 μM) of UCF 101 decreased the apoptosis rate of the PD cell model, but a high concentration (≥10 μM) increased the apoptosis rate, compared to that of controls. 6-OHDA upregulated the expression of HtrA2, α-syn, CHOP, Grp78 and active caspase-3 and reduced the levels of TH and XIAP[3].

Administration of UCF 101 shortly before reperfusion reduced postischemic myocardial apoptosis in a dose-dependent fashion, with the maximal protective effect observed at a dose of 1.5 μmol/kg. This dose of UCF 101 (ie, 1.5 μmol/kg) was used in all subsequent experiments. To further establish that inhibition of Omi/HtrA2 protease activity led to significant inhibition of apoptosis, the effect of UCF 101 on DNA ladder formation, a hallmark of apoptotic cell death, was determined. 30 minutes of ischemia followed by 3 hours of reperfusion resulted in significant DNA fragmentation, which was significantly reduced by treatment with UCF 101 before reperfusion[2].UCF 101 reduced the level of ERS and apoptosis in vivo. The ratio of p-GSK3β (Tyr216 to Ser9) increased in PD rats[3].

313649-08-0

C27H17N3O5S

495.51

UCF 101

DMSO:12.5 mg/mL (25.23 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years