UCF 101

Research use only, not for human use.

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

UCF 101 is a specific inhibitor of HtrA2 and reduces apoptosis in PC12 cells.(In Vitro):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.(In Vivo):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.UCF 101 reduced the level of ERS and apoptosis in vivo. The ratio of p-GSK3β (Tyr216 to Ser9) increased in PD rats.

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Animal Model:Adult male mice (20-25 g) with myocardial ischemia/reperfusion (MI/R) injury Dosage:0.6, 1.5, 1.8 μmol/kg Administration:I.p. 10 minutes before reperfusion Result:Reduced terminal dUTP nick end-labeling staining, incidence of DNA ladder fragmentation, and infarct size.

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Apoptosis

Apoptosis

nAChR

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313649-08-0

495.51

C27H17N3O5S

>98% (HPLC)

In Vitro:?DMSO : 12.5 mg/mL (25.23 mM)

[O-][N+](c(cccc1)c1-c1ccc(C=C(C(N(c2ccccc2)C(N2c3ccccc3)=S)=O)C2=O)o1)=O

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(-20℃)

With Ice Pack

≥ 2 years