UCF-101 Property

Boiling point:

651.8±65.0 °C(Predicted)

Density 

1.50±0.1 g/cm3(Predicted)

storage temp. 

-20°C

solubility 

DMSO: soluble5mg/mL, clear (warmed)

form 

powder

pka

-0.92±0.20(Predicted)

color 

light orange to dark orange

Stability:

Stable for 1 year from date of purchase as supplied. Solutions in DMSO or DMF may be stored at -20°C for up to 1 month.

Safety

Hazard Codes 

T

Risk Statements 

25

Safety Statements 

45

WGK Germany 

3

Hazard and Precautionary Statements (GHS)

Symbol(GHS)

Signal word

Danger

Hazard statements

H301Toxic if swalloed

Precautionary statements

P264Wash hands thoroughly after handling.

P264Wash skin thouroughly after handling.

P270Do not eat, drink or smoke when using this product.

P301+P310IF SWALLOWED: Immediately call a POISON CENTER or doctor/physician.

P321Specific treatment (see … on this label).

P330Rinse mouth.

P405Store locked up.

P501Dispose of contents/container to..…

UCF-101 Chemical Properties,Usage,Production

Description

UCF-101 (313649-08-0) is a potent, specific, competitive, and reversible inhibitor of the pro-apoptotic, mitochondrial serine protease Omi/HtrA2 (IC50?= 9.5 μM for His-Omi134-458). Shows very little activity against various other serine proteases tested (IC50?≥ 200 μM).1?Mitigates streptozotocin-induced cardiomyocyte dysfunction.2?Protects against cerebral oxidative injury and cognitive impairment in a rat model.3? Cell permeable.

Uses

UCF 101 is a specific inhibitor of Omi/HtrA2, a proapoptotic mitochondrial serine protease. UCF 101 has the neuroprotective effects on cerebral oxidative injury and cognitive impairment in septic rats.

in vitro

ucf 101 was identified in a hts of a combinatorial library using omi-(134-458) protease and fluorescein-casein as a generic substrate. ucf 101 exhibited specific activity against omi/htra2 and very little activity against other serine proteases. ucf 101 showed a natural fluorescence that was used to monitor its ability to enter mammalian cells. in addition, when tested in caspase-9 (-/-) null fibroblasts, ucf 101 was able to inhibit omi/htra2-induced cell death [1].

in vivo

in a previous study, rats were intraperitoneally administered ucf-101 at 1.5 micromol/kg 10 min prior to reperfusion. results showed that ucf-101 treatment could significantly decrease cerebral infarct size by about 16.27% and also improve neurological behavior. moreover, ucf-101 treatment was able to reduce tunel-positive cells in the cerebral cortex significantly. in addition, the upregulation in the expression of fasl and the cleavage products of active caspase-3 and caspase-8 induced by ischemia was attenuated in mice treated with ucf-101, while upregulation of flip levels was increased [2].

IC 50

9.5 μm

References

1) Cilenti?et al. (2003),?Characteristics of a novel and specific inhibitor for the pro-apoptotic protease Omi/HtrA2; J. Biol. Chem.,?278?11489 2) Li?et al.?(2009),?UCF-101 mitigates streptozotocin-induced cardiomyocyte dysfunction: role of AMPK; Am. J. Physiol. Endocrinol. Metab.,?297?E965 3) Hu?et al.?(2013),?Ucf-101 protects against cerebral oxidative injury and cognitive impairment in septic rat; Int. Immunopharmacol.,?16?108