Caspase-3 inhibitor,cell-permeable
货号:ajcx11434
CAS:
分子式:C29H40FN5O11S
分子量：685.72
溶解度:≥ 29.2mg/mL in DMSO
纯度：98%
存储：Store at -20°C
库存：现货

Background:

Inhibition of caspase-3 processing by Z-DQMD-FMK (Z-Asp(OMe)-Gln-Met-Asp(OMe)-fluoromethylketone) did not restore cell number in the zinc-deficient group, but resulted in processing of full-length PKC-δ to a 56-kDa fragment¹.

The inhibitory effect of specific caspase inhibitors (Z-DQMD-FMK, Z-IETD-FMK and Z-LEHD-FMK) suggests that the MG132-induced apoptotic cell death and depletion of GSH in SCLC cells are mediated by both activation of caspase-8 and mitochondrial damage, leading to the activation of caspase-9 and -3².

To investigate whether εPKC cleavage after stroke is caused by caspase-3 activation, we examined the effect of a cell-permeable caspase-3–specific inhibitor, Z-DQMD-FMK, on generation of cleaved εPKC fragments. Caspase-3 inhibition did not suppress the decrease in fulllength εPKC and the 43-kDa fragment in the ischemic core and penumbra after stroke³.

参考文献:
1. Susan S. CHOU*, Michael S. CLEGG, Alterations in protein kinase C activity and processing during zinc-de?ciency-induced cell death,Biochem. J. (2004) 383, 63–71
2. J. H. Banga, E. S. Han. Differential response of MG132 cytotoxicity against small cell lung cancer cells to changes in cellular GSH contents.Biochemical Pharmacology68 (2004) 659–666.
3. T. Shimohata, H. Zhao, εPKC May Contribute to the Protective Effect of Hypothermia in a Rat Focal Cerebral Ischemia Model.Stroke. 2007;38:375-380

Protocol:

Cell experiment [1]:
Cell lines	3T3-Swiss Albino cells
Preparation method	The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below - 20 °C for several months.
Reacting condition	25 μM; 24 hrs
Applications	In zinc-deficient 3T3-Swiss Albino cells, Z-DQMD-FMK (25 μM) prevented activation of caspase-3. Z-DQMD-FMK treatment did not restore cell number, but resulted in processing of full-length PKC-δ to a 56-kDa fragment.
参考文献: [1]. Susan S. CHOU*, Michael S. CLEGG, Alterations in protein kinase C activity and processing during zinc-deficiency-induced cell death, Biochem. J. (2004) 383, 63–71.