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Z-DQMD-FMK
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.
References:
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 Pharmacology 68 (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
- 1. Wang J, Shao L, et al. "Synergetic Inhibition of Human Colorectal Cancer Cells by Combining Polyyne-Enriched Fraction from Oplopanax elatus and Irinotecan." Nutr Cancer. 2018 Oct 29:1-11. PMID:30372160
- 2. Han J, Yang BP, et al. "RhoB/ROCK mediates oxygen-glucose deprivation-stimulated syncytiotrophoblast microparticle shedding in preeclampsia." Cell Tissue Res. 2016 PMID:27324125
- 3. Li, Lingfei, et al. "P38/MAPK contributes to endothelial barrier dysfunction via MAP4 phosphorylation-dependent microtubule disassembly in inflammation-induced acute lung injury." Scientific reports 5 (2015). PMID:25746230
Storage | Store at -20°C |
M.Wt | 685.72 |
Cas No. | 767287-99-0 |
Formula | C29H40FN5O11S |
Synonyms | Z-DQMD-FMK,Benzyloxycarbonyl-Asp(OMe)-Gln-Met-?Asp(OMe)-fluoromethylketone |
Solubility | ≥29.2 mg/mL in DMSO; insoluble in EtOH; insoluble in H2O |
Chemical Name | methyl (3S)-3-[[(2S)-2-[[(2S)-5-amino-2-[[(2S)-4-methoxy-4-oxo-2-(phenylmethoxycarbonylamino)butanoyl]amino]-5-oxopentanoyl]amino]-4-methylsulfanylbutanoyl]amino]-5-fluoro-4-oxopentanoate |
SDF | Download SDF |
Canonical SMILES | COC(=O)CC(C(=O)CF)NC(=O)C(CCSC)NC(=O)C(CCC(=O)N)NC(=O)C(CC(=O)OC)NC(=O)OCC1=CC=CC=C1 |
Shipping Condition | Small Molecules with Blue Ice, Modified Nucleotides with Dry Ice. |
General tips | We do not recommend long-term storage for the solution, please use it up soon. |
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. |
References: [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. |
Caspase-3 inhibitor. Inhibits MG 132-induced small cell lung cancer cell death in vitro. | ||||||
Targets | Caspase-3 | |||||
IC50 |
Quality Control & MSDS
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Chemical structure
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Related Biological Data
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Related Biological Data
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Related Biological Data
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