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Z-DQMD-FMK Caspase-3 inhibitor,cell-permeable

Catalog No.A1921
Size Price Stock Qty
10mM (in 1mL DMSO)
$330.00
In stock
Evaluation Sample
$28.00
In stock
1mg
$55.00
In stock
5mg
$150.00
In stock
10mg
$250.00
In stock
25mg
$400.00
In stock

Tel: +1-832-696-8203

Email: [email protected]

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Sample solution is provided at 25 µL, 10mM.

Product Citations

1.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
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

Quality Control

Chemical structure

Z-DQMD-FMK

Related Biological Data

Z-DQMD-FMK

Related Biological Data

Z-DQMD-FMK

Biological Activity

Caspase-3 inhibitor. Inhibits MG 132-induced small cell lung cancer cell death in vitro.
Targets Caspase-3          
IC50            

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.

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.

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Chemical Properties

Cas No. SDF Download SDF
Synonyms Z-DQMD-FMK,Benzyloxycarbonyl-Asp(OMe)-Gln-Met-​Asp(OMe)-fluoromethylketone
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
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
Formula C29H40FN5O11S M.Wt 685.72
Solubility >29.2mg/mL in DMSO Storage Store at -20°C
Shipping Condition Evaluation sample solution : ship with blue ice.All other available size: ship with RT , or blue ice upon request
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.

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.

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
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