Z-DEVD-FMK
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Z-DEVD-FMK

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Z-DEVD-FMK is a cell-permeant, irreversible caspase-3 inhibitor that can be used as an anaesthetic agent. It has been shown to suppress tumor cell apoptosis.

Category
Peptide Inhibitors
Catalog number
BAT-010236
CAS number
210344-95-9
Molecular Formula
C30H41FN4O12
Molecular Weight
668.67
Z-DEVD-FMK
Size Price Stock Quantity
10 mg $629 In stock
IUPAC Name
methyl (4S)-5-[[(2S)-1-[[(3S)-5-fluoro-1-methoxy-1,4-dioxopentan-3-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-4-[[(2S)-4-methoxy-4-oxo-2-(phenylmethoxycarbonylamino)butanoyl]amino]-5-oxopentanoate
Synonyms
Z-Asp(OMe)-Glu(OMe)-Val-Asp(OMe)-FMK; Caspase-3 Inhibitor; Z-D(OMe)E(Ome)VD(OMe)-FMK; benzyloxycarbonyl-Asp(OMe)-Glu(OMe)-Val-Asp(OMe)-fluoromethylketone; Caspase-3 Inhibitor II; Z-Asp(OMe)-Glu(OMe)-Val-Asp(OMe)-Fluoromethylketone; Z-DEVD-fluoromethylketone
Appearance
White to slightly brown Solid
Purity
≥95%
Density
1.260±0.06 g/cm3 (Predicted)
Boiling Point
914.2±65.0°C (Predicted)
Sequence
Cbz-Asp(OMe)-Glu(OMe)-Val-Asp(OMe)-FMK
Storage
Store at -20°C
Solubility
Soluble in DMSO, DMF
Application
Cysteine Proteinase Inhibitors
InChI
InChI=1S/C30H41FN4O12/c1-17(2)26(29(42)33-20(22(36)15-31)13-24(38)45-4)35-27(40)19(11-12-23(37)44-3)32-28(41)21(14-25(39)46-5)34-30(43)47-16-18-9-7-6-8-10-18/h6-10,17,19-21,26H,11-16H2,1-5H3,(H,32,41)(H,33,42)(H,34,43)(H,35,40)/t19-,20-,21-,26-/m0/s1
InChI Key
GBJVAVGBSGRRKN-JYEBCORGSA-N
Canonical SMILES
CC(C)C(C(=O)NC(CC(=O)OC)C(=O)CF)NC(=O)C(CCC(=O)OC)NC(=O)C(CC(=O)OC)NC(=O)OCC1=CC=CC=C1
1.Involvement of Bcl-2 family, cytochrome c and caspase 3 in induction of apoptosis by beauvericin in human non-small cell lung cancer cells.
Lin HI;Lee YJ;Chen BF;Tsai MC;Lu JL;Chou CJ;Jow GM Cancer Lett. 2005 Dec 18;230(2):248-59.
Beauvericin (BEA), a cyclic hexadepsipeptide from Codyceps cicadae, possesses anti-convulsion, anti-arrhythmia, sedation, and anti-tumor activities. It has been reported that BEA induces apoptosis in several cancer cell lines. However, the molecular mechanism underlying the BEA-induced apoptotic process is not yet clearly understood. In the present study, the intracellular signaling pathways of BEA-induced apoptosis in human non-small cell lung cancer (NSCLC) A549 cells were investigated using morphological analysis and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) technique. In this study, BEA-induced apoptosis in human NSCLC A549 cells demonstrated a BEA concentration- and treatment time-dependent manner. This BEA-induced apoptosis in human NSCLC A549 cells was also accompanied by the up-regulation of Bax, Bak, and p-Bad and down-regulation of p-Bcl-2, but no effect on the levels of Bcl-X(L) or Bad proteins. Moreover, the BEA treatment resulted in a significant reduction of mitochondrial membrane potential, increase in the release of mitochondrial cytochrome c (cyt c), and activation of caspase 3. Furthermore, treatment with caspase 3 inhibitor (z-DEVD-fmk) was capable to prevent the BEA-induced caspase 3 activity and cell death.
2.Increasing ceramides sensitizes genistein-induced melanoma cell apoptosis and growth inhibition.
Ji C;Yang YL;He L;Gu B;Xia JP;Sun WL;Su ZL;Chen B;Bi ZG Biochem Biophys Res Commun. 2012 May 11;421(3):462-7. doi: 10.1016/j.bbrc.2012.04.012. Epub 2012 Apr 7.
The aim of the current study is to investigate the effect of ceramides on genistein-induced anti-melanoma effects in vitro. We found that exogenously added cell-permeable short-chain ceramides (C6) dramatically enhanced genistein-induced growth inhibition and apoptosis in cultured melanoma cells. Genistein treatment only induced a moderate intracellular ceramides accumulation in B16 melanoma cells. Two different agents including 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), a ceramide glucosylation inhibitor, and the sphingosine kinase-1 (SphK1) inhibitor II (SKI-II), a sphingosine (ceramides precursor) phosphorylation inhibitor, both facilitated genistein-induced ceramides accumulation and melanoma cell apoptosis. Co-administration of ceramide (C6) and genistein induced a significant Akt inhibition and c-jun-NH(2)-kinase (JNK) activation, caspase-3 cleavage and cytochrome c release. Caspase-3 inhibitor z-DVED-fmk, JNK inhibitor SP 600125, or to restore Akt activation by introducing a constitutively active form of Akt (CA-Akt) diminished ceramide (C6) and genistein co-administration-induced in vitro anti-melanoma effect. Our study suggests that increasing cellular level of ceramides may sensitize genistein-induced anti-melanoma effects.
3.Involvement of the proteasome and caspase activation in hippocampal long-term depression induced by the serine protease subtilisin.
Forrest CM;Darlington LG;Stone TW Neuroscience. 2013 Feb 12;231:233-46. doi: 10.1016/j.neuroscience.2012.11.029. Epub 2012 Dec 1.
The serine protease subtilisin-A produces a long-term depression (LTD) of synaptic potentials in hippocampal slices which differs mechanistically from classical LTD. Since caspases have been implicated in hippocampal plasticity, this study examined a possible role for these enzymes in subtilisin-induced LTD. Subtilisin produced a concentration-dependent decrease in the size of field excitatory synaptic potentials (fEPSPs), which was not prevented or modified by the caspase inhibitors Z-VAD(OMe)-fmk and Z-DEVD-fmk. Similarly Z-VAD(OMe)-fmk did not modify the selective loss of protein expression produced by subtilisin. Subtilisin reduced the expression of procaspase-3 and caspase-9 but, while caspase-9 was converted to its conventionally activated form (39 kDa), caspase-3 was metabolised along a non-canonical pathway to a 29/30 kDa protein rather than the classical 17/19 kDa fragments. Both Z-VAD(OMe)-fmk and Z-DEVD-fmk were unable to prevent the reduced expression of Postsynaptic Density Protein-95, Vesicle-Associated Membrane Protein-1 and Unco-ordinated 5H3 proteins produced by subtilisin, although MG132 did produce partial recovery from subtilisin-induced depression of fEPSPs. When tested on long-term potentiation (LTP) induced by theta stimulation in the stratum radiatum, MG132 inhibited the immediate increase in fEPSP size but generated a higher plateau LTP.
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