Need Assistance?

  • US & Canada:
  • UK: +
* Please kindly note that our products are not to be used for therapeutic purposes and cannot be sold to patients.

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.

Peptide Inhibitors
Catalog number
CAS number
Molecular Formula
Molecular Weight
Size Price Stock Quantity
10 mg $629 In stock
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
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
White to slightly brown Solid
1.260±0.06 g/cm3 (Predicted)
Boiling Point
914.2±65.0°C (Predicted)
Store at -20°C
Soluble in DMSO, DMF
InChI Key
Canonical SMILES
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.

Online Inquiry

Verification code
Inquiry Basket