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Chemical Structure
Chemical Structure
Chemical Structure

Z-VAD-FMK (Cell permeable) [187389-52-2, 634911-81-2]

Research Use Only
AG-CP3-0002
AdipoGen Life Sciences
Estimated Purity>95% (HPLC)
Product group Chemicals
Molecular Weight467.5
Price on request
Packing Size
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Overview

  • Supplier
    AdipoGen Life Sciences
  • Product Name
    Z-VAD-FMK (Cell permeable) [187389-52-2, 634911-81-2]
  • Delivery Days Customer
    10
  • Certification
    Research Use Only
  • Estimated Purity
    >95% (HPLC)
  • Hazard Information
    Non-hazardous
  • Molecular Formula
    C22H30FN3O7
  • Molecular Weight
    467.5
  • Scientific Description
    Cell permeable, non-selective broad-spectrum caspase inhibitor [1, 3, 7, 8]. Binds irreversibly to the catalytic site of caspase proteases [1]. The peptide is O-methylated in the P1 position on aspartic acid, providing enhanced stability and increased cell permeability [1]. Inhibits ICE-family protease/caspase processing, leading to apoptosis and autophagy induction [2-4, 6, 9]. Decreases proteasome activity [5]. Potent inhibitor of caspase-1 activation in NLRP3/NALP3-induced cells [10]. Used in apoptosis and inflammasome studies. - Chemical. CAS: 187389-52-2 and 634911-81-2. Formula: C22H30FN3O7. MW: 467.5. Synthetic. Cell permeable, non-selective broad-spectrum caspase inhibitor. Binds irreversibly to the catalytic site of caspase proteases. The peptide is O-methylated in the P1 position on aspartic acid, providing enhanced stability and increased cell permeability. Inhibits ICE-family protease/caspase processing, leading to apoptosis and autophagy induction. Decreases proteasome activity. Potent inhibitor of caspase-1 activation in NLRP3/NALP3-induced cells. Used in apoptosis and inflammasome studies.
  • SMILES
    [H][C@](NC(=O)OCC1=CC=CC=C1)(C(C)C)C(=O)N[C@@H](C)C(=O)NC(CC(=O)OC)C(=O)CF
  • Storage Instruction
    2°C to 8°C,-20°C
  • UNSPSC
    12352200

References

  • Benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethylketone (Z-VAD.FMK) inhibits apoptosis by blocking the processing of CPP32: E.A. Slee, et al.; Biochem. J. 315, 21 (1996)
  • Different interleukin-1 beta converting enzyme (ICE) family protease requirements for the apoptotic death of T lymphocytes triggered by diverse stimuli: A. Sarin, et al.; J. Exp. Med. 184, 2445 (1996)
  • Processing/activation of at least four interleukin-1beta converting enzyme-like proteases occurs during the execution phase of apoptosis in human monocytic tumor cells: M. MacFarlane, et al.; J. Cell Biol. 137, 469 (1997)
  • Processing/activation of caspases, -3 and -7 and -8 but not caspase-2, in the induction of apoptosis in B-chronic lymphocytic leukemia cells: D. King, et al.; Leukemia 12, 1553 (1998)
  • Proteasome activities decrease during dexamethasone-induced apoptosis of thymocytes: J. Beyette, et al.; Biochem. J. 332, 315 (1998)
  • JNK (c-Jun N-terminal kinase) and p38 activation in receptor-mediated and chemically-induced apoptosis of T-cells: differential requirements for caspase activation: M. MacFarlane, et al.; Biochem. J. 348, 93 (2000)
  • Statin-induced proinflammatory response in mitogen-activated peripheral blood mononuclear cells through the activation of caspase-1 and IL-18 secretion in monocytes: W.R. Coward, et al.; J. Immunol. 176, 5284 (2006)
  • Broad-spectrum caspase inhibitors: from myth to reality? D. Chauvier, et al.; Cell Death Differ. 14, 387 (2007)
  • A calpain-like protease inhibits autophagic cell death: D.T. Madden, et al.; Autophagy 3, 519 (2007)
  • Malarial hemozoin is a Nalp3 inflammasome activating danger signal; C. Dostert, et al.; PLoS One 4, e6510 (2009)