Z-VAD-FMK

CAS No. 187389-52-2

Z-VAD-FMK( Z-Val-Ala-Asp-(OMe)-Fluoromethyl Ketone )

Catalog No. M12903 CAS No. 187389-52-2

Z-VAD-FMK is a cell-permeable, irreversible pan-caspase inhibitor, blocks all features of apoptosis.

Purity : >98% (HPLC)

COA Datasheet HNMR HPLC MSDS Handing Instructions
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2MG 76 In Stock
5MG 133 In Stock
10MG 224 In Stock
25MG 383 In Stock
50MG 493 In Stock
100MG 710 In Stock
200MG 981 In Stock
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Biological Information

  • Product Name
    Z-VAD-FMK
  • Note
    Research use only, not for human use.
  • Brief Description
    Z-VAD-FMK is a cell-permeable, irreversible pan-caspase inhibitor, blocks all features of apoptosis.
  • Description
    Z-VAD-FMK is a cell-permeable, irreversible pan-caspase inhibitor, blocks all features of apoptosis.(In Vitro):Z-VAD(OMe)-FMK (Z-Val-Ala-Asp(OMe)-FMK) is a broad-spectrum caspase inhibitor, has been shown to inhibit the intracellular activation of caspase-like proteases. The injection of Z-VAD(OMe)-FMK suppresses the caspase-3 activity in lung tissues, and significantly decreases the number of terminal dUTP nick-end labeling-positive cells. Z-VAD(OMe)-FMK effectively inhibits UCHL1's reaction with hemagglutinin-tagged ubiquitin vinylmethyl ester (HA-UbVME) at the concentration of 100 μM. Z-VAD(OMe)-FMK is administered intraperitoneally at 1 hour before and 6 hours after SAH. Expression of caspase-3 and positive TUNEL is examined as markers for apoptosis. Z-VAD(OMe)-FMK suppresses TUNEL and caspase-3 staining in endothelial cells, decreases caspase-3 activation, reduces BBB permeability, relieves vasospasm, abolishes brain edema, and improves neurological outcome. Z-VAD(OMe)-FMK is a cell-permeable caspase inhibitor, efficiently blocks cell death induced by SMN deficiency.(In Vivo):The survival rate of mice is prolonged significantly by the injection of Z-VAD(OMe)-FMK (Z-Val-Ala-Asp(OMe)-FMK). All mice succumbed to LPS within 30 hours. By contrast, the mice treated with Z-VAD(OMe)-FMK survive significantly longer and 27% of the mice survived more than 7 days.
  • In Vitro
    Z-VAD(OMe)-FMK (Z-Val-Ala-Asp(OMe)-FMK) is a broad-spectrum caspase inhibitor, has been shown to inhibit the intracellular activation of caspase-like proteases. The injection of Z-VAD(OMe)-FMK suppresses the caspase-3 activity in lung tissues, and significantly decreases the number of terminal dUTP nick-end labeling-positive cells. Z-VAD(OMe)-FMK effectively inhibits UCHL1's reaction with hemagglutinin-tagged ubiquitin vinylmethyl ester (HA-UbVME) at the concentration of 100 μM. Z-VAD(OMe)-FMK is administered intraperitoneally at 1 hour before and 6 hours after SAH. Expression of caspase-3 and positive TUNEL is examined as markers for apoptosis. Z-VAD(OMe)-FMK suppresses TUNEL and caspase-3 staining in endothelial cells, decreases caspase-3 activation, reduces BBB permeability, relieves vasospasm, abolishes brain edema, and improves neurological outcome. Z-VAD(OMe)-FMK is a cell-permeable caspase inhibitor, efficiently blocks cell death induced by SMN deficiency.
  • In Vivo
    The survival rate of mice is prolonged significantly by the injection of Z-VAD(OMe)-FMK (Z-Val-Ala-Asp(OMe)-FMK). All mice succumbed to LPS within 30 hours. By contrast, the mice treated with Z-VAD(OMe)-FMK survive significantly longer and 27% of the mice survived more than 7 days.
  • Synonyms
    Z-Val-Ala-Asp-(OMe)-Fluoromethyl Ketone
  • Pathway
    Apoptosis
  • Target
    Caspase
  • Recptor
    Pan-caspase
  • Research Area
    Cancer
  • Indication
    ——

Chemical Information

  • CAS Number
    187389-52-2
  • Formula Weight
    467.49
  • Molecular Formula
    C22H30FN3O7
  • Purity
    >98% (HPLC)
  • Solubility
    DMSO: 93 mg/mL (198.93 mM)
  • SMILES
    O=C(OC)C[C@H](NC([C@@H](NC([C@@H](NC(OCC1=CC=CC=C1)=O)C(C)C)=O)C)=O)C(CF)=O
  • Chemical Name
    methyl (3S)-5-fluoro-3-[[(2S)-2-[[(2S)-3-methyl-2-(phenylmethoxycarbonylamino)butanoyl]amino]propanoyl]amino]-4-oxopentanoate

Shipping & Storage Information

  • Storage
    (-20℃)
  • Shipping
    With Ice Pack
  • Stability
    ≥ 2 years

Reference

1.Slee EA, et al. Biochem J, 1996, 315 (Pt 1), 21-24.
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