2. Apoptosis
  3. Caspase
  4. Z-VAD(OMe)-FMK

Z-VAD(OMe)-FMK  (Synonyms: Z-Val-Ala-Asp(OMe)-FMK)

Cat. No.: HY-16658 Purity: ≥98.0%
COA Handling Instructions

Z-VAD(OMe)-FMK (Z-Val-Ala-Asp(OMe)-FMK) est un pan-caspase inhibiteur cellule-perméable et irréversible. Z-VAD(OMe)-FMK est un inhibiteur de l'ubiquitine carboxy-terminal hydrolase L1 (UCHL1). Z-VAD(OMe)-FMK modifie de manière irréversible UCHL1 en ciblant le site actif de UCHL1.

Z-VAD (OMe) -FMK (Z-Val-Ala-Asp (OMe) -FMK) ist ein zellpermeabler und irreversibler Pan-Caspase-Inhibitor. Z-VAD (OMe) -FMK ist ein Ubiquitin-Carboxy-terminaler Hydrolase L1 (UCHL1) -Inhibitor. Z-VAD (OMe) -FMK modifiziert UCHL1 irreversibel, indem es auf das aktive Zentrum von UCHL1 abzielt.

Z-VAD(OMe)-FMK (Z-Val-Ala-Asp(OMe)-FMK) is a cell-permeable and irreversible pan-caspase inhibitor. Z-VAD(OMe)-FMK is an ubiquitin carboxy-terminal hydrolase L1 (UCHL1) inhibitor. Z-VAD(OMe)-FMK irreversibly modifies UCHL1 by targeting the active site of UCHL1.

For research use only. We do not sell to patients.

Z-VAD(OMe)-FMK Chemical Structure

Z-VAD(OMe)-FMK Chemical Structure

CAS No. : 187389-52-2

Size Price Stock Quantity
Solid + Solvent
10 mM * 1 mL in DMSO
ready for reconstitution
 USD 185 In-stock
Solution
10 mM * 1 mL in DMSO USD 185 In-stock
Solid
1 mg USD 66 In-stock
5 mg USD 180 In-stock
10 mg USD 300 In-stock
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Customer Review

Based on 160 publication(s) in Google Scholar

Other Forms of Z-VAD(OMe)-FMK:

Z-VAD(OMe)-FMK Related Antibodies

Top Publications Citing Use of Products

145 Publications Citing Use of MCE Z-VAD(OMe)-FMK

WB

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: J Biol Chem. 2019 May 17;294(20):8161-8170.  [Abstract]

    HeLa cells are pretreated with or without the indicated concentrations of Z-VAD-FMK for 1 h before treatment with 3 μM T007-1 for 12, 24, or 48 h. Protein levels of cleaved PARP and caspase-3 are detected via western blot using GAPDH as a loading control.

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: Cell. 2018 Sep 6;174(6):1477-1491.e19.  [Abstract]

    WT and Tbk1-/-MEFs are pre-incubated with 20 μM zVAD-fmk in the presence or absence of Nec-1 s for 0.5 h and then stimulated with mTNFa for indicated periods of time. Complex II is isolated by anti-FADD immunoprecipitation and RIPK1 binding is revealed by immunoblotting.

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: Cell Death Dis. 2018 Jan 18;9(2):27.  [Abstract]

    Overexpression PCDHGA9 induces GC cell apoptosis, cell cycle arrest, and autophagy. Western blot analysis determines that 10 μg/mL V-ZAD-FMK inhibits the activation of caspases.

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: J Immunol. 2018 Jan 1;200(1):271-285.  [Abstract]

    RelA+/+ and RelA-/- MEFs are treated with TNF (20 ng/mL)/Smac Mimetics (10 nM) or TNF (20 ng/mL)/Smac Mimetics (10 nM)/Z-VAD (20 μM) at the indicated hours. Cell lysates are collected and subjected to western blot analysis using the indicated antibody.

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: Chem Res Toxicol. 2018 Dec 17;31(12):1418-1425.  [Abstract]

    HUVEC cells are stimulated with TCBQ for 6 h, pre-treated with either 10 μM Z-VADFMK (pan-caspase inhibitor) or 10 μM AC-YVAD-CHO (caspase 1/4/5 inhibitor) for 1 h. Then caspase 1/4/5 and GSDMD expressions are detected by Western blotting analysis.

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: Onco Targets Ther. 2018 Feb 26;11:1025-1035.  [Abstract]

    Reversine inhibits the expression levels of Cyclin A2, Cyclin B1, and p-Rb, but promotes p21 expression.

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: PLoS One. 2018 Aug 6;13(8):e0201920.  [Abstract]

    The pretreatment of Z-VAD-FMK significantly reduces the levels of cleaved caspase-3 and cleaved PARP. The pretreatment of 3-MA blocks the conversion of LC3-I to LC3-II.

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: Cell Physiol Biochem. 2018;46(5):1779-1792.  [Abstract]

    Western blot and quantitative analysis of the expressions of ZO-1, Claudin-1, and Occludin. Apoptosis inhibitor Z-VAD(OMe)-FMK is used.

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: Cancer Lett. 2017 Feb 16;393:22-32.  [Abstract]

    Effects of p38 MAPK inhibitor (SB203580), ERK inhibitor (U0126), JNK inhibitor (SP600125), caspase inhibitor (Z-VAD-FMK) and NAC on SGC-7901 and MGC-803 treated with DOX/VCPA combination treatment. VCPA pretreatment strategy is the same as above. SB203580 (20 μM), U0126 (10 μM), SP600125 (20 μM), Z-VAD-FMK (10 μM) and NAC (5 mM) are treated 2 h before DOX (2 μg/mL) added into the culture, respectively. MAPK pathway protein levels are determined.

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: Elife. 2017 Dec 12;6:e30590.  [Abstract]

    Cultured S2 cells are treated with DMSO or z-VAD-FMK as indicated, and then mock infected for 24 hr or infected with DCV (MOI=5) for indicated time.

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: Biomed Pharmacother. 2017 Apr 5;90:446-454.  [Abstract]

    Caspase-8, Caspase-9, Caspase-3 and PARP cleavage levels are calculated by western blotting analysis in PC-3 cells treated under various conditions as indicated for 24 h. After ZVAD combination treatment, CHI-induced high expression of cleaved Caspase-8, Caspase-9, Caspase-3 and PARP is impeded dramatically.

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: Sci Rep. 2017 Jun 7;7(1):2929.  [Abstract]

    Caspase signaling pathway. MCF7 and MDA-MB-231 cells are pretreated with 10 µM Z-VAD-FMK and BOC-D-FMK for 1 h and then exposed to 80 μM ω3-FFAs and 20 μM ATRA for 48 h. The expression of PARP protein.

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: Sci Rep. 2016 Dec 1;6:38267.  [Abstract]

    SHK-induced splicing events that occurred in PARP, Caspase 8, 9 and 3 are also blocked by ZVAD-FMK. SHK-induced apoptosis is caspase-dependent in SGC-7901 gastric cancer cells. Detection of apoptosis-related protein PARP and caspase-3, -8, -9. GAPDH is used as a loading control.

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: Oncotarget. 2016 Dec 20;7(51):84810-84825.  [Abstract]

    Effect of proteasome or caspase inhibition on BCR/Abl protein suppression under oxygen or glucose shortage.K562 cells are incubated at 0.1% O2 in standard medium (top panels) or 21% O2 in the absence of glucose (bottom panels) for the indicated times, treated with the pan-caspase inhibitor z-VAD-fmk (50 μM) for the indicated times and lysed. BCR/Abl protein expression is determined by Western blotting using α-Tubulin as loading control.

    Z-VAD(OMe)-FMK purchased from MedChemExpress. Usage Cited in: Chinese Journal of Cell Biology. 2016, 38(10): 1232-1243.

    TNFα induces activation of caspase signaling pathway in L929-A cells but not L929-N cells.

    View All Caspase Isoform Specific Products:

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    Caspase 1 Caspase 2 Caspase 3 Caspase 4 Caspase 5 Caspase 6 Caspase 7 Caspase 8 Caspase 9 Caspase 10 Caspase 12 Caspase Caspase 11 Caspase-13

    • Biological Activity

    • Protocol

    • Purity & Documentation

    • References

    • Customer Review

    Description

    Z-VAD(OMe)-FMK (Z-Val-Ala-Asp(OMe)-FMK) is a cell-permeable and irreversible pan-caspase inhibitor[1]. Z-VAD(OMe)-FMK is an ubiquitin carboxy-terminal hydrolase L1 (UCHL1) inhibitor. Z-VAD(OMe)-FMK irreversibly modifies UCHL1 by targeting the active site of UCHL1[2].

    IC50 & Target[1]

    Caspase

     

    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[1]. Z-VAD(OMe)-FMK effectively inhibits UCHL1's reaction with hemagglutinin-tagged ubiquitin vinylmethyl ester (HA-UbVME) at the concentration of 100 μM[2]. 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[3]. Z-VAD(OMe)-FMK is a cell-permeable caspase inhibitor, efficiently blocks cell death induced by SMN deficiency[4].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    Z-VAD(OMe)-FMK Related Antibodies
    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[1].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
    Molecular Weight

    467.49

    Appearance

    Solid

    Formula

    C22H30FN3O7
    CAS No.
    Sequence

    Z-Val-Ala-Asp(OMe)-FMK
    Sequence Shortening

    ZVA-D(OMe)-FMK
    SMILES

    O=C(CF)[C@H](CC(OC)=O)NC([C@H](C)NC([C@H](C(C)C)NC(OCC1=CC=CC=C1)=O)=O)=O
    Shipping

    Room temperature in continental US; may vary elsewhere.
    Storage
    Powder -20°C 3 years
    In solvent -80°C 2 years
    -20°C 1 year
    Solvent & Solubility
    In Vitro: 

    DMSO : 100 mg/mL (213.91 mM; Need ultrasonic)

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 2.1391 mL 10.6954 mL 21.3908 mL
    5 mM 0.4278 mL 2.1391 mL 4.2782 mL
    10 mM 0.2139 mL 1.0695 mL 2.1391 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  5% DMSO    40% PEG300    5% Tween-80    50% Saline

      Solubility: ≥ 2.62 mg/mL (5.60 mM); Clear solution

    • 2.

      Add each solvent one by one:  5% DMSO    95% (20% SBE-β-CD in Saline)

      Solubility: ≥ 2.62 mg/mL (5.60 mM); Clear solution

    • 3.

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% Saline

      Solubility: ≥ 2.5 mg/mL (5.35 mM); Clear solution

    • 4.

      Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in Saline)

      Solubility: ≥ 2.5 mg/mL (5.35 mM); Clear solution

    • 5.

      Add each solvent one by one:  10% DMSO    90% Corn Oil

      Solubility: ≥ 2.5 mg/mL (5.35 mM); Clear solution

    • 6.

      Add each solvent one by one:  1% DMSO    99% Saline

      Solubility: ≥ 0.52 mg/mL (1.11 mM); Clear solution

    *All of the co-solvents are available by MedChemExpress (MCE).
    Purity & Documentation

    Purity: 98.20%

    COA (248 KB) HNMR (199 KB) RP-HPLC (355 KB) LCMS (281 KB)

    Handling Instructions (2659 KB)
    References
    Cell Assay
    [4]

    PCR products containing coding sequences for the dSMN (forward primer: 5′-TAA TAC GAC TCA CTA TAG GG AAG ACG TAC GAC GAG TCG-3′; and reverse primer: 5′-TAA TAC GAC TCA CTA TAG GG GTG GTG CTG GCT TCT TTC-3′; product length, 601bps; bold and italics letters represent T7 promoter sequences) and control Drosophila Presenilin (dPsn) gene (forward primer: 5′-TAA TAC GAC TCA CTA TAG GG TG GCT GCT GTC AAT CTC-3′; and reverse primer: 5′-TAA TAC GAC TCA CTA TAG GG CGA TAG CAA CGC TTC TTG-3′; product length: 543bps) are obtained and gel-purified. Double-stranded RNAs (dsRNA) are generated by transcription with Ribomax T7 Transcription kit and digested with Rnase-free DNase. The dsRNA products are ethanol precipitated and annealed by incubation at 65°C for 30 min and then slowly allowed to cool at room temperature. The annealed dsRNA products are analyzed on a 1% agaorse gel to ensure the majority of dsRNA existed as a single band. The dsRNA (2 μg) and/or plasmid DNAs (2 μg) are introduced into cells by using Cellfectin. Caspase inhibition is achieved by using 50 μM of Z-VAD(OMe)-FMK in the culture medium[4].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.
    Animal Administration
    [1][3]

    Mice[1]
    Mice used in this study are 5- to 6-week-old (20 to 22 g) ICR males. Mice are injected with 30 mg/kg LPS from E. coli serotype O111:B4 through the tail vein. A single intravenous injection of Z-VAD(OMe)-FMK (0.25 mg) is made 15 minutes before LPS injection, followed by three intravenous injections of Z-VAD(OMe)-FMK (0.1 mg each) per hour. Control mice are injected with the same volume of 1% DMSO in sterile saline.
    Rats[3]
    Male Sprague-Dawley rats weighing 300 to 350 g are anesthetized with α-chloralose (40 mg/kg IP) and urethane (400 mg/kg IP). Animals are intubated, and respiration is maintained with a small animal respirator. Rectal temperature is maintained at 37±0.5°C with a heating pad. The left external carotid artery is isolated and a 4.0 monofilament nylon suture is inserted through the internal carotid artery to perforate the middle cerebral artery. SAH is confirmed at autopsy in each rat. Sham-operated rats underwent the same procedures except that the suture is withdrawn after resistance is felt. Z-VAD(OMe)-FMK (50 μM per 0.3 mL) is injected intraperitoneally at 1 hour before and 6 hours after SAH induction. In vehicle group, rats underwent SAH induction and are treated with the same volume of vehicle (DMSO diluted in physiological buffer solution). No treatment is applied in sham-operated animals.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.
    References
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    Z-VAD(OMe)-FMK Related Classifications

    Help & FAQs
    • Do most proteins show cross-species activity?

      Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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    Keywords:

    Z-VAD(OMe)-FMK187389-52-2Z-Val-Ala-Asp(OMe)-FMKCaspaseInhibitorinhibitorinhibit

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