1. Apoptosis
  2. Caspase

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

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

Z-VAD(OMe)-FMK is a cell-permeable, pan-caspase inhibitor.

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
10 mM * 1 mL in DMSO USD 185 In-stock
1 mg USD 66 In-stock
5 mg USD 180 In-stock
10 mg USD 300 In-stock
50 mg   Get quote  
100 mg   Get quote  

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Customer Review

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

    p53 and Cell apoptosis. MCF7 and MDA-MB-231 cells are treated with 80 μM ω-3 FFAs, 20 μM ATRA alone or in combination for 48 h. The expression of PARP and p53 protein. β-Actin is used as an internal control.

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

    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 MCE. Usage Cited in: Cancer Lett. 2016 Aug 28;379(1):134-142.

    Inhibition of HDAC6 by HDAC6-selective inhibitors impairs the proliferation of glioblastoma cells. U87 and U251 cells are treated with HDAC6 selective inhibitors and the cells are harvested for subsequent western blot analysis.

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

    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 MCE. Usage Cited in: Cancer Lett. 2017 Feb 16;393:22-32.

    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 MCE. Usage Cited in: Oncotarget. 2016 Dec 20;7(51):84810-84825.

    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 MCE. Usage Cited in: Oncol Rep. 2017 Feb;37(2):1270-1276.

    A375 cells are treated with indicated concentrations of ACY-1215. After 72 h, Western blotting assay are utilized to detect apoptosis.

    Z-VAD(OMe)-FMK purchased from MCE. 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.

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

    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 MCE. Usage Cited in: Sci Rep. 2017 Nov 23;7(1):16111.

    RIP1 does not mediate TNFα-induced apoptosis in RIP3 knockdown L929 cells. Nec-1 does not block the TNFα-induced death of RIP3 knockdown L929 cells. The cells are infected with the RIP3 shRNA or the negative control shRNA lentivirus, and western blotting is performed to determine RIP3 knockdown efficiency.

    Z-VAD(OMe)-FMK purchased from MCE. Usage Cited in: Elife. 2017 Dec 12;6. pii: e30590.

    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 MCE. Usage Cited in: J Immunol. 2018 Jan 1;200(1):271-285.

    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 MCE. Usage Cited in: Cell Death Dis. 2018 Jan 18;9(2):27.

    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 MCE. Usage Cited in: Cell Death Dis. 2018 Jan 18;9(2):27.

    The cellular locations of β-catenin are detected by western blot. GAPDH, Histone H3, and ATP1A1 are used to normalize protein expression in total lysates and nuclear and membrane fractions, respectively. SGC-7901 cells with PCDHGA9 overexpression or vector control cells are grown in media with or without 10 μg/mL inhibitor of β-catenin (XAV-939).

    Z-VAD(OMe)-FMK purchased from MCE. Usage Cited in: Chem Biol Interact. 2018 Mar 1;283:59-74.

    The expression levels of apoptosis-associated proteins after treatment with morusin or tumor necrosis factor-alpha (TNF-α)/Cycloheximide (CHX). A2780 cells are incubated with the indicated concentrations of morusin or TNF-α (50 ng/mL)/CHX (50 μM) for 24 h. GAPDH is used as a loading control in western blot analysis.

    Z-VAD(OMe)-FMK purchased from MCE. Usage Cited in: Chem Biol Interact. 2018 Mar 1;283:59-74.

    The expression levels of apoptosis-associated proteins after treatment with morusin or tumor necrosis factor-alpha (TNF-α)/Cycloheximide (CHX). SKOV-3 cells are incubated with the indicated concentrations of morusin or TNF-α (50 ng/mL)/CHX (50 μM) for 24 h. GAPDH is used as a loading control in western blot analysis.

    Z-VAD(OMe)-FMK purchased from MCE. Usage Cited in: Cell Physiol Biochem. 2018 Apr 25;46(5):1779-1792.

    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 MCE. Usage Cited in: Cell Physiol Biochem. 2018 Apr 25;46(5):1779-1792.

    Western blot bands of p38, phospho-p38, ZO-1, Clau-din-1, and Occludin. JNK inhibitor SP600125 and p38 inhibitor SB203580 are used.
    • Biological Activity

    • Protocol

    • Technical Information

    • Purity & Documentation

    • References

    Description

    Z-VAD(OMe)-FMK is a cell-permeable, pan-caspase inhibitor.

    IC50 & Target[1]

    Caspase

     

    In Vitro

    Z-VAD(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 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[2]. Z-VAD(OMe)-FMK is a cell-permeable caspase inhibitor, efficiently blocks cell death induced by SMN deficiency[3].

    In Vivo

    The survival rate of mice is prolonged significantly by the injection of Z-VAD(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].

    References
    Preparing Stock Solutions
    Concentration Volume 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.
    Cell Assay
    [3]

    Z-VAD(OMe)-FMK is dissolved in DMSO and stored, and then diluted with appropriate medium before use[3].

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

    Animal Administration
    [1][2]

    Z-VAD(OMe)-FMK is dissolved at 2 mg/mL in 1% DMSO in sterile saline (Mice)[1].
    Z-VAD(OMe)-FMK is dissolved in 1% DMSO and further diluted in physiological buffer solution (final <0.01% DMSO) (Rats)[2].

    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[2]
    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
    Molecular Weight

    467.49

    Formula

    C₂₂H₃₀FN₃O₇

    CAS No.

    187389-52-2

    SMILES

    O=C(CF)[[email protected]](CC(OC)=O)NC([[email protected]](C)NC([[email protected]](C(C)C)NC(OCC1=CC=CC=C1)=O)=O)=O

    Storage
    Powder -80°C 2 years
      -20°C 1 year
    In solvent -80°C 6 months
      -20°C 1 month
    Shipping

    Room temperature in continental US; may vary elsewhere

    Solvent & Solubility

    DMSO: ≥ 30 mg/mL

    * "<1 mg/mL" means slightly soluble or insoluble. "≥" means soluble, but saturation unknown.

    Purity: >98.0%

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    Product Name:
    Z-VAD(OMe)-FMK
    Cat. No.:
    HY-16658
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