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> Z-VAD(OMe)-FMK [187389-52-2]

Z-VAD(OMe)-FMK [187389-52-2]

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Cat# HY-16658-1mg

Size : 1mg

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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

CAS No. : 187389-52-2

*

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Z-VAD(OMe)-FMK Related Antibodies

WB
    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.
    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.
    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.
    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.
    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.
    Reversine inhibits the expression levels of Cyclin A2, Cyclin B1, and p-Rb, but promotes p21 expression.
    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.
    Western blot and quantitative analysis of the expressions of ZO-1, Claudin-1, and Occludin. Apoptosis inhibitor Z-VAD(OMe)-FMK is used.
    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.
    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.
    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.
    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.
    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.
    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.
    TNFα induces activation of caspase signaling pathway in L929-A cells but not L929-N cells.

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    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.

    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. 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.

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

    Z-VAD(OMe)-FMK Related Antibodies

      In Vivo Dissolution Calculator
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      Method for preparing stock solution: mg drug dissolved in μL  DMSO (Stock solution concentration: mg/mL).
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      Method for preparing in vivo working solution for animal experiments: Take μL DMSO stock solution, add μL . μL , mix evenly, next add μL Tween 80, mix evenly, then add μL Saline.
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      Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.

    • [1]. Kawasaki M, et al. Protection from lethal apoptosis in lipopolysaccharide-induced acute lung injury in mice by a caspaseinhibitor. Am J Pathol. 2000 Aug;157(2):597-603.  [Content Brief]

      [2]. Davies CW, et al. The co-crystal structure of ubiquitin carboxy-terminal hydrolase L1 (UCHL1) with a tripeptide fluoromethyl ketone (Z-VAE(OMe)-FMK). Bioorg Med Chem Lett. 2012 Jun 15;22(12):3900-4.  [Content Brief]

      [3]. Park S, et al. Neurovascular protection reduces early brain injury after subarachnoid hemorrhage. Stroke. 2004 Oct;35(10):2412-7.  [Content Brief]

      [4]. Ilangovan R, et al. Inhibition of apoptosis by Z-VAD-fmk in SMN-depleted S2 cells. J Biol Chem. 2003 Aug 15;278(33):30993-9.  [Content Brief]

    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.

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

    Mice
    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
    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.

    • [1]. Kawasaki M, et al. Protection from lethal apoptosis in lipopolysaccharide-induced acute lung injury in mice by a caspaseinhibitor. Am J Pathol. 2000 Aug;157(2):597-603.  [Content Brief]

      [2]. Davies CW, et al. The co-crystal structure of ubiquitin carboxy-terminal hydrolase L1 (UCHL1) with a tripeptide fluoromethyl ketone (Z-VAE(OMe)-FMK). Bioorg Med Chem Lett. 2012 Jun 15;22(12):3900-4.  [Content Brief]

      [3]. Park S, et al. Neurovascular protection reduces early brain injury after subarachnoid hemorrhage. Stroke. 2004 Oct;35(10):2412-7.  [Content Brief]

      [4]. Ilangovan R, et al. Inhibition of apoptosis by Z-VAD-fmk in SMN-depleted S2 cells. J Biol Chem. 2003 Aug 15;278(33):30993-9.  [Content Brief]

    • [1]. Kawasaki M, et al. Protection from lethal apoptosis in lipopolysaccharide-induced acute lung injury in mice by a caspaseinhibitor. Am J Pathol. 2000 Aug;157(2):597-603.

      [2]. Davies CW, et al. The co-crystal structure of ubiquitin carboxy-terminal hydrolase L1 (UCHL1) with a tripeptide fluoromethyl ketone (Z-VAE(OMe)-FMK). Bioorg Med Chem Lett. 2012 Jun 15;22(12):3900-4.

      [3]. Park S, et al. Neurovascular protection reduces early brain injury after subarachnoid hemorrhage. Stroke. 2004 Oct;35(10):2412-7.

      [4]. Ilangovan R, et al. Inhibition of apoptosis by Z-VAD-fmk in SMN-depleted S2 cells. J Biol Chem. 2003 Aug 15;278(33):30993-9.

    * Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
    Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

    Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
    DMSO 1 mM 2.1391 mL 10.6954 mL 21.3908 mL 53.4771 mL
    5 mM 0.4278 mL 2.1391 mL 4.2782 mL 10.6954 mL
    10 mM 0.2139 mL 1.0695 mL 2.1391 mL 5.3477 mL
    15 mM 0.1426 mL 0.7130 mL 1.4261 mL 3.5651 mL
    20 mM 0.1070 mL 0.5348 mL 1.0695 mL 2.6739 mL
    25 mM 0.0856 mL 0.4278 mL 0.8556 mL 2.1391 mL
    30 mM 0.0713 mL 0.3565 mL 0.7130 mL 1.7826 mL
    40 mM 0.0535 mL 0.2674 mL 0.5348 mL 1.3369 mL
    50 mM 0.0428 mL 0.2139 mL 0.4278 mL 1.0695 mL
    60 mM 0.0357 mL 0.1783 mL 0.3565 mL 0.8913 mL
    80 mM 0.0267 mL 0.1337 mL 0.2674 mL 0.6685 mL
    100 mM 0.0214 mL 0.1070 mL 0.2139 mL 0.5348 mL
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    Z-VAD(OMe)-FMK187389-52-2Z-Val-Ala-Asp(OMe)-FMKCaspaseInhibitorinhibitorinhibit

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