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Z-YVAD-FMK

  Cat. No.:  DC29098   Featured
Chemical Structure
210344-97-1
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More than 5000 active chemicals with high quality for research!
Field of application
AA-Z-YVAD-FMK is a cell-permeable, irreversible pan-caspase inhibitor with anti-inflammatory and anti-tumor activities.
Chemicals PropertiesBiological activity COA & MSDSRelated productsDatasheet
Cas No.: 210344-97-1
Chemical Name: Z-YVAD-FMK
Synonyms: N-[(benzyloxy)carbonyl]-L-tyrosyl-L-valyl-N-[(3S)-5-fluoro-1-methoxy-1,4-dioxopentan-3-yl]-L-alaninamide;L-Alaninamide, N-[(phenylmethoxy)carbonyl]-L-tyrosyl-L-valyl-N-[(1S)-3-fluoro-1-(2-methoxy-2-oxoethyl)-2-oxopropyl]-;Z-YVAD-FMK ( Z-Tyr-Val-Ala-Asp(OMe)-FMK );Z-YVAD-FMK
SMILES: CC([C@H](NC([C@@H](NC(OCC1=CC=CC=C1)=O)CC2=CC=C(O)C=C2)=O)C(N[C@H](C(N[C@H](C(CF)=O)CC(OC)=O)=O)C)=O)C
Formula: C31H39N4O9F
M.Wt: 630.66116
Purity: >98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: AA-Z-YVAD-FMK is a cell-permeable, irreversible pan-caspase inhibitor with anti-inflammatory and anti-tumor activities.
Target: Caspase
In Vivo: Z-VAD-FMK (intraperitoneal injection; 10mg/kg; pre- 30 minutes) significantly delayed preterm delivery at 18 hours, but after 36 hours treatment, non different exists between Z-VAD-FMK-pretreated and control groups[3]. Animal Model: Day 14.5 pregnant CD1 mice[3] Dosage: 10 mg/kg Administration: Intraperitoneal injection; 10mg/kg; pre-30 minutes Result: Prevented HK-GBS-induced preterm delivery.
In Vitro: Z-YVAD-FMK (100 μM; 24 hours) significantly downregulated the growth inhibition induced by butyrate in Caco-2 cells[1]. Z-YVAD-FMK (20 μM; pre 1 hour; 24 hours) attenuates the apoptotic induction of III-10 on both HepG2 and BEL-7402 cells, the apoptotic rate of -10 on HepG2 cells is reduced by Z-VAD-FMK from 19.88% to 8.34%, while that on BEL-7402 cells is reduced from 17.56% to 11.98%[4]. Z-YVAD-FMK (1-10 μM; 24 hours) shows inhibitory effect in various cells against TNFr- or anti-CD95-induced cell death, exhibits IC50 values of 0.0015 μM (Murine hepatocytes), 0.027 μM (Murine hepatocytes), 4.8 μM (HepG2), 5.8 μM (HepG2), 1.6 μM (Hela) and 1.1 μM (Jurkat), respectively[5]. Cell Viability Assay[1] Cell Line: Caco-2 cells Concentration: 0-100 μM Incubation Time: 24 hours Result: Inhibited Caco-2 cells growth. Apoptosis Analysis[1] Cell Line: BEL-7402 and HepG2 cells Concentration: 20 μM Incubation Time: Pre 1 hour; 24 hours Result: Induced a caspase-dependent apoptosis in cells.
References: [1]. Li H1,et al.Aluminum hydroxide adjuvants activate caspase-1 and induce IL-1beta and IL-18 release.J Immunol. 2007 Apr 15;178(8):5271-6. [2]. Avivi-Green C, et al. Different molecular events account for butyrate-induced apoptosis in two human colon cancer cell lines.J Nutr. 2002 Jul;132(7):1812-8. [3]. Equils O, et al. Pretreatment with pancaspase inhibitor (Z-VAD-FMK) delays but does not prevent intraperitoneal heat-killed group B Streptococcus-induced preterm delivery in a pregnant mouse model.infect Dis Obstet Gynecol. 2009;2009:749432. [4]. Künstle G,et al. ICE-protease inhibitors block murine liver injury and apoptosis caused by CD95 or by TNF-alpha.Immunol Lett. 1997 Jan;55(1):5-10.
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Cat. No. Product name Field of application
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