(1S)-Z-FA-FMK MedChemExpress (MCE)

Product Name	Z-PHE-DL-ALA-FLUOROMETHYLKETONE
Synonyms	CS-1504 Z-Phe-DL-Ala-FMK Z-PHE-DL-ALA-FLUOROMETHYLKETONE Nalpha-[(Benzyloxy)Carbonyl]-N-(4-Fluoro-3-Oxo-2-Butanyl)Phenylalaninamide Nalpha-[(Benzyloxy)Carbonyl]-N-(4-Fluoro-3-Oxo-2-Butanyl)Phenylalaninamide z-fa-fmk Synonyms CS-1504 Z-Phe-DL-Ala-FMK Z-PHE-DL-ALA-FLUOROMETHYLKETONE Nalpha-[(Benzyloxy)Carbonyl]-N-(4-Fluoro-3-Oxo-2-Butanyl)Phenylalaninamide Nalpha-[(Benzyloxy)Carbonyl]-N-(4-Fluoro-3-Oxo-2-Butanyl)Phenylalaninamide z-fa-fmk Carbamic acid,N-[(1S)-2-[(3-fluoro-1-methyl-2-oxopropyl)amino]-2-oxo-1-(phenylmethyl)ethyl]-,phenylmethyl ester
CAS	197855-65-5
EINECS
Chemical Formula	C21H23FN2O4
Molecular Weight	386.42
inchi
Package	25 mg
Price	Email to quote
Descriptions	Z-FA-FMK Z-FA-FMK MedChemExpress (MCE) HY-P0109A 197855-65-5 (1S)-Z-FA-FMK 99.14% -20°C, sealed storage, away from moisture In solvent : -80°C, 6 months Descriptions Z-FA-FMK Z-FA-FMK MedChemExpress (MCE) HY-P0109A 197855-65-5 (1S)-Z-FA-FMK 99.14% -20°C, sealed storage, away from moisture In solvent : -80°C, 6 months -20°C, 1 month (sealed storage, away from moisture) Room temperature in continental US may vary elsewhere. Z-FA-FMK ((1S)-Z-FA-FMK) is a potent Cathepsin B and L inhibitor. Z-FA-FMK blocks the induction of DEVDase activity, DNA fragmentation, and externalization of phosphatidylserine by selective synthetic retinoid-related molecules (RRMs). Z-FA-FMK inhibits apoptosis. Z-FA-FMK inhibits caspase activity and selectively inhibits recombinant effector caspases 2, -3, -6, and -7. Z-FA-FMK is a viral inhibitor. Z-FA-FMK inhibits reovirus replication in a susceptible host. Z-FA-FMK ((1S)-Z-FA-FMK 5-100 μM 1 h Jurkat cells) reduces levels of DEVDase activity and DNA fragmentation. Z-FA-FMK inhibits the externalization of phosphatidylserine induced by either MX2870-1 or MX781[1]. Z-FA-FMK (100 μM 1 h Jurkat cells) inhibits apoptosis. Z-FA-FMK inhibited the induction of DEVDase activity not only by the RRMs but also by other apoptotic insults, including etoposide-, ceramide-, and CD95/Fas receptor-mediated pathways[1]. Z-FA-FMK (0-100 μM 1 h Jurkat cells) inhibits caspases 2, -3, -6, and -7 activity through repressed induction of DEVDase activity in Jurkat cells[1]. Z-FA-FMK (0-20 μM 48 h HT1080 and mouse embryonic stem cells) blocks reoviral replication and cures cells of a persistent infection with reovirus in vitro[2]. Z-FA-FMK (20 μM 48 h HT1080 cells) induces defects in reoviral maturation[2]. Z-FA-FMK (1 mg/kg intratumor injection every 2 d, for 27 d SCID mice with HT1080 xenograft) blocks reovirus infection in vivo[2]. Z-FA-FMK (8 mg/kg i.v. every 2 d, once male BALB/c mice) markedly lessens the degree of impairment seen in D-GalN/TNF-α-induced kidney injury[3]. Cathepsin B cathepsin L Caspase-2 Caspase-3 Caspase-6 Caspase-7 \| \| \| \| \| \| \| \| \| \| [1]. Lopez-Hernandez FJ, et, al. Z-FA-fmk inhibits effector caspases but not initiator caspases 8 and 10, and demonstrates that novel anticancer retinoid-related molecules induce apoptosis via the intrinsic pathway. Mol Cancer Ther. 2003 Mar 2(3):255-63. [Content Brief] [2]. Kim M, et, al. Z-FA-FMK as a novel potent inhibitor of reovirus pathogenesis and oncolysis in vivo. Antivir Ther. 2010 15(6):897-905. [Content Brief] [3]. Gezginci-Oktayoglu S, et, al. Effects of Z-FA.FMK on D-galactosamine/tumor necrosis factor-alpha-induced kidney injury and oxidative stress in mice : effects of Z-FA.FMK on TNF-alpha-mediated kidney injury. Mol Cell Biochem. 2008 Feb 309(1-2):9-20. [Content Brief]
Last Update	2025-04-01 14:45:47

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