Z-FA-FMK

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^[1][2][3]. In Vitro: 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].
In Vivo: 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].