Irreversible MALT1 inhibitor. Suppresses T cell activation-induced cleavage of Bcl-10 in a dose-dependent manor. Reduces Jurkat cell adhesion to fibronectin. Cell permeable.
When compared to other caspase inhibitors, Z-DRHD-FMK inhibited caspase 6 activity more effectively than the general caspase inhibitor of Z-Val-Ala-Asp (OMe)-fluoromethy ketone (Z-VAD-FMK) or the caspase 6 inhibitor Z-Val-Glu(Ome)-Ile-Asp(OMe)-fluorometh
Z-AEVD-FMK is an irreversible inhibitor of caspase-10 and related caspases.[1] At 10 µM, it can prevent the initiation of Fas signaling by caspase-10 in Jurkat T lymphoma cells, preventing Bid cleavage into its active form, caspase cascade activation, and apoptosis.[2]
Z-LEHD-FMK TFA is a specific and irreversible inhibitor of caspase-9, offering protection against detrimental reperfusion injury and moderating apoptosis. Additionally, Z-LEHD-FMK TFA demonstrates its neuroprotective potential in a rat model of spinal cord trauma.
Z-VAE(OMe)-fmk is a cell-permeable and irreversible UCHL1 inhibitor. The inhibitor approaches the active-site cleft from the opposite side of the crossover loop as compared to the direction of approach of ubiquitin's C-terminal tail, thereby occupying the P1' (leaving group) site, a binding site perhaps used by the unknown C-terminal extension of ubiquitin in the actual in vivo substrate(s) of UCHL1.
Z-VRPR-FMK (TFA) (VRPR) is a tetrapeptide and a selective and irreversible inhibitor of lymphoma translocation protein 1 (MALT1) in mucosa-associated lymphoid tissue.
Z-WEHD-FMK is a cell-permeable and irreversible inhibitor of caspase-1 5. It also shows a robust inhibitory effect on cathepsin B activity (IC50: 6 μM).