fmk

FMK is an irreversible inhibitor of RSK2 kinase.

Z-VAD(OMe)-FMK is a pan-caspase inhibitor with irreversible properties; Z-VAD(OMe)-FMK is also an inhibitor of ubiquitin C terminal hydrolase L1 (UCHL1), which is irreversibly modified by targeting the UCHL1 active site.

Z-VAD-FMK (Caspase Inhibitor VI) is a broad-spectrum inhibitor of caspases.Z-VAD-FMK binds to activated caspases and inhibits apoptosis.Z-VAD-FMK does not inhibit UCHL1 activity, even at concentrations up to 440 μM.

FMK-MEA is a potent and selective inhibitor of p90 Ribosomal S6 Kinase (RSK).

FMK 9a is an irreversible inhibitor of ATG4B with IC50 values of 80 and 73 nM in the TR-FRET and cellular-based LRA assays.

(Iso)-Z-VAD(OMe)-FMK is an isomer of Z-VAD(OMe)-FMK, which is a pan-caspase inhibitor with irreversible properties. Z-VAD(OMe)-FMK is also an inhibitor of ubiquitin C-terminal hydrolase L1 (UCHL1), irreversibly modified by targeting the UCHL1 active site.

Biotin-VAD-FMK is a cell-permeable, irreversible biotin-labeled inhibitor of caspase. It is used to identify active caspases in cell lysates.

Z-LEHD-FMK is a selective and potent caspase-9 inhibitor that protects against reperfusion injury and slows apoptosis. Z-LEHD-FMK exhibits antitumor and neuroprotective activity, increases the yield of in vitro-produced preimplantation embryos of [Bubalus bubalis], and alters the cellular stress response.

Z-VEID-FMK is a selective and cell-permeable caspase-6 peptide inhibitor that irreversibly covalently binds to the active site of the enzyme, thereby inhibiting apoptosis and DNA breakage.

Z-AEVD-FMK (Z-Ala-Glu-Val-Asp-Fluoromethyl Ketone) is a degradable ADC linker and caspase-10 inhibitor, reducing TNF-α/butyrate-induced apoptosis, and inhibiting Gal-9-induced apoptosis.

(Rac)-Z-Phe-Phe-FMK (Cathepsin L-IN-2) is a cathepsin L inhibitor that inhibits the tendency of β-amyloid to induce apoptotic changes .

Z-VDVA-(DL-Asp)-FMK, a derivative of Z-VDVAD-FMK, is specifically designed as a caspase-2 inhibitor.

Z-LEHD-FMK TFA is a specific and irreversible inhibitor of caspase-9, providing protection against detrimental reperfusion injury and moderating apoptosis, with demonstrated neuroprotective potential in a rat model of spinal cord trauma.

Z-DEVD-FMK (Caspase-3 Inhibitor) is a Caspase-3 inhibitor (IC50=18 μM), featuring selectivity, irreversibility and cell permeability. Z-DEVD-FMK can inhibit caspase activation induced apoptosis.

Z-FA-FMK can irreversibly inhibit cysteine protease and also inhibit effector caspases.

Z-IETD-FMK (Z-IE(OMe)TD(OMe)-FMK) is a cell-permeable, selective inhibitor of caspase 8.

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.

Ac-PLVE-FMK (Ac-Pro-Leu-Val-Glu(OMe)-CH2F), a tetrapeptidyl fluoromethylketone (FMK), acts as a cathepsin inhibitor and is used in cancer research [1].

Ac-VLPE-FMK, a tetrapeptidyl mono-fluoromethyl ketone (m-FMK), inhibits Cathepsin B (Cat-B) and Cathepsin L (Cat-L) and is used in cancer aggressiveness research [1] [2].

AA-Z-YVAD-FMK is a Irreversible caspase-1 inhibitor,with anti-inflammatory and anti-tumor activities.

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).

Boc-D-FMK is an irreversible, cell-permeable, and broad-spectrum caspase inhibitor and inhibits apoptosis stimulated by TNF-α (IC50: 39 µM).

Z-VA-DL-D-FMK (Z-VA-DL-D(OH)-FMK) acts as an inhibitor of caspases. It irreversibly binds to caspases, enhancing the sensitivity to TNF-α and stimulating HIV replication in infected T cells ACH-2.

Boc-Asp(OMe)-fluoromethyl ketone (Boc-Asp(OMe)-FMK) is a broad range caspase inhibitor. Boc-Asp(OME)-Fluoromethyl Ketone inhibits Fas-mediated phagocytosis and oxidative rupture inhibition, but does not affect the chemotactic activity of IL-8.