cmk

CMK, an RSK2 kinase inhibitor, shows similar potency but less chemical stability compared with FMK.

Decanoyl-RVKR-CMK (DecRVKRcmk) TFA effectively hinders the processing of over-expressed gp160 and suppresses HIV-1 replication.

Boc-Asp(OBzl)-CMK, an inhibitor of IL-1 converting enzyme (ICE, caspase1), prevents the death of CHP100 neuroblastoma cells and inhibits IL-1β release induced by the viral coat protein [1].

MeOSuc-AAPA-CMK is a potent inhibitor of human neutrophil elastase (HNE) [1].

MeOSuc-AAPF-CMK (MeOSuc-Ala-Ala-Pro-Phe-CH2Cl) is a potent inhibitor of proteinase K [1].

Ac-YVAD-CMK (Ac-Tyr-Val-Ala-Asp-CMK) is a selective and irreversible inhibitor of Caspase-1 and inhibits pyroptosis, IL-1β and IL-18. Ac-YVAD-CMK shows neuroprotective and anti-inflammatory capacity.

Tripeptidyl peptidase II (TPPII) is a serine peptidase of the subtilisin-type which removes tripeptides from the free NH2 terminus of oligopeptides. AAF-CMK is an irreversible inhibitor of TPPII commonly used at 10-100 μM. It does not significantly interfere with the chymotrypsin-like activity of the proteasome. AAF-CMK also inhibits bleomycin hydrolase and puromycin-sensitive aminopeptidase when used at 50 μM.

D-Val-Phe-Lys-CMK (D-Val-Phe-Lys Chloromethyl ketone) inhibits plasmin activity [1].

Ac-DEVD-CMK (Caspase-3 Inhibitor III) TFA is a selective, irreversible caspase-3 inhibitor, preventing apoptosis induced by elevated glucose levels or 3,20-dibenzoate (IDB) in various experimental contexts, as supported by references [1] [2] [3].

Z-APF-CMK is a selective inhibitor of the calcium (Ca2+)-regulated nuclear scaffold protease (CRNSP), as reported in reference [1].

Z-GGF-CMK, a protease inhibitor, impedes ClpP1P2 and proteasome activity and demonstrates cytotoxic effects on HepG2 cells, with a CC50 value of 125 μM [1].

Z-DEVD-CMK irreversibly inhibits various cathepsins in vitro [1].

Subtilisin/Kex2p-like proprotein convertase inhibitor; blocks activity of all seven convertases (PC1, PC2, PC4, PACE4, PC5, PC7 and furin). Abolishes proET-1 processing in endothelial cells; inhibits regulated secretion of the neuronal polypeptide VGF in

Decanoyl-Arg-Val-Arg-Lys-chloromethylketone (DEC-RVRK-CMK) is a small, synthetic, irreversible cell-permeable competitive inhibitor of furin that exhibits strong antiviral activity against Zika virus (ZIKV) and Japanese encephalitis virus (JEV) [1].

Ac-FEID-CMK, a potent peptide inhibitor derived from zebrafish-specific GSDMEb, effectively reduces mortality and kidney injury during septic shock by inhibiting pyroptosis and mitigating acute kidney injury (AKI) in vivo. Additionally, it suppresses the caspy2-mediated noncanonical inflammasome pathway [1].

Ac-FLTD-CMK is an inhibitor derived from abscisicin D (GSDMDD) with specific inhibitory effects on inflammatory caspases. ac-FLTD-CMK showed inhibitory effects on caspases-1, caspases-4 and caspases-11 with IC50s of 46.7 nM, 1.49 μM and 329 nM, respectively. Ac-FLTD-CMK showed potency against caspases-1, caspases-4 and caspases-11, but not against apoptosis-associated caspase-3.

Z-YVAD-CMK is an inhibitor of both caspase-1 and caspase-3, as referenced in [1].

Ac-FEID-CMK TFA is a selective zebrafish GSDMEb-derived peptide inhibitor that reduces mortality and renal injury in infectious shock. It inhibits pyroptosis in vivo, attenuates septic AKI (acute kidney injury), and inhibits the caspy2-mediated atypical inflammatory vesicle pathway.

Z-Ala-Ala-Asp-chloromethylketone (Z-AAD-CMK) is a selective inhibitor of granzyme B [1].

AAF-CMK, a tripeptidylpeptidase II (TPPII) inhibitor, exhibits anti-tumor activity and induces apoptosis, making it applicable in leukemia research.

DEC-RVRK-CMK (Decanoyl-Arg-Val-Arg-Lys-chloromethylketone) TFA is a peptide-based CMK (chloromethylketone) inhibitor that targets and inactivates the secreted soluble kexin (Kex2) with a Ki value of 8.45 μM. Kex2, a yeast enzyme and a member of the mammalian subtilisin-like proprotein convertase family within the serine protease class, is a calcium-dependent transmembrane protease. The binding mechanism of Kex2 with different CMK inhibitors depends on substrate selectivity, particularly noting the differences in selectivity between lysine and arginine at the P1 position, which influences their varying binding affinities.

Ac-VAD-CMK is a pan-inhibitor for caspase-1 [1].

MeOSuc-AAPV-CMK (Elastase Inhibitor III) inhibits elastase, cathepsin G, and proteinase 3, impeding leukocyte elastase-mediated cleavage of adiponectin [1].

CMKLR1 antagonist 1 (compound S-26d) is a potent, orally active antagonist of the chemokine-like receptor 1 (CMKLR1) with a pIC50 of 7.44 in hCMKLR1-transfected CHO cells, applicable in the research of psoriasis and metabolic diseases [1].