cmk

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

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.

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.

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

Z-Ala-Ala-Asp-CMK (Z-AAD-CMK) is a selective granzyme B inhibitor that blocks granzyme B protease activity, suitable for studies in inflammatory diseases and tumours.

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

Ala-Ala-Pro-Val-chloromethylketone serves as an irreversible inhibitor of human neutrophil elastase (NE), utilized in researching chronic inflammatory airway diseases.

Caspase-9 Inhibitor III (Ac-LEHD-cmk), a caspase-9 inhibitor, demonstrates protective effects against ischemia-reperfusion-induced myocardial injury.

MeO-Suc-Ala-Ala-Pro-Ala-CMK (MSACK) is an inhibitor of human neutrophil elastase (HNE) with an IC50 of 20.3 μM. It effectively inhibits the hydrolysis of substrates like lung tissue elastin by HNE and is applicable in studies related to conditions such as chronic obstructive pulmonary disease (COPD).

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

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].

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-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.

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

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

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

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

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

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

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].

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].

Ac-DMLD-CMK is a peptide designed to target the caspase3-Gsdme signaling pathway in mice. It specifically inhibits the activation of caspase 3 and Gsdme, preventing the cleavage of Gsdme by caspase 3, which reduces pyroptosis. This process helps alleviate damage to renal tubular epithelial cells and decrease the secretion of inflammatory cytokines. Ac-DMLD-CMK can lower serum creatinine and blood urea nitrogen levels in mice induced by Cisplatin, thereby mitigating the progression of renal dysfunction. It holds potential for research into chemotherapy-induced nephrotoxicity.

D-Val-Phe-Lys-CMK (D-Val-Phe-Lys Chloromethyl ketone) diTFA effectively inhibits fibrinolytic enzyme activity.