pan-caspase

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.

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.

Emricasan (IDN-6556) is a pan-caspase inhibitor with irreversible properties. Emricasan has anti-inflammatory and anti-apoptotic activity and can be used in the treatment of infections and liver failure, etc. Emricasan also inhibits Zika virus infections.

(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.

Q-VD-OPH (Quinoline-Val-Asp-Difluorophenoxymethylketone) is a pan-caspase inhibitor with potent antiapoptotic properties.

(R)-Q-VD-OPh is the less active enantiomer of Q-VD-OPha. Q-VD-OPha is an irreversible inhibitor of pan-caspase, with potent antiapoptotic properties.

TD1092, a pan-IAP degrader, effectively degrades cIAP1, cIAP2, and XIAP, catalyzing the activation of Caspase 3 7 and fostering apoptosis in cancer cells through IAP degradation. It also obstructs the TNFα-mediated NF-κB pathway, diminishing the phosphorylation of IKK, IkBα, p65, and p38, and operates as a PROTAC. This compound is utilized in cancer research [1].

(2R,3S)-Emricasan ((2R,3S)-PF 03491390) is an isomer of Emricasan. This compound acts as an orally effective irreversible pan-caspase inhibitor. (2R,3S)-Emricasan inhibits the increase in caspase-3 activity induced by Zika virus (ZIKV) and protects human cortical neural progenitor cells.

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

MX1013, a dipeptide pan-caspase inhibitor, inhibits caspase-1, -3, -6, -7, -8, and -9.

VX-166 is a pan-caspase inhibitor applicable in the study of non-alcoholic steatohepatitis (NASH), alcoholic steatohepatitis (ASH), and other conditions involving liver fibrosis, steatosis, or inflammation.

CGP74514A is a CDK1 inhibitor with potential anticancer activity. In U937 cells, CGP74514A - induced apoptosis (5 microM) became apparent within 4 hr and approached 100% by 24 hr. The pan- caspase inhibitor Boc-fmk and the caspase-8 inhibitor lETD-fmk opposed CGP74514A -induced caspase-9 activation and PARP degradation, but not cytochrome c or Smac DIABLO release. CGP74514A -mediated apoptosis was substantially blocked by ectopic expression of full-length Bel- 2, a loop-deleted mutant Bcl-2, and Bcl-x(L). CGP74514A treatment (5 microM; 18 hr) resulted in increased p21(CIP1) expression, p27(KIP1) degradation, diminished E2F1 expression, and dephosphorylation of p34(CDC2). It also induced early (i.e., within 2 hr) inhibition of CDK1 activity and dephosphorylation of pRb, followed by pRb degradation, but did not block pRb phosphorylation at CDK2- and CDK4- specific sites. These findings indicate that the selective CDK1 inhibitor, CGP74514A , induces complex changes in cell cycle......

Cantrixil (TRX-E-002-1) is a second-generation super-benzopyran (SBP) compound, derived from TRX-E-002. It elicits an increase in phosphorylated c-Jun levels, leading to caspase-mediated apoptosis in ovarian cancer cells. Cantrixil exhibits potent pan anti-cancer activity against various cancer phenotypes.

Ac-Val-Ala-Asp-CHO (Ac-VAD-CHO) serves as a pan-caspase inhibitor and preserves mitochondrial membrane potential (MMP) while preventing the release of cytochrome c in cells subjected to hypoxia [1].