Biotin-VAD-FMK is a cell permeable, irreversible biotin-labeled caspase inhibitor, used to identify active caspases in cell lysates.
TRP-601 is a caspase inhibitor.
Ac-LEHD-AMC is a fluorogenic substrate for caspase-9 (Excitation: 341 nm; Emission: 441 nm). Caspase-9 can induce hydrolysis of Ac-LEHD-AMC, resulting in the release of AMC fluorophore and its fluorescence can be used to quantify caspase-9 activity[1].
Z-VAD-AMC is a substrate of caspase-9[1].
Sesaminol, isolated from Justicia orbiculata, has antioxidative activity, Sesaminol inhibits lipid peroxidation and shows neuroprotection effect. Sesaminol potently inhibits MAPK cascades by preventing phosphorylation of JNK, p38 MAPKs, and caspase-3 but not ERK-MAPK expression[1][2][3][4].
Limonin glucoside can be isolated from seeds of Citrus reticulata. Limonin glucoside induces activation of caspase-3. Limonin glucoside inhibits the proliferation of human colon adenocarcinoma (SW480) cells (IC50: 37.39 μM)[1].
Apoptotic agent-2 (compound 14b) induces apoptosis by down-regulation of Bcl-2 and up-regulation of Bax and caspase-3. Apoptotic agent-2 exhibits anti-proliferative activities and can be used for cancer research[1].
PAC-1 is an activator of procaspase-3 induces apoptosis in cancer cells with EC50 of 2.08 μM.
Procaspase-3/6 activator 1 (compound 1541) is a highly specific and robust activator of executioner procaspases-3 and -6, with EC50 values of 2.4 ± 0.2 and 2.8 ± 0.3 μM, respectively. Procaspase-3/6 activator 1 does not activate procaspases-1 or -7[1].
Fenbufen-d9 (CL-82204-d9) is the deuterium labeled Fenbufen. Fenbufen (CL-82204) is an orally active non-steroidal anti-inflammatory drug (NSAID), with analgetic and antipyretic effects. Fenbufen has potent activity in a variety of animal model, including carageenin edema, UV erythema and adjuvant arthritis. Fenbufen has inhibitory activities against COX-1 and COX-2 with IC50s of 3.9 μM and 8.1 μM, respectively. Fenbufen is a caspases (caspase-1, 3, 4, 5, 9) inhibitor[1][2][3][4][5].
Ac-VRPR-AMC is a fluorogenic metacaspase substrate. Ac-VRPR-AMC can be used to tests metacaspase activity[1].
cRIPGBM(chloride), an orally active, proapoptotic derivative. cRIPGBM can be generated from glioblastoma multiforme (GBM) cancer stem cells (CSCs). cRIPGBM(chloride) targets to receptor-interacting protein kinase 2 (RIPK2) to induce caspase 1-dependent apoptosis. cRIPGBM(chloride) suppresses the formation of RIPK2/TAK1 (prosurvival complex), and increases the formation of RIPK2/caspase 1 (proapoptotic complex). cRIPGBM(chloride) exerts potent anti-tumor activity in vivo in animal models[1].
JQAD1 is a CRBN-dependent PROTAC that selectively targets EP300 for degradation. JQAD1 suppresses EP300 expression and the H3K27ac modification. JQAD1 induces apoptosis. JQAD1 can be used in research of cancer[1].
Paris saponin VII (Chonglou Saponin VII) is a steroidal saponin isolated from the roots and rhizomes of Trillium tschonoskii Maxim. Paris saponin VII-induced apoptosis in K562/ADR cells is associated with Akt/MAPK and the inhibition of P-gp. Paris saponin VII attenuates mitochondrial membrane potential, increases the expression of apoptosis-related proteins, such as Bax and cytochrome c, and decreases the protein expression levels of Bcl-2, caspase-9, caspase-3, PARP-1, and p-Akt. Paris saponin VII induces a robust autophagy in K562/ADR cells and provides a biochemical basis in the treatment of leukemia[1].
ALK-IN-26 is an ALK inhibitor with IC50 value of 7.0 μM for ALK tyrosine kinase. ALK-IN-26 has good pharmacokinetic properties and blood-brain barrier (BBB) permeability. ALK-IN-26 can induce apoptosis, autophagy and necrosis. ALK-IN-26 can be used in glioblastoma studies[1].
Topoisomerase I inhibitor 2 (ZML-8) is a highly selective inhibitor of DNA topoisomerase I (Top1). Topoisomerase I inhibitor 2 inhibits Top1 activity and results DNA damage. Topoisomerase I inhibitor 2 blocks G2/M phase and induces apoptosis, exhibits anti-tumor effect[1].
Rosamultic acid is an A-ring contracted triterpene, that can be isolated from the roots of Rosa rnultiflora. Rosamultic acid inhibits gastric cancer cells proliferation by inducing Apoptosis mediated through cell cycle arrest, downregulation of cell cycle related protein expressions, inhibition of cell migration, DNA damage, and activation of caspases[1][2].
ML132 (NCGC 00185682) is a potent and selective caspase 1 inhibitor with an IC50 of 0.316 nM.
Boc-AEVD-CHO is a Caspase 8 inhibitor useful in the study of apoptosis and immune and inflammatory diseases[1][2].
Thevetiaflavone could upregulate the expression of Bcl‑2 and downregulate that of Bax and caspase‑3.
Z-VAD(OMe)-FMK is a cell-permeable and irreversible pan-caspase inhibitor.
ZYZ-488 is a competitive apoptotic protease activating factor-1 (Apaf-1) inhibitor, which inhibits the activation of binding protein procaspase-9 and procaspase-3[1].
Aspidin BB is a phloroglucinol derivative, which can be isolated from the aerial part of Dryopteris championii. Aspidin BB has anticancer activity. Aspidin BB induces cell cycle arrest and apoptosis in human ovarian HO-8910 cells[1][2].
SDZ 224-015 is an orally active inhibitor of the interleukin-1 beta (IL-1β) converting enzyme and caspase-1. SDZ 224-015 possesses anti-COVID-19 activity, targeting Mpro (IC50 of 30 nM)[1][2].
Ginsenoside Rh4 is a rare saponin obtained from Panax notoginseng. Ginsenoside Rh4 activates Bax, caspase 3, caspase 8, and caspase 9. Ginsenoside Rh4 also induces autophagy.
Boc-Asp(OME)-Fluoromethyl Ketone is a broad range caspase inhibitor that inhibits Fas-mediated phagocytosis and oxidative rupture inhibition, but does not affect the chemotactic activity of IL-8[1][2].
Trijuganone C, a natural product extracted from Salvia miltiorrhiza, inhibits the proliferation of cancer cells through induction of apoptosis mediated by mitochondrial dysfunction and caspase activation[1].
Ac-DEVD-CHO is a specific Caspase-3 inhibitor with a Ki value of 230 pM.
N1,N11-Diethylnorspermine (DENSPM) is a potent anticancer agent. N1,N11-Diethylnorspermine is a spermine analog that activates polyamine catabolism. N1,N11-Diethylnorspermine induces the release of cytochrome c from mitochondria, resulting in activation of caspase 3. N1,N11-Diethylnorspermine kills glioblastoma multiforme (GBM) cells through induction of SSAT (spermidine/spermine N1-acetyltransferase) coupled with H2O2 production[1][2][3].