GPR is a three amino acid peptide. GPR can rescue cultured rat hippocampal neurons from Aβ-induced neuronal death by inhibiting caspase-3/p53 dependent apoptosis. GPR can be used for the research of Alzheimer's disease (AD).
Ginsenoside Rh2 is isolated from the root of Ginseng. Ginsenoside Rh2 induces the activation of caspase-8 and caspase-9. Ginsenoside Rh2 induces cancer cell apoptosis in a multi-path manner.
Cimiside E (25-Anhydrocimigenol xyloside) is a triterpene xyloside, Cimiside E possesses apoptotic action on gastric cancer cells, with an IC50 value of 14.58 μM. Cimiside E induces cell cycle arrest at G2/M phase, and mediates apoptosis through the induction of the Caspase cascade for both the extrinsic and intrinsic pathways[1][2].
Z-VEID-AFC is a fluorescent substrate for caspase-6[1].
MX1013 is a potent, irreversible dipeptide caspase inhibitor vith antiapoptotic activity. MX1013 inhibits recombinant human caspase 3 with an IC50 of 30 nM[1].
2-HBA is a potent inducer of NAD(P)H:quinone acceptor oxidoreductase 1 (NQO1) which can also activate caspase-3 and caspase-10.
Anticancer agent 56 (compound 4d) is a potent anti-cancer agent with drug-likeness properties, possessing anticancer activity against several cancer cell lines (IC50<3 μM). Anticancer agent 56 induces cell cycle arrest at G2/M phase and triggers mitochondrial apoptosis pathway. Anticancer agent 56 acts by accumulation of ROS, up regulation of BAX, down regulation of Bcl-2 and activation of caspases 3, 7, 9[1].
Estrogen receptor modulator 10 (compound G-5b) is an Estrogen receptor (ER) antagonist (IC50=6.7 nM) and degrader (DC50=0.4 nM). Estrogen receptor modulator 10 can induce apoptosis. Estrogen receptor modulator 10 can block cells at the G1/G0 phase. Estrogen receptor modulator 10 can be used in cancer studies[1].
Z-IETD-pNA (Z-Ile-Glu-Thr-Asp-pNA) is a colorimetric caspase-8 and granzyme B substrate. Z-IETD-pNA is hydrlyzed by caspase 8 to generate pNA[1].
Anticancer Agent 43 is a potent anticancer agent. Anticancer Agent 43 induces apoptosis by caspase 3, PARP1, and Bax dependent mechanisms. Anticancer Agent 43 induces DNA damage[1].
Z-WEHD-FMK is a potent, cell-permeable and irreversible caspase-1/5 inhibitor. Z-WEHD-FMK also exhibits a robust inhibitory effect on cathepsin B activity (IC50=6 μM). Z-WEHD-FMK can be used to investigate cells for evidence of apoptosis[1][2][4].
GDC-2394 is an orally active and selective NLRP3 inhibitor, and also inhibits IL-1β with IC50s of 0.4 μM (human IL-1β) and 0.1 μM (mouse IL-1β). GDC-2394 inhibits NLRP3-induced caspase-1 activity without inhibiting NLRC4-dependent inflammasome activation[1][2].
Z-VAD-FMK (Z-VAD(OH)-FMK) is a well-know pan caspase inhibitor, which does not inhibit ubiquitin carboxy-terminal hydrolase L1 (UCHL1) activity even at concentrations as high as 440 μM[1].
Ac-FLTD-CMK, a gasdermin D (GSDMD)-derived inhibitor, is a specific inflammatory caspases inhibitor. Ac-FLTD-CMK is effective against caspases-1 (IC50 of 46.7 nM), caspases-4 (IC50 of 1.49 μM), caspases-5 (IC50 of 329 nM), and caspases-11 , but not the apoptotic caspases such as caspase-3[1].
Duocarmycin A, which is one of well-known antitumor antibiotics, efficiently alkylates adenine N3 at the 3′ end of AT-rich sequences in the DNA. Duocarmycin A, as a chemotherapeutic agent, results HLC-2 cells typically apoptotic changes, including chromatin condensation, sub-G1 accumulation in DNA histogram pattern, and decrease in procaspase-3 and 9 levels[1].
Ac-LEHD-AFC is a fluorescent substrate for caspase-9, can be used to assess the activity of caspase[1].
Caspase-9 Inhibitor III (Ac-LEHD-cmk) is a caspase-9 inhibitor. Caspase-9 Inhibitor III exhibits protective effects on ischemia-reperfusion-induced myocardial injury[1].
VRT-043198, the drug metabolite of VX-765 (Belnacasan), is a potent, selective and blood-brain barrier permeable inhibitor of interleukin-converting enzyme/caspase-1 subfamily caspases. VRT-043198 exhibits Ki values of 0.8 nM and 0.6 nM for ICE/caspase-1 and caspase-4, respectively[1].
Z-LEHD-FMK is a selective and irreversible inhibitor of caspase-9, protects against lethal reperfusion injury and attenuates apoptosis. Z-LEHD-FMK exhibits the neuroprotective effect in a rat model of spinal cord trauma[1][2][3].
Mca-DEVDAP-K(Dnp)-OH is a fluorogenic substrate for caspase-3[1].
Nivalenol, classified as type B trichotecenes toxins produced by Fusarium graminearum, is a fungal metabolite present in agricultural product[1]. Nivalenol induces cell death through caspase-dependent mechanisms and via the intrinsic apoptotic pathway. Nivalenol affects the immune system, causes emesis, growth retardation, reproductive disorders and has a haematotoxic/myelotoxic effect[2].
Demethoxyfumitremorgin C is a secondary metabolite of the marine fungus, Aspergillus fumigatus. Demethoxyfumitremorgin C induces prostate cancer cell apoptosis. Demethoxyfumitremorgin C activates caspase-3, -8, and -9, leading to PARP/ cleavage[1].
GRI977143 is a specific LPA2 receptor agonist, with an EC50 of 3.3 μM [1].
Q-VD-OPha is a irreversible pan-caspase inhibitor with potent antiapoptotic properties; inhibits caspase 7 with IC50 of 48 nM and 25-400 nM for other caspases including caspase 1, 3, 8, 9, 10, and 12. Q-VD-OPha is able to cross the blood-brain barrier.
Caspase-3-IN-1 (compound 11b) is a potent Caspase-3 inhibitor, with an IC50 of 14.5 nM[1].
Z-YVAD-pNA (Z-Tyr-Val-Ala-Asp-pNA) is a caspase-1 substrate[1].
Senkyunolide I, isolated from Ligusticum chuanxiong Hort, is an anti-migraine compound. Senkyunolide I protects rat brain against focal cerebral ischemia-reperfusion injury by up-regulating p-Erk1/2, Nrf2/HO-1 and inhibiting caspase 3[1][2].
Z-YVAD-CMK is a caspase-1 and caspase-3 inhibitor[1].
Tauroursodeoxycholate-d4-1 is the deuterium labeled Tauroursodeoxycholate. Tauroursodeoxycholate (Tauroursodeoxycholic acid) is an endoplasmic reticulum (ER) stress inhibitor. Tauroursodeoxycholate significantly reduces expression of apoptosis molecules, such as caspase-3 and caspase-12. Tauroursodeoxycholate also inhibits ERK.
QM31 (SVT016426, Apaf-1 inhibitor QM31) is a cytoprotective agent that inhibits the formation of the apoptosome (IC50=7.9 uM in vitro), the caspase activation complex composed by Apaf-1, cytochrome c, dATP and caspase-9; suppresses the Apaf-1-dependent intra-S-phase DNA damage checkpoint; QM31 can interfere with the two known functions of Apaf-1, namely apoptosome assembly/activation and intra-S-phase cell cycle arrest.