|S2228||Belnacasan (VX-765)||<1 mg/mL||100 mg/mL||100 mg/mL|
|S7023||Z-VAD-FMK||<1 mg/mL||93 mg/mL||<1 mg/mL|
|S7313||Z-LEHD-FMK||44 mg/mL||100 mg/mL||100 mg/mL|
|S7314||Z-IETD-FMK||<1 mg/mL||91 mg/mL||<1 mg/mL|
|S7312||Z-DEVD-FMK||<1 mg/mL||100 mg/mL||<1 mg/mL|
|S7311||Q-VD-OPh||<1 mg/mL||100 mg/mL||100 mg/mL|
|S8102||Z-VAD-FMK (Caspase Inhibitor VI)||<1 mg/mL||90 mg/mL||90 mg/mL|
|S7775||Emricasan||<1 mg/mL||100 mg/mL||100 mg/mL|
|S7901||Ac-DEVD-CHO||100 mg/mL||-1 mg/mL||-1 mg/mL|
|S2738||PAC-1||<1 mg/mL||78 mg/mL||16 mg/mL|
|S2927||Apoptosis Activator 2||<1 mg/mL||61 mg/mL||<1 mg/mL|
|S7326||Tasisulam||<1 mg/mL||83 mg/mL||83 mg/mL|
|S2448||Gambogic Acid||<1 mg/mL||100 mg/mL||100 mg/mL|
Belnacasan (VX-765) is a potent and selective inhibitor of caspase-1 with Ki of 0.8 nM in a cell-free assay. Phase 2.
BMMs were treated as above for 1 h. Cell lysates, as well as cell culture supernatants, were analyzed by western blot for cleavage of caspase-1. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) served as loading control.
Z-VAD-FMK is a cell-permeable, irreversible pan-caspase inhibitor, blocks all features of apoptosis in THP.1 and Jurkat T-cells.
(A) LAN5 cells were untreated (top panels) or treated with 50 µM of the caspase inhibitor Z-VAD-FMK (bottom panels). Cells were co-treated with nothing (No Rx), 1 µM GSK-J4, or 1 µM venetoclax for 48 hours and assayed for apoptosis by flow cytometry.
Z-LEHD-FMK is a specific, irreversible Caspase-9 inhibitor.
Z-IETD-FMK is a specific Caspase-8 inhibitor.
Z-DEVD-FMK is a specific, irreversible Caspase-3 inhibitor, and also shows potent inhibition on caspase-6, caspase-7, caspase-8, and caspase-10.
Immunoblotting analysis was performed for the active-caspase-3 and cleavage of MCL-1 in MM.1S cells treated with z-DEVD-fmk (20 μM, 1 h) and following GSK126 (25 μM, 24 h).
Q-VD-Oph is a potent pan-caspase inhibitor with IC50 ranged from 25 to 400 nM for caspases 1,3,8, and 9.
Z-VAD-FMK (Caspase Inhibitor VI) is an irreversible pan-caspase inhibitor.
Effect on the RAS of CFZ, z-VAD-fmk, or CFZ+z-VAD-fmk treatments administered 5 or 12 days after C26 inoculation and control groups. Serum levels of a renin and b ANGII. c The mRNA expression of ATF2. d Western blot analysis of ATF2 and pATF2. e pATF2-to-ATF2 ratio. Significant differences were detected between most of the groups, with the exceptionsof (A and B) CP and UT (D) and ZP and ZT (#); and (C and E) CP and UP (*), CT and UT (#), and HC, ZP, ZT and CC (&). ZP:z-VAD-fmk.
Emricasan is a potent irreversible pan-caspase inhibitor.
Ac-DEVD-CHO is a potent aldehyde inhibitor of Group II caspases with Ki values of 0.2 nM and 0.3 nM for for caspase-3 and caspase-7, respectively. Weak inhibition for caspase-2.
PAC-1 is a potent procaspase-3 activator with EC50 of 0.22 μM and the first small molecule known to directly activate procaspase-3 to caspase-3.
The effects of PAC-1 (activator of ROS) administration on the newborn pups' weight and the plasma IGF-1 and ROS levels in graviditas gp91phox-/- mice. The values are presented as the means ± SD derived from six animals. *P<0.05 in comparison to the non-treatment mice.
Apoptosis Activator 2 strongly induces caspase-3 activation, PARP cleavage, and DNA fragmentation which leads to the destruction of cells (Apaf-1 dependent) with IC50 of ~4 μM, inactive to HMEC, PREC, or MCF-10A cells.
Tasisulam is an antitumor agent and an apoptosis inducer via the intrinsic pathway. Phase 3.
Alisol B acetate, a triterpene from Alismatis rhizoma, induces Bax up-regulation and nuclear translocation, the activation of initiator caspase-8 and caspase-9, and executor caspase-3, suggesting the involvement of both extrinsic and intrinsic apoptosis pathways.
Gambogic Acid activates caspases with EC50 of 0.78-1.64 μM and competitively inhibits Bcl-XL, Bcl-2, Bcl-W, Bcl-B, Bfl-1 and Mcl-1 with IC50 of 1.47, 1.21, 2.02, 0.66, 1.06 and 0.79 μM, respectively.