SC75741 is a broad and efficient NF-κB inhibitor with an IC50 of 200 nM for p65[1]. SC75741 blocks influenza viruses (IV) replication in non-toxic concentrations. SC75741 impairs DNA binding of the NF-κB subunit p65, resulting in reduced expression of cytokines, chemokines, and pro-apoptotic factors. SC75741 subsequently inhibits caspase activation and blocks caspase-mediated nuclear export of viral ribonucleoproteins[2].
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].
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].
TC11 is a MCL1 degradator and Caspase-9 and CDK1 activator. TC11 structurally relates to immunomodulatory drugs as phenylphthalimide derivative. TC11 induces apoptotic death caused by degradation of MCL1 during prolonged mitotic arrest[1][2].
Ivachtin (Caspase-3 Inhibitor VII; compound 7a) is a nonpeptide, noncompetitive and reversibl caspase-3 inhibitor with an IC50 of 23 nM. Ivachtin has modest selectivity for the remaining caspases[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].
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].
Ac-AAVALLPAVLLALLAP-YVAD-CHO is a cell-permeable caspase-1 inhibitor that has antitumor activity[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].
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].
Akt1/Akt2-IN-2 (compound 7) is an allosteric dual Akt1 and Akt2 inhibitor (IC50=138 nM and 212 nM, respectively). Akt1/Akt2-IN-2 increases activity of caspase-3, and inhibits viability of a number of tumor cells[1].
Aspirin (Acetylsalicylic Acid) lithium is an orally active, potent and irreversible inhibitor of cyclooxygenase COX-1 and COX-2, with IC50 values of 5 and 210 μg/mL, respectively. Aspirin lithium induces apoptosis. Aspirin lithium inhibits the activation of NF-κB. Aspirin lithium also inhibits platelet prostaglandin synthetase, and can prevent coronary artery and cerebrovascular thrombosis[1][2][3][4][5][6].
Boc-Ala-Ala-Asp-pNA is a chromogenic substrate of granzyme B. Boc-Ala-Ala-Asp-pNA can be used to test functional activity of granzyme B[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].
Coenzyme Q0 (CoQ0) is a potent, oral active ubiquinone compound can be derived from Antrodia cinnamomea. Coenzyme Q0 induces apoptosis and autophagy, suppresses of HER-2/AKT/mTOR signaling to potentiate the apoptosis and autophagy mechanisms. Coenzyme Q0 regulates NFκB/AP-1 activation and enhances Nrf2 stabilization in attenuation of inflammation and redox imbalance. Coenzyme Q0 has anti-angiogenic activity through downregulation of MMP-9/NF-κB and upregulation of HO-1 signaling[1][2][3].
Cystamine-d8 (dihydrochloride） is the deuterium labeled Cystamine (dihydrochloride）[1]. Cystamine (dihydrochloride) is the disulfide form of the free thiol, cysteamine. Cystamine is an orally active transglutaminase (Tgase) inhibitor. Cystamine also has inhibition activity for caspase-3 with an IC50 value of 23.6 μM. Cystamine can be used for the research of severals diseases including Huntington's disease (HD)[2][3][4].
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].
Ac-Trp-Glu-His-Asp-Aldehyde is a potent and selective caspase-1 inhibitor with a Ki value of 56 pM[1][2].
ML132 (NCGC 00185682) is a potent and selective caspase 1 inhibitor with an IC50 of 0.316 nM.
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].
Boc-AEVD-CHO is a Caspase 8 inhibitor useful in the study of apoptosis and immune and inflammatory diseases[1][2].
Ac-VETD-AMC is a synthetic peptide substrate for caspase 8. Ac-VETD-AMC also has potential to assess functional activity of recombinant phytaspase[1].
AKN-028 is an orally active and potent FLT3 tyrosine kinase inhibitor (IC50 = 6 nM). AKN-028 causes dose-dependent inhibition of FLT3 autophosphorylation[1].
Thevetiaflavone could upregulate the expression of Bcl‑2 and downregulate that of Bax and caspase‑3.
Ac-Trp-Glu-His-Asp-AMC (Ac-Trp-Glu-His-Asp-AMC) is a potent fluorogenic substrate of caspase-1[1].
Lycopodine, a pharmacologically important bioactive component derived from Lycopodium clavatumspores, triggers apoptosis by modulating 5-lipoxygenase, and depolarizing mitochondrial membrane potential in refractory prostate cancer cells without modulating p53 activity[1]. Lycopodine inhibits proliferation of HeLa cells through induction of apoptosis via caspase-3 activation[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].