Pyridoclax is a potential Mcl-1 inhibitor.
BH3I-1 is a Bcl-2 family antagonist, which inhibits the binding of the Bak BH3 peptide to Bcl-xL with a Ki of 2.4±0.2 μM in FP assay. BH3I-1 has a Kd of 5.3 μM against the p53/MDM2 pair.
CDK1/2/4-IN-1 (compound 3a) is a potent CDK inhibitor with IC50 values of 1.47, 0.78 and 0.87 μM for CDK1, CDK2 and CDK4, respectively. CDK1/2/4-IN-1 arrests cell cycle at G2/M phase and induces apoptosis. CDK1/2/4-IN-1 elevates Bax, caspase-3, P53 levels and decreases Bcl-2 level. CDK1/2/4-IN-1 can be used for cancer research[1].
(E)-Mcl-1 inhibitor 7 (Example 34) is a Mcl-1 inhibitor (Ki: <1 nM, IC50: <500 nM). (E)-Mcl-1 inhibitor 7 can be used for research of cancers[1].
A09-003 is a CDK-9 inhibitor (IC50: 16 nM). A09-003 inhibits leukemia cell proliferation (IC50: 1.90, 0.86, 2.49, 1.84, 0.48 μM for BDCM, Molm-14, THP-1, U937, MV4-11 cells). A09-003 induces apoptosis and decreases Mcl-1 expression through Thr163 dephosphorylation[1].
MNK8 is a potent STAT3 (signal transducer and activator of transcription 3) inhibitor. MNK8 inhibits STAT3 activation and reduced its DNA binding ability. MNK8 shows good growth inhibition against hepatocellular carcinoma (HCC) cells. MNK8 induces apoptosis in HCC cells. MNK8 reduces prosurvival proteins expression and migration/invasion of HCC cells[1].
ML311 is a potent and selective inhibitor of the Mcl-1/Bim interaction.
BCL2-IN-1 is a potent Bcl-2 inhibitor. BCL2-IN-1 binds Bcl-2 with a Ki of <0.01 nM[1].
S63845 is a potent and selective myeloid cell leukemia 1 (MCL1) inhibitor with a Kd of 0.19 nM for human MCL1.
Bax activator-1 (compound 106) is a Bax activator that induces Bax-dependent tumor cell apoptosis[1].
BTSA1 is a potent, high affinity and orally active BAX activator with an IC50 of 250 nM and an EC50 of 144 nM. BTSA1 binds with high affinity and specificity to the N-terminal activation site and induces conformational changes to BAX leading to BAX-mediated apoptosis[1].
Apoptotic agent-3 (compound 15f) promotes apoptosis through the potential mitochondria-mediated Bcl-2/Bax pathway and activation of the Caspase 3 pathway. Apoptotic agent-3 exhibits anti-proliferative activities and can be used for cancer research[1].
Bcl-xL antagonist 2 is a potent, selective, and orally active antagonist of BCL-XL with an IC50 and Ki of 0.091 μM and 65 nM, respectively. Bcl-xL antagonist 2 promotes the apoptosis of cancer cells. Bcl-xL antagonist 2 has the potential for the research of the chronic lymphocytic leukemia (CLL) and non-Hodgkin’s lymphoma (NHL)[1][2].
Gambogic acid is derived from the gamboges resin of the tree Garcinia hanburyi. Gambogic acid inhibits Bcl-XL, Bcl-2, Bcl-W, Bcl-B, Bfl-1 and Mcl-1 with IC50s of 1.47 μM, 1.21 μM, 2.02 μM, 0.66 μM, 1.06 μM and 0.79 μM.
Dehydrocorydaline (13-Methylpalmatine) is an alkaloid isolated from traditional Chinese herb Corydalis yanhusuo W.T. Wang. Dehydrocorydaline regulates protein expression of Bax, Bcl-2; activates caspase-7, caspase-8, and inactivates PARP.
Mcl1-IN-9 is a potent myeloid cell leukemia-1 (Mcl-1) Inhibitor with an IC50 of 446 nM in reengineered BCR-ABL+ B-ALL cells and a Ki of 0.03 nM[1].
IDO1/TDO-IN-1 (30) is a potent dual IDO1 (uncompetitive, Ki of 0.23 μM) and TDO (competitive, Ki of 0.73 μM) inhibitor. IDO1/TDO-IN-1 (30) significantly promotes cell apoptosis through the potential mitochondria-mediated Bcl-2/Bax pathway[1].
Bcl-2-IN-9 is a novel proapoptotic Bcl-2 inhibitor with IC50 value of 2.9 μM and low cytotoxic. Bcl-2-IN-9 mediates apoptosis by down-regulating expression of Bcl-2 in cancer cells and has a high selectivity against leukemia cells[1].
MSN-50 is a Bax and Bak oligomerization inhibitor. MSN-50 efficiently inhibits liposome permeabilization, prevents genotoxic cell death and promotes neuroprotection[1][2].
NPB is a specific and potent inhibitor of BAD phosphorylation at Ser99, with an IC50 of 0.41 μM[1].
CYD-2-11 is a novel potent, selective Bax agonist that targets the structural pocket proximal to S184 in the C-terminal region of Bax (Ki=34.1 nM); shows no affinity for other Bcl-2 family members; directly activates Bax proapoptotic activity by inducing a conformational change enabling formation of Bax homooligomers in mitochondrial membranes; suppresses malignant growth without evident significant toxicity to normal tissues in mutant KRAS-driven lung cancer models; displays strong synergistic activity and overcomes rapalog resistance combined with RAD001.
BBR-BODIPY is a fluorescent probe that allows screening its interaction with the targeted cells. BBR-BODIPY induces apoptosis and changes the expression of apoptosis-related proteins[1].
Apogossypolone (ApoG2) is an orally active Bcl-2 family proteins inhibitor with Ki values of 35, 25 and 660 nM for Bcl-2, Mcl-1 and Bcl-XL, respectively. Apogossypolone shows antitumor activities, induces cell apoptosis[1] and autophagy[2]. Apogossypolone also has antifungal activity[3].
BAI1 is a direct allosteric inhibitor of BAX.
BM-1074 is a potent and specific Bcl-2/Bcl-xL inhibitor with Ki values of < 1 nM and IC50 values of 1.8 nM and 6.9 nM for Bcl-2 and Bcl-xL, respectively. BM-1074 induces apoptosis, and exhibits antiproliferative activity against four small-cell lung cancer cell lines (H146, H1963, H187 and H1417) with IC50 values of 1-2 nM[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].
Mcl1-IN-8 (Comp8) is a Mcl-1-PUMA interface inhibitor, with a Ki of 0.3 μM. Mcl1-IN-8 (Comp8) exhibits dual activity on reduce PUMA-dependent apoptosis while deactivating Mcl-1-mediated anti-apoptosis in cancer cells[1].
Mcl-1 inhibitor 3 (compound 1) is a highly potent and orally activate macrocyclic Mcl-1 inhibitor (Ki= 0.061 nM; IC50=19 nM in an OPM-2 cell viability assay). Mcl-1 inhibitor 3 shows good pharmacokinetic properties and excellent in vivo efficacy without toxicity[1]. .
Clezutoclax is a potent payload and also a Bcl-XL inhibitor. Clezutoclax can be used in the synthesis of antibody-drug conjugates (ADCs)[1].
TCPOBOP is a constitutive androstane receptor (CAR) agonist that induces robust hepatocyte proliferation and hepatomegaly without any liver injury or tissue loss[1]. TCPOBOP attenuates Fas-induced murine liver injury by altering Bcl-2 proteins[2].