BCL

Bcl-2-IN-16 is a Bcl-2 (B-cell lymphoma 2) inhibitor [1].

Bcl-2-IN-14 (Compound 13c), a BCL-2 inhibitor, exhibits an inhibitory concentration (IC 50) of 0.471 μM, and is applicable in cancer research [1].

Bcl-2-IN-12 (Compound 1) is a potent Bcl-2 inhibitor with an IC50 value of 6 nM, utilized in cancer research [1].

Bcl-B inhibitor 1 is a Bcl-B inhibitor with antitumor activity that binds to and inactivates pro-apoptotic proteins in the BH3 structural domain.

Bcl-2-IN-15 (Compound 13d) is a Bcl-2 inhibitor with an IC50 of 363 nM, which impedes the proliferation of the NCI leukemia cancer cell line [1].

Bcl-2-IN-5 is a potent inhibitor of BCL-2, demonstrating inhibitory concentrations (IC50) of 0.12 nM, 0.14 nM, and 0.22 nM against wild type Bcl-2, Bcl-2 D103Y, and Bcl-2 G101V, respectively. Additionally, it effectively suppresses cell growth in Bcl 2-G101V knock-in RS4;11 cells, with IC50 values of 0.2 nM and 0.44 nM.

Beclin1-Bcl-2 Interaction Inhibitor 1 effectively disrupts the binding of Beclin 1 to Bcl-2, and is utilized in cancer and neurodegeneration research [1].

Bcl-2-IN-13 is a potent inhibitor of Bcl-2, exhibiting an IC50 of 17 nM, and holds potential for use in cancer research [1].

PROTAC Bcl-xL degrader-3 is a potent ROTAC Bcl-xL degrader.

TAT-BH4 (Bcl-xL) TFA, primarily localized at the mitochondria, inhibits apoptotic cell death. This compound comprises an eosin-labeled cysteine at the N-terminal and the protein transduction domain from the HIV TAT protein (amino acids 49 to 57), fused to the Bcl-xL BH4 peptide. It is utilized in research concerning diseases associated with accelerated apoptosis [1].

Bcl-2-IN-9 is a novel, pro-apoptotic, low cytotoxic Bcl-2 inhibitor (IC50: 2.9 μM). Bcl-2-IN-9 downregulates Bcl-2 expression, induces apoptosis in cancer cells, and exhibits high selectivity for leukemia cells.

MCL-1/BCL-2-IN-4 is a selective and potent Mcl-1 and Bcl-2 dual inhibitor.

PROTAC Bcl-xL degrader-1 is a potent PROTAC composed of a Bcl-xL (Bcl-2 family member) ligand-binding group, a linker, and an IAP E3 ligases binding group, demonstrating effectiveness as a Bcl-xL degrader. It exhibits toxicity towards human platelets and MyLa 1929 cells, with IC50 values of 62 nM and 8.5 μM, respectively [1].

PROTAC Bcl-xL ligand-1 serves as a ligand targeting Bcl-xL, essential in synthesizing PROTACs [1].

Bcl-2-IN-4, an orally active and selective inhibitor of Bcl-2, demonstrates potent efficacy with an IC50 value of 1.5 nM and exhibits more than 200-fold selectivity over Bcl-xL (IC50 of 411 nM). Additionally, it effectively inhibits the proliferation of RS4;11 cells, achieving an IC50 of 2.7 nM.

Bcl-2/Mcl-1-IN-3 is a Bcl-2/Mcl-1 inhibitor that acts on Mcl-1 (Ki: 0.14 μM) and Bcl-2 (Ki: 0.23 μM) and can be used in cancer research.

Bcl-2/Mcl-1-IN-2 is a Bcl-2 (Ki: 4.70 μM) and Mcl-1 (Ki: 0.88 μM) inhibitor.Bcl-2/Mcl-1-IN-2 can be used in cancer research.

TAT-BH4 (Bcl-xL), primarily localized at the mitochondria, inhibits apoptotic cell death. This compound comprises an N-terminal eosin-labeled cysteine and the protein transduction domain of the HIV TAT protein (amino acids 49 to 57), fused to the Bcl-xL BH4 peptide. It serves as a tool for research into diseases characterized by accelerated apoptosis [1].

PROTAC Bcl-xL degrader-2, based on von Hippel-Lindau ligand, is a potent degrader of Bcl-xL (a Bcl-2 family member), demonstrating an IC 50 of 0.6 nM.

Bcl-2-IN-7 is a potent inhibitor of Bcl-2 (b-cell lymphoma-2), which can downregulate the expression of Bcl-2, increase the expression of p53, Bax, caspase-7 mRNA, and induce cell cycle arrest and apoptosis in MCF-7 cells of breast cancer. Bcl2-IN-7 showed good antitumor activity against MCF-7 cells (IC50: 20.17 μM), LoVo cells (IC50: 22.64 μM), HepG2 cells (IC50: 45.57 μM) and A549 cells (IC50: 51.50 μM).

Bcl-2-IN-6 is a potent inhibitor of Bcl-2 (b-cell lymphoma-2) that downregulates Bcl-2 expression and increases the expression of p53, Bax, and caspase-7 mRNA. bcl-2-IN-7 induces cell cycle arrest and apoptosis in breast cancer MCF-7 cells. bcl-2-IN-7 acts on MCF-7 cells ( Bcl2-IN-7 showed good antitumor effects on MCF-7 cells (IC50: 20.91 μM), LoVo cells (IC50: 22.30 μM), HepG2 cells (IC50: 42.29 μM) and A549 cells (IC50: 48.00 μM).

MCL-1/BCL-2-IN-2 is a selective Mcl-1 and Bcl-2 inhibitor with potential antitumor activity for tumor research.

MCL-1/BCL-2-IN-3 is a selective and potent Mcl-1 and Bcl-2 dual inhibitor with IC50s of 5.95 and 4.78 μM, respectiely.

MCL-1/BCL-2-IN-2 (Compound Nap-1) is a potent and selective dual inhibitor of Mcl-1 and Bcl-2 with IC 50 s of 4.45 and 3.18 μM, respectively [1].

Bcl-2-IN-8 is a potent anti-cancer agent. bcl-2-IN-8 exhibits anti-proliferative effects on both drug-sensitive and drug-resistant cancer cells. bcl-2-IN-8 inhibits cell migration in a dose-dependent manner. bcl-2-IN-8 blocks the cell cycle in the G1 phase and induces apoptosis. bcl-2-IN-8 has shown research potential in triple-negative breast cancer. Bcl-2-IN-8 has shown potential for research in triple negative breast cancer.

Bcl-2-IN-11 (compound 6) is a potent and selective inhibitor of Bcl-2 activity, exhibiting an IC50 of 0.9 nM, and demonstrates minimal inhibition against Bcl-xl (IC50 > 1000 nM). This compound is utilized in researching various cancers linked to the overexpression of Bcl-2 family proteins, primarily malignant hematologic conditions such as acute lymphoid leukemia. Importantly, Bcl-2-IN-11 minimizes the risk of toxic side effects, including thrombocytopenia [1], by sparing Bcl-xl.

Bcl-2-IN-2 is a highly potent and selective inhibitor targeting Bcl-2 and Bcl-xL. It displays an IC50 value of 0.034 nM, suggesting its strong inhibitory activity specifically against Bcl-2. Additionally, Bcl-2-IN-2 exhibits an IC50 value of 43 nM against Bcl-xL, demonstrating over 1000-fold selectivity for Bcl-2 compared to Bcl-xL.

Bcl-2/Mcl-1-IN-1 is an inhibitor of Bcl-2 (Ki: 4.53 μM) and Mcl-1 (Ki: 1.19 μM).Bcl-2/Mcl-1-IN-1 can be used in cancer research.

Bcl-xL antagonist 2 is an effective and selective antagonist of Bcl-xL with an IC50 of 91 nM and a Ki of 65 nM. Bcl-xL antagonist 2 induces apoptosis in cancer cells and can be used in studies about chronic lymphocytic leukemia and non-Hodgkin’s lymphoma.

BCL6-IN-3 is a potent BCL6 inhibitor with GI50 of 70 nM in SU-DHL4 cells. BCL6-in-3 regulates cell activation, differentiation, DNA damage and apoptosis, and has antitumor activity.

BCL6 PROTAC 1 is a selective B-cell lymphoma 6 (BCL6) proteolysis targeting chimera (PROTAC) that inhibits the BCL6 cell reporter with an IC50 value of 8.8 µM and significantly degrades BCL6 in diffuse large B-cell lymphoma (DLBCL) cell lines, making it valuable for tumor-related research [1].

CDK2/Bcl2-IN-1 (compound 1) is a saponin-based inhibitor of CDK-2 (IC50=117.6 nM) that exhibits potent cytotoxic effects on cancer cells. Additionally, it inhibits Bcl-2 and promotes apoptosis in A549 lung cancer cells [1].

BCL6-IN-4, a potent inhibitor of B-cell lymphoma 6 (BCL6), exhibits anti-tumor activities with an inhibitory concentration 50 (IC50) value of 97 nM[1].

BCL6-IN-5 is a highly effective inhibitor of BCL6. It exhibits a pIC50 value of 5.82.

BCL6-IN-6 is an inhibitor of Bcl-6 and can be used in studies about diffuse large B-cell lymphoma. BCL6-IN-6 blocks the interaction of Bcl-6 with its corepressors and dose-dependently reactivates Bcl-6 target genes.

BCL6-IN-9 (compound 1) is a potent inhibitor of B-cell lymphoma 6 protein (BCL6) (IC50: 3.9 nM) and can be used to study cancer.

Lisaftoclax (Bcl-2/Bcl-xl inhibitor 1) is an oral dual inhibitor of Bcl-2 and Bcl-xl, with IC50 values of 2 nM and 5.9 nM for Bcl-2 and Bcl-xl, respectively. Lisaftoclax is used to treat chronic lymphocytic leukemia (CLL) by inhibiting the action of the BCL-2 protein, which promotes the death of leukemia cells.

Navitoclax (ABT-263) is a Bcl-2 inhibitor that binds to Bcl-xL, Bcl-2, and Bcl-w proteins (Ki<1 nM) with potent and oral activity. Navitoclax has antitumor activity and induces apoptosis.

Venetoclax (ABT-199) is a Bcl-2 inhibitor (Ki<0.01 nM) with potent, selective, and orally active properties. Venetoclax has a 3-order-of-magnitude lower affinity for Bcl-xL and Bcl-W (Kis=48/245 nM). Venetoclax induces autophagy and apoptosis.

S63845 is a selective MCL-1 inhibitor(Kd: 0.19 nM)

Procyanidin C1 is a natural product, with anti-inflammatory effects, and induces apoptosis.

UMI-77, a specific Mcl-1 inhibitor (Ki: 490 nM), has selectivity over other members of Bcl-2 family.

Gossypol (BL 193) Acetate is a polyphenolic aldehyde that permeates cells and acts as an inhibitor for several dehydrogenase enzymes.

BCL2-IN-1 is a potent Bcl-2 inhibitor (Ki <0.01 nM).

Magnolin reduces the renal oxidative stress, suppresses caspase-3 activity, and increases Bcl-2 expression in vivo and in vitro. Magnolin has anti-inflammatory and antioxidative effects.

Vanillyl Alcohol (3-Methoxy-4-hydroxybenzyl alcohol) possesses anti-angiogenic, anticonvulsive, anti-inflammatory, anti-oxidant, neuroprotective, and anti-nociceptive activities. Vanillyl alcohol can effectively inhibit the cytotoxicity and improved cell viability in 1-methyl-4-phenylpyridinium (MPP+)-induced MN9D dopaminergic cells, it also can attenuate the elevation of reactive oxygen species (ROS) levels, decrease in the Bax/Bcl-2 ratio and poly (ADP-ribose) polymerase proteolysis.

NSC 122393 is a fluorescent dye that inhibits the interaction between Bax and Bcl-X and induces apoptosis in Bcl-X overexpressing breast cancer cells.

TV 3279 is a novel ChE-MAI inhibitor , and the neuroprotective properties depend on their ability to induce the anti-apoptotic proteins PKC, Bcl-2, Bcl-x, and SOD, and to block the nuclear translocation of the pro-apoptotic enzyme glyceraldehyde phosphate dehydrogenase in PC-12 and neuroblastoma cells.

BAD (103-127) (human) acetate is a 25-mer Bad polypeptide from the BAD BH3 domain that antagonizes the effects of Bcl-xl.

Nitroaspirin (NCX 4016) is a nitric oxide donor and a nitro-derivative of Aspirin, which combines with Nitroaspirin to inhibit cyclooxygenase. Nitroaspirin induces significant induction of cell cycle arrest and apoptosis in Cisplatin-resistant human ovarian cancer cells via down-regulation of EGFR/PI3K/STAT3 signaling and modulation of Bcl-2 family proteins. Nitroaspirin has antithrombotic and antiplatelet properties and acts as a direct and irreversible inhibitor of COX-1.