bcl

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.

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

MCL-1 BCL-2-IN-2 (Compound Nap-1) is a potent and selective dual inhibitor of Mcl-1 and Bcl-2, with IC50 values of 4.45 μM and 3.18 μM, respectively [1].

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

MCL-1 BCL-2-IN-3 is a selective and potent dual inhibitor of Mcl-1 and Bcl-2, with IC50 values of 5.95 and 4.78 μM, respectively.

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

Bcl-2-IN-22 (compound 1), a gold (I) NHC complex, exhibits anticancer activity. It induces cell death (apoptosis) via the mitochondrial pathway with an IC50 value of 0.014 μM. Additionally, Bcl-2-IN-22 targets members of the BCL-2 family, promoting apoptosis and sensitization in multidrug-resistant leukemia cells overexpressing BCL-2.

BCL-XL-IN-1 (Compound 11) is a selective inhibitor of BCL-XL, exhibiting a Ki of less than 0.01 nM against BCL-XLTR-FERT. It is primarily used in cancer research.

Bcl-2-IN-3 (Compound 10) is an inhibitor of Bcl-2, utilized in cancer research.

BCL-XL-IN-3 (Compound 11) is an inhibitor of BCL-XL, with a Ki of less than 0.01 nM. It suppresses cell viability in both normal Molt-4 cells and digitonin-permeabilized Molt-4 cells, with EC50 values of 77.8 nM and 0.07 nM, respectively. BCL-XL-IN-3 can be utilized as an ADC toxin for synthesizing Clezutoclax.

Bcl-2-IN-2 is a highly potent and selective inhibitor targeting Bcl-2 and Bcl-xL, displaying an IC50 value of 0.034 nM against Bcl-2 and 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), and can be used in cancer research.

Bcl-2 Mcl-1-IN-2 is an inhibitor of Bcl-2 [Ki: 4.70 μM] and Mcl-1 [Ki: 0.88 μM], suitable for use in cancer research.

Bcl-2 Mcl-1-IN-3 is a Bcl-2 Mcl-1 inhibitor, targeting Mcl-1 (Ki: 0.14 μM) and Bcl-2 (Ki: 0.23 μM), suitable for cancer research.

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).

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

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

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

PROTAC Bcl-xL ligand-1 serves as a ligand targeting Bcl-xL, essential in synthesizing PROTACs [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-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-IN-5 is a potent BCL-2 inhibitor with 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. It also suppresses cell growth in Bcl 2-G101V knock-in [RS4;11] cells, with IC50 values of 0.2 nM and 0.44 nM.