mcl-1/bcl-2-in-1

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.

Mcl1-IN-11 (Compound G) is a selective Mcl-1 inhibitor with Kis of 0.06 μM and 4.2 μM for Mcl-1 and Bcl-2, respectively.

Mcl1-IN-12 has anti-tumor activity.It is a selective Mcl-1 inhibitor, less potent at Bcl-2, with Kis of 0.29 and 3.1 μM, respectively.

IMB-XH1 (Mcl1-IN-2) is a myeloid cell factor 1 (Mcl-1) inhibitor.

Ch282-5, an orally active inhibitor targeting the Bcl-2 protein, promotes mitochondria-dependent apoptosis (Apoptosis) by disrupting mitophagy and the mTOR pathway. It demonstrates antiproliferative effects on colorectal cancer cells, effective both in vitro and in vivo, while also inhibiting metastasis. Further, Ch282-5 augments Oxaliplatin-induced autophagy (Autophagy) by downregulating Mcl-1 protein and raising platelet count, which helps mitigate the adverse effects of Navitoclax.

Mcl-1-IN-20 (Compound 26d) is an Mcl-1 inhibitor displaying Ki values of 0.59 μM for Mcl-1, 6.6 μM for Bcl-xL, and 3.6 μM for Bcl-2. It exhibits significant antiproliferative activity against pancreatic cancer cells and induces apoptosis in BxPC-3 cells. Mcl-1-IN-20 is applicable in pancreatic cancer research.

Mcl-1-IN-16 is an effective macrolide inhibitor of myeloid cell leukemia 1 (Mcl-1) with a Ki of less than 0.08 nM. It demonstrates over 50,000-fold selectivity for Mcl-1 compared to other anti-apoptotic Bcl-2 family members, Bcl-2 and Bcl-xL. Mcl-1-IN-16 activates caspase-3/7, thereby inducing apoptosis. In tumor xenograft mouse models derived from lung cancer, it achieves tumor regression. Mcl-1-IN-16 is useful for research on solid tumors, including non-small cell lung cancer (NSCLC).

Tubulin polymerization-IN-85 (Compound C21) is a microtubule polymerization inhibitor with an IC50 value of 1.59 μM, targeting the colchicine binding site. It exhibits antiproliferative activity against HeLa, HepG2, MCF-7, and A549 cells with IC50 values of 0.08, 0.21, 0.27, and 0.32 μM, respectively, while demonstrating low toxicity to normal renal epithelial 293T cells (IC50 value of 187 μM). Tubulin polymerization-IN-85 induces G2/M phase arrest and triggers apoptosis in cancer cells. It downregulates the expression of Bcl-2, Bcl-xl, Mcl-1, Cyclin B1, cdc25, and cdc2 proteins, and upregulates P53, P21, Bad, and Bax levels. This compound is applicable in cancer research, such as cervical cancer studies.

S65487 (VOB560) is a potent and selective inhibitor of the anti-apoptotic protein Bcl-2, displaying activity not only against the wild-type protein but also against clinically relevant BCL-2 mutations such as G101V and D103Y. S65487 demonstrates poor affinity toward other Bcl-2 family members, including MCL-1, BFL-1, and BCL-XL, which underlines its selectivity profile. S65487 induces apoptosis in cancer cells and exhibits robust anticancer activities in preclinical studies.

Mcl-1 inhibitor 6 is a potent, orally active small molecule that selectively targets the anti-apoptotic protein myeloid cell leukemia 1 (Mcl-1). Mcl-1 inhibitor 6 binds with high affinity, with a dissociation constant (K d) of 0.23 nM, and exhibits binding activity with a K i of 0.02 μM. Mcl-1 inhibitor 6 displays exceptional selectivity over other anti-apoptotic Bcl-2 family proteins, including Bcl-2, Bcl2A1, Bcl-xL, and Bcl-w, all of which display binding constants greater than 10 μM. Notably, Mcl-1 inhibitor 6 demonstrates strong antitumor activity in preclinical models, highlighting its potential as a therapeutic candidate in oncology.

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.

(S)-Sabutoclax ((S)-BI-97C1), an optically pure derivative of apogossypol, serves as a pan-active inhibitor of the antiapoptotic B-cell lymphoma/leukemia-2 (Bcl-2) family proteins. It effectively blocks the binding of BH3 peptides to key proteins in the family, including Bcl-XL, Bcl-2, Mcl-1, and Bfl-1, displaying inhibitory concentration (IC50) values of 0.31, 0.32, 0.20, and 0.62 μM, respectively. Furthermore, (S)-Sabutoclax demonstrates potent efficacy in inhibiting the growth of various cancer cell lines, such as those from human prostate cancer, lung cancer, and lymphoma, with half-maximal effective concentration (EC50) values of 0.13, 0.56, and 0.049 μM, respectively. This compound is utilized in research focusing on apoptosis-based cancer therapies [1].

Mcl-1 inhibitor 17 is an effective inhibitor of the Mcl-1 protein. Mcl-1 is a critical anti-apoptotic member of the Bcl-2 family, frequently overexpressed in various malignancies, where it suppresses apoptosis by sequestering pro-apoptotic proteins such as Bak and Bax. Mcl-1 inhibitor 17 functions by competitively binding to the BH3-binding groove of Mcl-1, thereby releasing pro-apoptotic factors and restoring apoptotic sensitivity in cancer cells. This compound is utilized for research into cancer and other diseases associated with Mcl-1 dysregulation.

Bcl-2/Mcl-1-IN-4 (compound 20) acts as a dual inhibitor targeting Bcl-2 (Ki=0.49 μM) and Mcl-1 (Ki=0.51 μM). This compound effectively suppresses cancer cell proliferation and induces apoptosis in U937 cells. It is utilized in cancer research.

(-)BI97D6 is a broad-spectrum inhibitor of the Bcl-2 protein family, exhibiting inhibitory effects on Mcl-1, Bcl-2, Bcl-xL, and Bcl-w, with IC50 values of 0.025, 0.031, 0.076, and 0.122 μM respectively. This compound stimulates cell death through the mitochondrial apoptosis pathway mediated by Bak and Bax. Additionally, (-)BI97D6s inhibition of Mcl-1 effectively induces apoptosis in acute myeloid leukemia (AML) cells.

Gambogic Acid (Standard) is a reference standard for research and analysis in studies involving Gambogic Acid. Gambogic Acid (Guttic Acid) ( EC50=0.78-1.64 uM) activates caspases. Gambogic Acid competitively suppresses Bcl-XL, Bcl-2, Bcl-W, Bcl-B, Bfl-1 and Mcl-1. The IC50s of Gambogic Acid for Bcl-XL, Bcl-2, Bcl-W, Bcl-B, Bfl-1 and Mcl-1 are 1.47, 1.21, 2.02, 0.66, 1.06 and 0.79 uM, respectively.