bcl-xl-bh3

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

ABT-737 is a BH3 mimetic and an inhibitor of Bcl-2, Bcl-xL, and Bcl-w (EC50=30.3 nM 78.7 nM 197.8 nM). ABT-737 exhibits antitumor activity and anti-aging activity.

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

(S)-Gossypol acetic acid ((S)-(+)-Gossypol acetic acid) is a conformational isomer of Gossypol that acts as a BH3 mimic capable of binding Bcl-xL and Bcl-2 proteins, with the potential to induce apoptosis and inhibit cell growth.

BH3I-1 (BHI1) is a Bcl-2 antagonist.

JY-1-106 is a BH3 α-helix mimetic, inducing apoptosis in a subset of cancer cells (lung cancer, colon cancer and mesothelioma) by disrupting Bcl-xL and Mcl-1 protein-protein interactions with Bak.

BAD (103-127) (human) is a 25-mer peptide obtained from the BH3 domain of BAD. It effectively counteracts the activity of Bcl-xL. Notably, BAD (103-127) (human) exhibits an approximately 800-fold greater binding affinity for Bcl-xL compared to the 16-mer peptide.

BH3 hydrochloride, a peptide that crosses the blood-brain barrier, induces apoptosis either through direct activation of the pro-apoptotic proteins Bax Bak or by inhibiting anti-apoptotic Bcl-2 proteins (Bcl-2, Bcl-XL, Bcl-w, Mcl-1, and A-1) through their BH3 domain [1][2].

BAD (103-127) (human), a FAM-labeled 25-mer peptide derived from the BH3 domain of human BAD, antagonizes the function of Bcl-xL [1].

(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].

GQN-B37-E is an effective selective binder and inhibitor of MCL-1. It binds to the BH3-binding domain of MCL-1. GQN-B37-E demonstrates binding affinity for MCL-1 within the sub-micromolar range (Ki= 0.6 μM), yet shows negligible binding to BCL-2 or BCL-XL.

This peptide, generated from the BH3 domain of Bak (Flu-BakBH3), has been shown to have high-affinity binding to a surface pocket of the Bcl-XL protein that is required for its death antagonist function.