2. Signaling Pathways
  3. Apoptosis
  4. Bcl-2 Family
  5. Bcl-B Isoform

Bcl-B

Bcl-B (BCL2L10) is an atypical anti-apoptotic member of the BCL-2 family that primarily regulates mitochondrial apoptosis through selective interactions with pro-apoptotic proteins and intracellular survival pathways[1][2]. Mechanistically, Bcl-B localizes mainly to the outer mitochondrial membrane, where it suppresses apoptosis by binding Bax, limiting mitochondrial outer membrane permeabilization and downstream caspase activation[1][3]. Beyond canonical apoptosis control, Bcl-B also participates in autophagy, mitophagy, and Ca2+ signaling regulation through interactions with Beclin 1, Parkin, and the inositol 1,4,5-trisphosphate receptor (IP3R), linking mitochondrial homeostasis to cell survival programs[1]. In disease models, dysregulated BCL2L10 expression has been reported in multiple malignancies, including melanoma, breast cancer, hepatocellular carcinoma, and hematologic cancers, where its biological role appears highly context dependent[1][4]. In melanoma, BCL2L10 functions as a pro-survival factor that promotes resistance to cytotoxic agents and BCL-2 family-targeted therapies, supporting tumor cell survival under therapeutic stress[4]. Compared with related anti-apoptotic isoforms such as BCL-2, BCL-xL, and MCL-1, Bcl-B exhibits a more restricted interaction profile, selectively binding Bax while showing limited interaction with several other BCL-2 family proteins, highlighting a distinct regulatory mechanism within the family[1]. For experimental applications, the unique interaction network, context-dependent oncogenic activity, and potential sensitivity to proteasomal regulation have positioned Bcl-B as a candidate target for studies investigating apoptosis resistance and therapeutic response in cancer models[1][4].

Bcl-B Related Products (5):

Cat. No. Product Name Effect Purity
  • HY-50907
    ABT-737
    		Inhibitor 99.64%
    ABT-737, a BH3 mimetic, is a potent Bcl-2, Bcl-xL and Bcl-w inhibitor with EC50s of 30.3 nM, 78.7 nM, and 197.8 nM, respectively. ABT-737 induces the disruption of the BCL-2/BAX complex and BAK-dependent but BIM-independent activation of the intrinsic apoptotic pathway. ABT-737 induces autophagy and has the potential for acute myeloid leukemia (AML) research.
  • HY-10969
    Obatoclax Mesylate
    		Inhibitor 99.85%
    Obatoclax Mesylate (GX15-070 Mesylate), a BH3 mimetic, is a pan-BCL-2 family proteins inhibitor with a Ki of 220 nM for BCL-2. Obatoclax Mesylate induces autophagy-dependent cell death and targets cyclin D1 for proteasomal degradation. Obatoclax Mesylate has anti-cancer and broad-spectrum antiparasitic activity.
  • HY-N0087
    Gambogic Acid
    		Inhibitor 98.34%
    Gambogic Acid (Beta-Guttiferrin) is derived from the gamboges resin of the tree Garcinia hanburyi. Gambogic Acid (Beta-Guttiferrin) 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.
  • HY-10969A
    Obatoclax
    		Inhibitor ≥99.0%
    Obatoclax (GX15-070), a BH3 mimetic, is a pan-BCL-2 family proteins inhibitor with a Ki of 220 nM for BCL-2. Obatoclax induces autophagy-dependent cell death and targets cyclin D1 for proteasomal degradation. Obatoclax has anti-cancer and broad-spectrum antiparasitic activity.
  • HY-122275
    A-371191
    		Antagonist
    A-371191 is a selective Bcl-XL antagonist with a Ki <0.5 μM, and also acts as a mitochondria-targeting agent and chemosensitizer. A-371191 restores the sensitivity of cancer cells overexpressing Bcl-XL to Cisplatin (HY-17394) and Doxorubicin (HY-15142A). A-371191 reduces tumor volume in mice with intraperitoneal tumors. A-371191 can be used in the research of acute myeloid leukemia.