Bcl-2
Bcl-2 (B-cell lymphoma 2) is a central anti-apoptotic regulator that preserves mitochondrial integrity by preventing mitochondrial outer membrane permeabilization (MOMP), a critical checkpoint controlling cytochrome c release and caspase activation during intrinsic apoptosis[1][2]. Mechanistically, Bcl-2 functions through direct interactions with pro-apoptotic BCL-2 family proteins, including Bax and Bak, thereby suppressing their oligomerization and limiting mitochondrial membrane disruption[3][4]. The protein also integrates signals transmitted by BH3-only proteins, which regulate the balance between cell survival and programmed cell death under physiological and pathological stress conditions[3][5]. Dysregulated Bcl-2 expression contributes to apoptosis resistance in multiple malignancies and supports tumor cell survival by maintaining mitochondrial homeostasis despite cellular stress[6][7]. In disease models, the anti-apoptotic activity of Bcl-2 is closely linked to mitochondrial apoptosis pathways that represent major therapeutic targets in hematologic and solid cancers[6][8]. Compared with related anti-apoptotic isoforms such as Mcl-1 and Bcl-B, Bcl-2 displays broader interactions with both Bax and Bak, whereas Mcl-1 and Bcl-B show preferential regulation of Bak- and Bax-dependent apoptotic pathways, respectively[4]. For experimental applications, BH3-mimetic inhibitors disrupt the interaction between Bcl-2 and pro-apoptotic partners, thereby restoring mitochondrial apoptosis and providing a widely used strategy for mechanistic studies and targeted cancer research[7][8].
References:
- [1]. Harris MH, et al. The role of the Bcl-2 family in the regulation of outer mitochondrial membrane permeability. Cell Death Differ. 2000;7:1182-1191.
- [2]. Breckenridge DG, et al. Regulation of mitochondrial membrane permeabilization by BCL-2 family proteins and caspases. Curr Opin Cell Biol. 2004;16(6):647-652.
- [3]. Kale J, et al. BCL-2 family proteins: changing partners in the dance towards death. Cell Death Differ. 2018;25:65-80.
- [4]. Zhai D, et al. Differential regulation of Bax and Bak by anti-apoptotic Bcl-2 family proteins Bcl-B and Mcl-1. J Biol Chem. 2008 Apr 11;283(15):9580-6. [Content Brief]
- [5]. Lomonosova E, et al. BH3-only proteins in apoptosis and beyond: an overview. Oncogene. 2008 Dec;27 Suppl 1(Suppl 1):S2-19. [Content Brief]
- [6]. Danial NN. BCL-2 family proteins: critical checkpoints of apoptotic cell death. Clin Cancer Res. 2007;13(24):7254-7263.
- [7]. Akl H, et al. A dual role for the anti-apoptotic Bcl-2 protein in cancer: Mitochondria versus endoplasmic reticulum. Biochim Biophys Acta. 2014;1843(10):2240-2252.
- [8]. Kang MH, et al. Bcl-2 inhibitors: targeting mitochondrial apoptotic pathways in cancer therapy. Clin Cancer Res. 2009 Feb 15;15(4):1126-32. [Content Brief]
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Bcl-2 Related Products (328)
Related Products (328)
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Antibodies (6)
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EGFR-IN-201
0 ImagesCat. No.: HY-181659CAS No.: 3103654-99-2EGFR-IN-201 is a potent EGFR inhibitor, with an IC50 of 0.091 μM against wild-type EGFR; for mutant EGFR variants, the IC50 values of EGFRT790M, EGFRL858R and EGFRC797S are 0.147 μM, 0.221 μM and 0.703 μM, respectively. EGFR-IN-201 inhibits EGFR downstream signaling proteins AKT1 (IC50 = 0.225 μg/mL) and ERK1 (IC50 = 0.705 μg/mL). EGFR-IN-201 induces G0/G1 cell cycle arrest, apoptosis and low-level necrosis in cancer cells. EGFR-IN-201 is applicable to research on cancers such as colon cancer.
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EGFR-IN-134
0 ImagesCat. No.: HY-168623EGFR-IN-134 (compound 3f), a triazolo[3,4-a]isoquinoline derivative, is a potent EGFR inhibitor with an IC50 of 0.023 µM. EGFR-IN-134 induces apoptosis and necrosis. EGFR-IN-134 initiates cell cycle arrest at the G2/M and pre-G1 phases, downregulates anti-apoptotic protein Bcl2 and upregulates pro-apoptotic proteins: p53, Bax, and caspases 3, 8, and 9. EGFR-IN-134 shows antiproliferative and anticancer activity.
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Bcl-2-IN-26
0 ImagesCat. No.: HY-184443CAS No.: 3119834-80-6Bcl-2-IN-26 is an inhibitor targeting β-tubulin and BCL-2. Bcl-2-IN-26 disrupts the intracellular microtubule network and interferes with cell mitosis, inducing G2/M phase cell cycle arrest. Bcl-2-IN-26 suppresses antiapoptotic BCL-2 function via p53 upregulation, thereby triggering mitochondrial dysfunction, elevated ROS production and robust tumor cell apoptosis. Bcl-2-IN-26 can be used in lung cancer research.
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Topoisomerase I-IN-25
0 ImagesCat. No.: HY-189630Topoisomerase I-IN-25 is a moderate inhibitor of Topoisomerase I-mediated DNA relaxation. Topoisomerase I-IN-25 inhibits the cAMP-PKA-CREB and PI3K-AKT-mTOR signaling pathways. Topoisomerase I-IN-25 downregulates Bcl-2, upregulates Bax, and induces Apoptosis, G2/M phase arrest, mitochondrial dysfunction, and reactive oxygen species accumulation. Topoisomerase I-IN-25 exhibits anticancer activity against hepatocellular carcinoma. Topoisomerase I-IN-25 can be used for research on hepatocellular carcinoma.
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Isomeldenin
0 ImagesCat. No.: HY-N22057CAS No.: 186892-52-4Isomeldenin is a natural product derived from the leaves of Azadirachta indica. Isomeldenin possesses antifungal activity and inhibits pustule formation in Puccinia arachidis. Isomeldenin exhibits antitumor activity, showing cytotoxic activity against SK-OV-3, MCF-7, and 3SKBr cells, and also decreases Bax and increases Bcl2 expression. Isomeldenin can be used in research related to fungal infections and has potential for research related to coronavirus infection.
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PZ15227
0 ImagesCat. No.: HY-152179CAS No.: 2143464-25-7PZ15227 is a potent and selective Bcl-XL PROTAC degrader with a DC50 of 46 nM, and its Ki values for Bcl-XL, Bcl-2 and Bcl-w are 1.90 nM, 3.52 nM and >1 mM, respectively. PZ15227 recruits Bcl-XL to CRBN, induces polyubiquitination of Bcl-XL and promotes its proteasome-dependent degradation, thereby selectively killing senescent cells that rely on Bcl-XL for survival without causing severe thrombocytopenia. PZ15227 can be used for research related to age-related diseases, aging and renal cancer.
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YC137
0 ImagesCat. No.: HY-123244CAS No.: 810659-53-1YC137 is a potent Bcl-2 antagonist with Kis of 1.3 μM and >100 μM for Bcl-2 and Bcl-xL when assayed in Bis-Tris buffer, respectively. YC137 inhibits the binding of the Bid BH3 peptide to Bcl-2, thus disrupting an interaction essential for the antiapoptotic activity of Bcl-2. YC137 selectively induces apoptosis of Bcl-2-dependent cells. YC137 has the potential for breast cancer research.
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STAT3-IN-51
0 ImagesCat. No.: HY-180245STAT3-IN-51 is a STAT3 inhibitor that directly binds to the STAT3 SH2 domain. STAT3-IN-51 induces apoptosis, ferroptosis, and immunogenic cell death (ICD) to potentiate anti-tumor immunity. STAT3-IN-51 inhibits STAT3 activation (phosphorylation, p-STAT3) and its downstream signaling. STAT3-IN-51 induces ROS generation, decreases Bcl-2 expression, disruptes mitochondrial function, suppresses GPX4 activity, and promotes lipid peroxidation. STAT3-IN-51 can be used for the study of colorectal carcinoma, breast adenocarcinoma, non-small cell lung cancer (NSCLC) and Cisplatin (HY-17394)-resistant pulmonary adenocarcinoma.
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CDC25A/NF-κB-IN-1
0 ImagesCat. No.: HY-184446CDC25A/NF-κB-IN-1 is an effective dual-target inhibitor of CDC25A and NF-κB, and is a prodrug of Pt(IV). CDC25A/NF-κB-IN-1 has anticancer activity and low cytotoxicity to normal cells. CDC25A/NF-κB-IN-1 can trigger a variety of anticancer mechanisms, including S phase cell cycle arrest, mitochondrial endogenous apoptosis, endoplasmic reticulum stress, autophagy-dependent ferroptosis. CDC25A/NF-κB-IN-1 has good safety and can be used for ovarian cancer research.
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Mito-fisetin mF7
0 ImagesCat. No.: HY-185559CAS No.: 3106880-06-9Mito-fisetin mF7 is a lipophilic derivative of Fisetin (HY-N0182). Mito-fisetin mF7 interacts with AKT and Bcl-2, limiting their stability and functionality. Mito-fisetin mF7 stimulates impairs mitochondrial function and reduces metabolic activity of cancer cells. Mito-fisetin mF7 can be used for the research of ER-positive breast cancer.
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NSC 850745
0 ImagesCat. No.: HY-175848NSC 850745 is a selective and potent c-Met/STAT3 inhibitor with IC50 values of 210 and 670 nM. NSC 850745 can inhibit cell proliferation, induce G2/M phase arrest and induce apoptosis. NSC 850745 can downregulate AKT-1, VEGF and Bcl-2 expression and upregulate p53, Bax and caspase expression. NSC 850745 can be used for the research of cancer, such as leukemia and colon cancer.
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Topoisomerase I-IN-23
0 ImagesCat. No.: HY-187459Topoisomerase I-IN-23 is a topoisomerase I inhibitor with anticancer activity. Topoisomerase I-IN-23 competitively binds to the hydrophobic pocket at the Topo I-DNA interface, stabilizes the covalent DNA-Topo I complex, downregulates Topo I protein expression in a concentration-dependent manner, induces S-phase cell cycle arrest in tumor cells, regulates the expression of apoptosis-related proteins Bax, Bcl-2 and cleaved caspase-3 to trigger apoptosis, and inhibits the migration and invasion of tumor cells. Topoisomerase I-IN-23 exhibits in vivo antitumor efficacy in xenograft models. Topoisomerase I-IN-23 can be used in research related to colorectal cancer, lung cancer and hepatocellular carcinoma.
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Desethylamiodarone hydrochloride (Standard)
0 ImagesCat. No.: HY-130353RCAS No.: 96027-74-6Synonyms: N-Desethylamiodarone hydrochloride (Standard); LB 33020 hydrochloride (Standard)Desethylamiodarone hydrochloride (Standard) (N-Desethylamiodarone hydrochloride (Standard); LB 33020 hydrochloride (Standard)) is the analytical standard of Desethylamiodarone hydrochloride (HY-130353). This product is intended for research and analytical applications. Desethylamiodarone hydrochloride (N-Desethylamiodarone hydrochloride; LB 33020 hydrochloride) is the major active metabolite of Amiodarone (HY-14187) generated via CYP3A4 metabolism. Desethylamiodarone hydrochloride downregulates p‑Akt, p‑Bad and Bcl‑2, upregulates Bax, promotes mitochondrial release of cytochrome c, activates caspase‑3 and cleaves PARP‑1, thereby inducing cell cycle arrest and apoptosis. Desethylamiodarone hydrochloride can be used in cervical cancer-related research.
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EGFR-IN-170
0 ImagesCat. No.: HY-175588EGFR-IN-170 (Compound 5c) is an EGFR inhibitor with an IC50 of 5.17 μM. EGFR-IN-170 induces apoptosis by inhibiting Bcl2 expression and activating Bax expression with a significantly increased ratio of Bax/Bcl2. EGFR-IN-170 has potent anticancer activity and inhibits the cell growth of resistant lung cancer cells.
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MAPK-IN-5
0 ImagesCat. No.: HY-175175CAS No.: 2579683-39-7MAPK-IN-5 is a potent MAPK inhibitor with an IC50 of 1.35 μM against HeLa cells. MAPK-IN-5 inhibits HeLa cell proliferation by inducing ROS-mediated DNA damage and mitochondrial apoptosis via the MAPK pathway. MAPK-IN-5 significantly inhibits colony formation, reduces the number of live cells, suppresses cell migration, and causes cell cycle arrest in the G2/M phase in HeLa cells. MAPK-IN-5 can be used for the study of cervical cancer.
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Anticancer agent 306
0 ImagesCat. No.: HY-181769CAS No.: 3043892-01-6Anticancer agent 306 is a spiro tetramic acid derivative and a inhibitor of MMP1, MMP7 and PLK1. Anticancer agent 306 exerts antiproliferative activity against H1299, RKO and MCF-7 cells with IC50 values of 19.25 μM, 3.29 μM and 102.36 μM, respectively. Anticancer agent 306 can up-regulate p21 protein and down-regulate CCND1 and CCNB1 proteins to induce cell cycle arrest, regulate the expression of Bcl-2 and Bax to induce cell apoptosis. Anticancer agent 306 can down-regulate MMP1 and MMP7 proteins to inhibit tumor invasion and metastasis. Anticancer agent 306 can be used for the research of lung cancer, colorectal cancer, breast cancer.
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CSN5-IN-3
0 ImagesCat. No.: HY-181795CSN5-IN-3 (Compound 30) is a CSN5 inhibitor with an IC50 of 0.58 μM. CSN5-IN-3 inhibits the enzymatic activity of CSN5, leading to increased accumulation of NEDD8-Cul1 and promoting the degradation of PD-L1. CSN5-IN-3 downregulates Bcl-2, and upregulates P53 and Cleaved caspase-3. CSN5-IN-3 exhibits anticancer activity against triple-negative breast cancer.
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Topo I/II-IN-2
0 ImagesCat. No.: HY-170912Topo I/II-IN-2 (Compound 3g) is an inhibitor of Topo I and Topo II. Topo I/II-IN-2 inhibits NCI-H446 cells and NCI-H1048 cells with IC50s of 1.30 μM and 1.42 μM, respectively. Topo I/II-IN-2 induces mitochondrial Apoptosis, mitochondrial dysfunction and activity generation. Topo I/II-IN-2 inhibits the PI3K/Akt/mTOR pathway. Topo I/II-IN-2 prevents SCLC (small cell lung cancer) cell proliferation, invasion, and migration in vitro. .
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Tubulin polymerization-IN-85
0 ImagesCat. No.: HY-180190Tubulin polymerization-IN-85 (Compound C21) is a tubulin polymerization inhibitor (IC50 = 1.59 μM) targeting the colchicine binding site. Tubulin polymerization-IN-85 can cause cancer cells G2/M phase arrest and induce apoptosis. Tubulin polymerization-IN-85 downregulates the expression of Bcl-2, Bcl-xl, Mcl-1, Cyclin B1, cdc25, cdc2 protein and upregulates P53, P21, Bad and Bax levels. Tubulin polymerization-IN-85 can be used for the research of cancer, such as cervical cancer.
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Lisaftoclax-d8
0 ImagesCat. No.: HY-129179SSynonyms: APG-2575-d8; Bcl-2/Bcl-xl inhibitor 1-d8Lisaftoclax-d8 is the deuterated-labeled Lisaftoclax (HY-129179). Lisaftoclax is an orally active, selective BCL-2 inhibitor with a Ki of < 0.1 nM against human BCL-2. Lisaftoclax selectively binds to BCL-2, disrupts the BCL-2:BIM complex, and antagonizes the antiapoptotic function of BCL-2. Lisaftoclax induces BAX/BAK-dependent, caspase-mediated apoptosis, upregulates the pro-death proteins BIM and Noxa, and downregulates mitochondrial respiratory function and ATP production. Lisaftoclax can be used in the research of hematological malignancies including chronic lymphocytic leukemia, multiple myeloma, and diffuse large B-cell lymphoma.
