Bcl-xL
Bcl-xL, encoded by BCL2L1, is a major anti-apoptotic member of the BCL-2 family that regulates mitochondrial apoptosis through interactions with pro-apoptotic proteins and preservation of mitochondrial integrity[1][2]. Mechanistically, Bcl-xL suppresses mitochondrial outer membrane permeabilization, limits BAX/BAK activation, and modulates cellular bioenergetics, calcium signaling, and autophagy, linking survival pathways with metabolic adaptation under cellular stress[1][3]. Beyond canonical apoptosis control, Bcl-xL interacts with Beclin-1 and intracellular calcium regulators, including IP3 receptors and VDAC1, thereby influencing autophagy, endoplasmic reticulum-mitochondrial communication, and stress responses[1][4]. In disease models, elevated Bcl-xL expression promotes tumor cell survival, therapeutic resistance, angiogenesis, and metastatic progression across hematologic malignancies and solid tumors, including melanoma and breast cancer[1][5]. Compared with related BCL2L1 splice isoforms, Bcl-xL functions predominantly as a pro-survival protein, whereas the alternatively spliced Bcl-xS isoform exhibits pro-apoptotic activity, highlighting the biological significance of isoform-specific regulation in apoptosis research[2][6]. For experimental applications, Bcl-xL is a validated target of BH3 mimetics and other apoptosis-directed strategies, and its inhibition is widely used to investigate mitochondrial apoptotic priming, drug resistance mechanisms, and cancer cell dependency on anti-apoptotic signaling networks[1][7].
References:
- [1]. Silva JPN, et al. BCL-2 and BCL-xL in Cancer: Regulation, Function, and Therapeutic Targeting. Int J Mol Sci. 2026;27(2):1123.
- [2]. Warren CFA, et al. BCL-2 family isoforms in apoptosis and cancer. Cell Death Dis. 2019 Feb 21;10(3):177. [Content Brief]
- [3]. Li M, et al. Bcl-XL: A multifunctional anti-apoptotic protein. Pharmacol Res. 2020;151:104547.
- [4]. Bcl-xL gene information from NCBI.
- [5]. Kim TJ, et al. Risk of Second Primary Malignancies among Patients with Early Gastric Cancer Exposed to Recurrent Computed Tomography Scans. Cancers (Basel). 2021 Mar 7;13(5):1144. [Content Brief]
- [6]. Chen W, et al. Alternative splicing of BCL-X and implications for treating hematological malignancies. Oncol Lett. 2021;22(4):670. [Content Brief]
- [7]. Campbell KJ, et al. Targeting BCL-2 regulated apoptosis in cancer. Open Biol. 2018;8(5):180002. [Content Brief]
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Bcl-xL Related Products (121)
Related Products (121)
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Antibodies (1)
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Venetoclax
0 ImagesSynonyms: ABT-199; GDC-0199; RG7601
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Sorafenib
0 ImagesSynonyms: Bay 43-9006Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.
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Navitoclax
0 ImagesSynonyms: ABT-263Navitoclax (ABT-263) is a potent and orally active Bcl-2 family protein inhibitor that binds to multiple anti-apoptotic Bcl-2 family proteins, such as Bcl-xL, Bcl-2 and Bcl-w, with a Ki of less than 1 nM.
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ABT-737
0 ImagesABT-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.
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ARV-825
0 ImagesARV-825 is a BET protein PROTAC degrader that recruits cereblon, and it targets BRD2, BRD3, and BRD4 for degradation via the ubiquitin-proteasome pathway. ARV-825 downregulates c-MYC, PLK1, MYCN, CDK4/6, JAK2, pSTAT3/5, PIM1, and Bcl-xL, upregulates p21 and p27, and modulates H3K27Ac-mediated transcription, the G2/M checkpoint, the Wnt/β-catenin pathway, and amino acid transport pathways. ARV-825 induces G1 phase cell cycle arrest, caspase 3/PARP-mediated apoptosis, DNA damage, and reactive oxygen species (ROS) production, reduces mitochondrial respiration, and simultaneously inhibits cell proliferation, clonogenic growth, and cell migration. ARV-825 is used in research on gastric cancer, leukemia, neuroblastoma, and cholangiocarcinoma.
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Sorafenib tosylate
0 ImagesSynonyms: Bay 43-9006 tosylateSorafenib (Bay 43-9006) tosylate is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib tosylate induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib tosylate inhibits tumor growth and metastasis in mouse and rat models. Sorafenib tosylate can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.
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Obatoclax Mesylate
0 ImagesSynonyms: GX15-070 MesylateObatoclax 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.
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Dihydrocapsaicin
0 ImagesDihydrocapsaicin, a capsaicin, is a potent and selective TRPV1 (transient receptor potential vanilloid channel 1) agonist. Dihydrocapsaicin reduces AIF, Bax, and Caspase-3 expressions, and increased Bcl-2, Bcl-xL and p-Akt levels. Dihydrocapsaicin enhances the hypothermia-induced neuroprotection following ischemic stroke via PI3K/Akt regulation in rat.
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Sorafenib-d3
0 ImagesSynonyms: Donafenib; Bay 43-9006-d3Sorafenib-d3 (Donafenib) is the deuterated-labeled Sorafenib (HY-10201). Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.
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AZD4320
0 ImagesAZD4320 is a novel BH3-mimicking dual BCL2/BCLxL inhibitor with IC50s of 26 nM, 17 nM, and 170 nM for KPUM-MS3, KPUM-UH1, and STR-428 cells, respectively.
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Lisaftoclax
0 ImagesSynonyms: APG-2575; Bcl-2/Bcl-xl inhibitor 1Lisaftoclax 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.
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Gossypol (acetic acid)
0 ImagesSynonyms: (±)-Gossypol-acetic acid; BL-193 (acetic acid)
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N-Hydroxyphthalimide
0 ImagesN-Hydroxyphthalimide is a blocking agent and catalyst. N-Hydroxyphthalimide promotes oxidation reactions by generating PINO free radicals and activating hydrogen atom transfer processes. N-Hydroxyphthalimide reduces the expression of anti-apoptotic proteins Survivin and Bcl-xL and activates caspase 9 and caspase 3. N-Hydroxyphthalimide induces Apoptosis. N-Hydroxyphthalimide inhibits the phosphorylation of mTOR (Ser2448, Ser2481) and Akt (Ser473). N-Hydroxyphthalimide has anticancer effects against breast and colon cancer.
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Ganoderma lucidum polysaccharide
0 ImagesCat. No.: HY-159059Ganoderma Lucidum/Reishi Extract is a Ganoderma lucidum extract. Ganoderma Lucidum/Reishi Extract reduces the expression of c-Myc, BCL-2, BCL-XL, TERT, PDGFB, eIF4G, Survivin, β-catenin, and eIF4E. Ganoderma Lucidum/Reishi Extract downregulates the gene expression of MMP-9. Ganoderma Lucidum/Reishi Extract upregulates the expression of IL8. Ganoderma Lucidum/Reishi Extract is applicable to the research of inflammatory breast cancer. Ganoderma Lucidum is used in the research of various diseases, such as allergy, arthritis, hypertension, neurasthenia, inflammation, and cancer.
