Bax
BAX (BCL2-associated X protein) is a pro-apoptotic member of the BCL-2 family that regulates programmed cell death through mitochondrial apoptosis and functions as a critical determinant of cellular survival following apoptotic stimuli[1][2]. BAX forms heterodimers with anti-apoptotic BCL-2 proteins, and the balance between BAX and BCL-2 influences mitochondrial outer membrane permeabilization (MOMP), cytochrome c release, and activation of the intrinsic apoptotic pathway[2][3][4]. Mechanistically, BAX belongs to the pore-forming executioner subgroup of the BCL-2 family and undergoes activation in response to cellular stress signals, including p53-dependent apoptotic signaling, thereby promoting mitochondrial membrane permeabilization and irreversible cell death commitment[1][3][5]. In disease models, dysregulated BAX activity contributes to the pathophysiology of cancer, neurodegenerative disorders, and other apoptosis-associated conditions, making mitochondrial apoptosis a major target for therapeutic intervention[3][4][6]. Compared with related BCL-2 family isoforms, BAX is distinguished by its direct executioner function in apoptosis, whereas many alternative BCL-2 family isoforms display variable anti-apoptotic or context-dependent activities that remain incompletely characterized[3]. A notable BAX isoform, BaxΔ2, retains pro-apoptotic activity despite N-terminal alterations, highlighting functional diversity within the BAX locus and providing experimental models for studying non-canonical apoptotic mechanisms[7]. For experimental applications, BAX-dependent signaling is widely used to evaluate mitochondrial apoptosis, while therapeutic strategies targeting BCL-2 family interactions, including BH3 mimetics, are actively investigated to modulate BAX-mediated cell death in cancer research[3][6].
References:
- [1]. Brady HJ, et al. Bax. The pro-apoptotic Bcl-2 family member, Bax. Int J Biochem Cell Biol. 1998 Jun;30(6):647-50. [Content Brief]
- [2]. Bax gene information from NCBI.
- [3]. Warren CFA, et al. BCL-2 family isoforms in apoptosis and cancer. Cell Death Dis. 2019 Feb 21;10(3):177. [Content Brief]
- [4]. Vogler M, et al. The BCL2 family: from apoptosis mechanisms to new advances in targeted therapy. Signal Transduct Target Ther. 2025 Mar 21;10(1):91. [Content Brief]
- [5]. Maes ME, et al. BAX to basics: How the BCL2 gene family controls the death of retinal ganglion cells. Prog Retin Eye Res. 2017 Mar;57:1-25. [Content Brief]
- [6]. Huang Y, et al. The adjuvant treatment role of ω-3 fatty acids by regulating gut microbiota positively in the acne vulgaris. J Dermatolog Treat. 2024 Dec;35(1):2299107. [Content Brief]
- [7]. Rabezanahary H, et al. Live virus neutralizing antibodies against pre and post Omicron strains in food and retail workers in Québec, Canada. Heliyon. 2024 May 21;10(10):e31026. [Content Brief]
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Bax Related Products (220)
Related Products (220)
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Antibodies (3)
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Astin B
0 ImagesCat. No.: HY-P3148CAS No.: 151201-76-2Astin B is a orally active and potent cyclic pentapeptide, that can be isolated from Aster tataricus. Astin B has hepatotoxic effects in vitro and in vivo and that hepatic injury was primarily mediated by apoptosis in a mitochondria/caspase-dependent manner. Astin B induces autophagy in L-02 cells, increases LC3-II and decreases p62 expression.
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TKL002
0 ImagesTKL002 is a blood-brain barrier-permeable inhibitor of the CTH/H2S/NF-κB/EMT signaling axis. TKL002 induces G2/M phase cell cycle arrest and apoptosis in glioblastoma cells. TKL002 inhibits the migration and invasion of glioblastoma cells by upregulating E-cadherin and downregulating N-cadherin and vimentin. TKL002 is applicable to relevant research on glioblastoma.
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Topoisomerase I/II-IN-10
0 ImagesCat. No.: HY-189664Topoisomerase I/II-IN-10 is a Topoisomerase I/II inhibitor. Topoisomerase I/II-IN-10 inhibits TrxR1 activity, impairs the thioredoxin antioxidant system, and promotes oxidative stress. Topoisomerase I/II-IN-10 does not intercalate into DNA and does not induce DNA relaxation in the absence of topoisomerase. Topoisomerase I/II-IN-10 induces Apoptosis, increases the intracellular total oxidation state, and increases the Bax/Bcl-2 ratio. Topoisomerase I/II-IN-10 can be used for research on lung cancer.
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COX/5-LO-IN-2
0 ImagesCat. No.: HY-181061COX/5-LO-IN-2 is a COX2, EGFR, COX1, 5-LOX, BRAF and FAK inhibitor with IC50 of 1.22 μM, 2.5 μM, 2.95 μM, 4.65 μM, 7.4 μM, 12.2 μM, respectively. COX/5-LO-IN-2 induces cell growth arrest at G2/M phase. COX/5-LO-IN-2 triggers apoptotic activity by up-regulating proapoptotic proteins p53, Bax, and caspase-7 and down-regulating anti-apoptotic protein Bcl-2. COX/5-LO-IN-2 can be used for the research of breast cancer.
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EGFR-IN-109
0 ImagesCat. No.: HY-162360CAS No.: 3019971-97-9
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CDK1/2/4-IN-1
0 ImagesCat. No.: HY-146253CAS No.: 2414633-49-9CDK1/2/4-IN-1 (compound 3a) is a potent CDK inhibitor with IC50 values of 1.47, 0.78 and 0.87 μM for CDK1, CDK2 and CDK4, respectively. CDK1/2/4-IN-1 arrests cell cycle at G2/M phase and induces apoptosis. CDK1/2/4-IN-1 elevates Bax, caspase-3, P53 levels and decreases Bcl-2 level. CDK1/2/4-IN-1 can be used for cancer research.
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HDAC-IN-91
0 ImagesCat. No.: HY-175021HDAC-IN-91 is a multiple inhibitor of HDAC (IC50 = 134.22 nM for HDAC1, 66.29 nM for HDAC2), carbonic anhydrase (CA) (Ki = 72.03 nM for CA IX, 50.76 nM for XII), and tubulin polymerization ( IC50 = 2.56 μM). HDAC-IN-91 inhibits PARP1 and increases the Bax/Bcl-2 ratio. HDAC-IN-91 blocks the cell cycle at the G2/M phase and induces apoptosis through a mitochondrial apoptosis activation mechanism. HDAC-IN-91 can exert potent cytotoxic activity through tubulin polymerization inhibition. HDAC-IN-91 can be used in breast, colorectal, cervical and lung cancer research.
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Dehydrobruceine B
0 ImagesCat. No.: HY-N10313CAS No.: 53730-90-8Dehydrobruceine B, a quassinoid, can be isolated from Brucea javanica. Dehydrobruceine B shows a synergistic effect with Cisplatin (HY-17394) to induce apoptosis via mitochondrial method. Dehydrobruceine B increases apoptosis-inducing factor (AIF) and Bax expression and suppresses Keap1-Nrf2.
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EGFR/BRAFV600E-IN-6
0 ImagesCat. No.: HY-180154CAS No.: 3120155-78-1EGFR/BRAFV600E-IN-6 (Compound 7c) is a dual EGFR/BRAFV600E inhibitor with IC50 values of 0.12 and 0.05 μM. EGFR/BRAFV600E-IN-6 can activate caspase-3/8/9, unregulate Bax expression and downregulate Bcl-2 levels. EGFR/BRAFV600E-IN-6 can induce apoptosis and shows antioxidant activity. EGFR/BRAFV600E-IN-6 can be used for the research of cancer, such as colon cancer.
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Antiproliferative agent-83
0 ImagesCat. No.: HY-189636Antiproliferative agent-83 is an orally active STAT3 inhibitor (Kd = 5.63 μM) with antiproliferative activity against Huh-7 cells (IC50 = 1.30 μM). Antiproliferative agent-83 inhibits dual phosphorylation of STAT3 at tyrosine and serine residues, blocking nuclear translocation and downstream transcriptional activation. Antiproliferative agent-83 induces apoptosis, ROS accumulation, and mitochondrial depolarization. Antiproliferative agent-83 suppresses tumor growth in a hepatocellular carcinoma xenograft mouse model. Antiproliferative agent-83 can be used for research on hepatocellular carcinoma.
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Multitarget AD-IN-8
0 ImagesCat. No.: HY-189262Multitarget AD-IN-8 is a blood-brain barrier-penetrant, orally active multitarget inhibitor. Multitarget AD-IN-8 inhibits abnormal Tau phosphorylation at Thr181 and Ser396 sites and attenuates NF-κB phosphorylation. Multitarget AD-IN-8 downregulates BACE1 expression to reduce Aβ production, inhibits the Bax/Bcl-2 pathway, and suppresses Caspase-1 activation. Multitarget AD-IN-8 attenuates p38, ERK1/2, and JNK phosphorylation and inhibits Aβ25-35-induced Apoptosis. Multitarget AD-IN-8 exhibits neuroprotective effects against Aβ25-35-induced injury, ameliorates learning and memory deficits in AD mouse models, and alleviates hippocampal neuronal pathological damage. Multitarget AD-IN-8 can be used for research on Alzheimer's disease.
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Aurora kinase-IN-15
0 ImagesCat. No.: HY-184386Aurora kinase-IN-15 is a potent dual Aurora A and Aurora B kinase inhibitor. Aurora kinase-IN-15 has broad-spectrum anticancer activity and low toxicity to normal cells. Aurora kinase-IN-15 induces G2/M phase arrest, apoptosis, and activates the intrinsic apoptotic pathway through upregulation of Caspase 3 and Bax, along with downregulation of Bcl-2. Aurora kinase-IN-15 can be used for the study of breast cancer, hepatocellular carcinoma, colorectal cancer and prostate cancer.
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CHNQD-01522
0 ImagesCat. No.: HY-181675CHNQD-01522 is a microtubule inhibitor targeting the colchicine binding site on β-tubulin. CHNQD-01522 binds to the colchicine binding site on β-tubulin, inhibits microtubule polymerization, and evades P-glycoprotein transport in cancer cells. CHNQD-01522 inhibits proliferation, suppresses tumor cell colony formation, arrests cell cycle in G2/M phases, and induces apoptosis in cancer cells. CHNQD-01522 upregulates of Bax and activation of caspase-9 and caspase-3. CHNQD-01522 shows anti-tumor efficacy in subcutaneous and orthotopic hepatocellular carcinoma xenograft tumor models. CHNQD-01522 can be used for the research of hepatocellular carcinoma.
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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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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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CDL36
0 ImagesCat. No.: HY-187706CAS No.: 951529-42-3CDL36 is a BAX inhibitor with an EC50 of 23.6 µM. CDL36 inhibits pro-apoptotic peptide-induced mitochondrial outer membrane permeabilization (MOMP). CDL36 exerts cytoprotective effects against Doxorubicin (HY-15142A)-induced cell death.
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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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EGFR/HER2-IN-20
0 ImagesCat. No.: HY-184301EGFR/HER2-IN-20 is a dual EGFR/HER2 inhibitor. EGFR/HER2-IN-20 induces G1/S phase cell cycle arrest by downregulating CCND1. EGFR/HER2-IN-20 induces cell apoptosis by upregulating BAX and caspase-3. EGFR/HER2-IN-20 inhibits cancer cell migration. EGFR/HER2-IN-20 can be used in the research of cervical cancer and breast cancer.
