Date published: 2026-4-23

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Bax channel blocker

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Application:
Bax channel blocker is a cell-permeable dibromocarbazolo-piperazinyl derivative that displays anti-apoptotic properties
Purity:
≥95%
Molecular Weight:
695.3
Molecular Formula:
C19H21Br2N3O•2CF3CO2H
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.
* Refer to Certificate of Analysis for lot specific data.

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Bax Channel Blocker, a cell-permeable dibromocarbazolo-piperazinyl derivative, exhibits potent anti-apoptotic characteristics primarily through its inhibition of the Bax channel-forming activity. This compound is adept at preventing the release of cytochrome c from mitochondria within HeLa cells, a process typically initiated by Bid, a pro-apoptotic member of the Bcl-2 family. Its mechanism of action involves the direct blockade of the Bax protein′s ability to integrate into mitochondrial membranes and form channels, an essential step in the intrinsic pathway of apoptosis. This action not only highlights its potential utility in dissecting the molecular pathways of cell death but also emphasizes its significance in research areas focused on understanding the intricate balance between cell survival and apoptosis. By effectively modulating the Bax-mediated apoptotic pathway, Bax Channel Blocker serves as a critical tool in cellular and molecular biology research, offering insights into the regulation of apoptosis and its implications in the maintenance of cellular homeostasis.


Bax channel blocker References

  1. Azoxystrobin Induces Apoptosis of Human Esophageal Squamous Cell Carcinoma KYSE-150 Cells through Triggering of the Mitochondrial Pathway.  |  Shi, XK., et al. 2017. Front Pharmacol. 8: 277. PMID: 28567017
  2. Feedback activation of AMPK-mediated autophagy acceleration is a key resistance mechanism against SCD1 inhibitor-induced cell growth inhibition.  |  Ono, A., et al. 2017. PLoS One. 12: e0181243. PMID: 28704514
  3. Attribution of Bax and mitochondrial permeability transition pore on cantharidin-induced apoptosis of Sf9 cells.  |  Cui, G., et al. 2017. Pestic Biochem Physiol. 142: 91-101. PMID: 29107253
  4. Activation of the apoptotic pathway during prolonged prometaphase blocks daughter cell proliferation.  |  Uetake, Y. and Sluder, G. 2018. Mol Biol Cell. 29: 2632-2643. PMID: 30133342
  5. Chemical proteasome inhibition as a novel animal model of inner retinal degeneration in rats.  |  Kageyama, M., et al. 2019. PLoS One. 14: e0217945. PMID: 31150519
  6. Optogenetic perturbation of the biochemical pathways that control cell behavior.  |  Haar, LL., et al. 2019. Methods Enzymol. 622: 309-328. PMID: 31155059
  7. Computational Cancer Cell Models to Guide Precision Breast Cancer Medicine.  |  Cheng, L., et al. 2020. Genes (Basel). 11: PMID: 32121160
  8. Staurosporine and venetoclax induce the caspase-dependent proteolysis of MEF2D-fusion proteins and apoptosis in MEF2D-fusion (+) ALL cells.  |  Tange, N., et al. 2020. Biomed Pharmacother. 128: 110330. PMID: 32504922
  9. Aspirin Induced Glioma Apoptosis through Noxa Upregulation.  |  Chang, CY., et al. 2020. Int J Mol Sci. 21: PMID: 32545774
  10. Ipriflavone Suppresses Growth of Esophageal Squamous Cell Carcinoma Through Inhibiting mTOR In Vitro and In Vivo.  |  Shi, X., et al. 2021. Front Oncol. 11: 648809. PMID: 34178634
  11. pNiPAM-Nanoparticle-Based Antiapoptotic Approach for Pro-Regenerative Capacity of Skeletal Myogenic Cells.  |  Nowaczyk, M., et al. 2021. Nanomaterials (Basel). 11: PMID: 34684935
  12. In Vitro Study of Cytotoxic Mechanisms of Alkylphospholipids and Alkyltriazoles in Acute Lymphoblastic Leukemia Models.  |  Jesus, LOP., et al. 2022. Molecules. 27: PMID: 36500726
  13. Chemical Activation and Mechanical Sensitization of Piezo1 Enhance TRAIL-Mediated Apoptosis in Glioblastoma Cells.  |  Knoblauch, SV., et al. 2023. ACS Omega. 8: 16975-16986. PMID: 37214705

Ordering Information

Product NameCatalog #UNITPriceQtyFAVORITES

Bax channel blocker, 5 mg

sc-221285
5 mg
$152.00