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Submit ReviewProbucol is an ABCA1 (CERP) inhibitor. Inhibits cholesterol efflux from J774 macrophages expressing ABCA1 by up to 80%. Inhibits atherogenesis in genetically hypercholesterolemic rabbits (Watanabe) and attenuates ischemia/reperfusion-induced cardiomyocyte apoptosis. Antioxidant, anti-inflammatory and hypocholesterolemic agent.
M. Wt | 516.84 |
Formula | C31H48O2S2 |
Storage | Desiccate at +4°C |
Purity | ≥99% (HPLC) |
CAS Number | 23288-49-5 |
PubChem ID | 4912 |
InChI Key | FYPMFJGVHOHGLL-UHFFFAOYSA-N |
Smiles | CC(SC2=CC(C(C)(C)C)=C(O)C(C(C)(C)C)=C2)(C)SC1=CC(C(C)(C)C)=C(O)C(C(C)(C)C)=C1 |
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
References are publications that support the biological activity of the product.
Ruixing et al (2006) Pretreatment with prob. attenuates cardiomyocyte apoptosis in a rabbit model of ischemia/reperfusion. Scand.J.Clin.Lab.Invest. 66 549 PMID: 17101546
Wu et al (2007) Probucol [4,4'-[(1-methylethylidene)bis(thio)]bis-[2,6-bis(1,1-dimethylethyl)phenol]] inhibits compensatory remodeling and promotes lumen loss associated with atherosclerosis in apolipoprotein E-deficient mice. J.Pharmacol.Exp.Ther. 321 477 PMID: 17293560
Favari et al (2004) Probucol inhibits ABCA1-mediated cellular lipid efflux. Arterioscler.Thromb.Vasc.Biol. 24 2345 PMID: 15514211
Wu et al (2004) Probucol inactivates ABCA1 in the plasma membrane with respect to its mediation of apolipoprotein binding and high density lipoprotein assembly and to its proteolytic degradation. J.Biol.Chem. 279 30168 PMID: 15140889
Keywords: Probucol, Probucol supplier, Antioxidant, anti-inflammatory, hypocholesterolemic, hypocholesterolaemic, agent, ATP-binding, cassette, ABCA1, CERP, Antioxidants, Multidrug, Transporters, 2775, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for Probucol include:
Guo et al (2016) VCP recruitment to mitochondria causes mitophagy impairment and neurodegeneration in models of Huntington's disease. Nat Commun 7 12646 PMID: 27561680
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There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.