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Potent P-glycoprotein (P-gp) inhibitor (IC50 = 5.1 nM). Reverses drug resistance in multiple MDR cell lines. Acts as a substrate for breast cancer resistance protein (BCRP) at low concentrations and acts as an inhibitor of BCRP when used at >100 nM concentration. Potentiates the cytotoxic effects of doxorubicin (Cat. No. 2252) and mitoxantrone (Cat. No. 4250) in vitro.
|Storage||Store at -20°C|
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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 719.66. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||1.39 mL||6.95 mL||13.9 mL|
|5 mM||0.28 mL||1.39 mL||2.78 mL|
|10 mM||0.14 mL||0.69 mL||1.39 mL|
|50 mM||0.03 mL||0.14 mL||0.28 mL|
References are publications that support the biological activity of the product.
Kannan et al (2011) The "specific" P-glycoprotein inhibitor Tariquidar is also a substrate and an inhibitor for breast cancer resistance protein (BCRP/ABCG2). ACS Chem.Neurosci. 2 82 PMID: 22778859
Loo et al (2015) Mapping the binding site of the inhibitor Tariquidar that stabilizes the first transmembrane domain of P-glycoprotein. J.Biol.Chem. 290 29389 PMID: 26507655
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Keywords: Tariquidar dihydrochloride, Tariquidar dihydrochloride supplier, Potent, P-glycoprotein, P-gp, inhibitors, inhibits, multidrug, resistance, MDR, breast, cancer, resistant, protein, BCRP, substrates, cytotoxic, abcb1, atp, binding, cassette, 206873-63-4, Multidrug, Transporters, 5757, Tocris Bioscience
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Programmed Cell Death Poster
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.