High affinity P-glycoprotein (P-gp) inhibitor (Kd = 79 nM). Restores doxorubicin (Cat. No. 2252) sensitivity in P-gp-expressing multidrug (MDR) resistant cancer cell lines. Also potentiates antitumor efficacy of taxol (Cat. No. 1097) in a MDR human non-small cell lung carcinoma xenograft mouse model.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 636.99. Batch specific molecular weights may vary from batch to batch due to solvent 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||1.57 mL||7.85 mL||15.7 mL|
|5 mM||0.31 mL||1.57 mL||3.14 mL|
|10 mM||0.16 mL||0.78 mL||1.57 mL|
|50 mM||0.03 mL||0.16 mL||0.31 mL|
References are publications that support the products' biological activity.
Dantzig et al (1999) Selectivity of the multidrug resistance modulator, LY335979, for P-glycoprotein and effect on cytochrome P-450 activities. J.Pharmacol.Exp.Ther. 290 854 PMID: 10411602
Dantzig et al (1996) Reversal of P-glycoprotein-mediated multidrug resistance by a potent cyclopropyldibenzosuberane modulator, LY335979. Cancer Res. 56 4171 PMID: 8797588
If you know of a relevant reference for Zosuquidar trihydrochloride, please let us know.
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Keywords: Zosuquidar trihydrochloride, supplier, LY335979, RS33295198, high, affinity, p-glycoprotein, p-gp, inhibitors, inhibits, multidrug, transporters, resistance, LY, 335979, Multidrug, Transporters, Multidrug, Transporters, 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.