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Purity: ≥98%
Tariquidar (formerly XR9576; D06008; XR-9576; D-06008) is a potent and selective noncompetitive inhibitor of P-glycoprotein (P-gp) with potential antineoplastic activity. It inhibits P-gp with a Kd of 5.1 nM in CHrB30 cell line, it reverses drug resistance in MDR cell Lines. Tariquidaris is currently undergoing research as an adjuvant against multidrug resistance in cancer. Tariquidar non-competitively binds to the p-glycoprotein transporter, thereby inhibiting transmembrane transport of anticancer drugs. Inhibition of transmembrane transport may result in increased intracellular concentrations of an anticancer drug, thereby augmenting its cytotoxicity.
| ln Vitro |
Tariquidar (XR9576) increases the steady-state accumulation of P-gp, making it a potent modulator of P-gp-mediated transport of [3H]-Vinblastine and [3H]-Paclitaxel. The levels of P-gp observed in AuxB1 cells (EC50=487±50 nM) are not required for the cytotoxic effects observed in CHrB30 cells. [3H]-Tariquidar has the strongest affinity (Kd=5.1±0.9 nM, n=7) and a binding capacity (Bmax) of 275±15 pmol/mg membrane protein when it comes to CHrB30 membranes. The modulator Tariquidar (EC50=487±50 nm) increased the accumulation of [3H]-vinblastine in a dose-dependent manner when compared to the parental cell line. With an effective IC50 value of 43±9 nM, the MDR modulator Tariquidar can inhibit 60–70% of vanadate-sensitive ATPase activity[1]. Several medications, such as doxorubicin, paclitaxel, etoposide, and vincristine, are made more cytotoxic by tiriquidar (XR9576); in the presence of 25–80 nM XR9576, resistance is completely reversed. Strong photoaffinity labeling of P-gp by [3H]Azidopine is inhibited by tariquidar, suggesting a direct interaction with the protein [2].
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| ln Vivo |
In mice with intrinsically resistant MC26 colon cancers, coadministration of Tariquidar (XR9576) at a dose of 2.5–4.0 mg/kg maximally increased the anticancer efficacy of doxorubicin without appreciably increasing toxicity was noted. Moreover, in nude mouse xenografts of two highly resistant MDR human cancers (2780AD, H69/LX4), coadministration with Tariquidar (6–12 mg/kg po) completely restored the efficacy of paclitaxel, etoposide, and vincristine Antitumor activity. Additionally, when doxorubicin is subcutaneously injected in vivo against MC26 tumors, tartiquidar greatly increases its anti-tumor effectiveness [2].
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| References |
[1]. Martin C, et al. The molecular interaction of the high affinity reversal agent XR9576 with P-glycoprotein. Br J Pharmacol, 1999, 128(2), 403-411.
[2]. Mistry P, et al. In vitro and in vivo reversal of P-glycoprotein-mediated multidrug resistance by a novel potent modulator, XR9576. Cancer Res, 2001, 61(2), 749-758. [3]. Zimmermann ES, et al. Simultaneous Semimechanistic Population Analyses of Levofloxacin in Plasma, Lung, and Prostate To Describe the Influence of Efflux Transporters on Drug Distribution following Intravenous and Intratracheal Administration. Antimicrob Agents Chemother. 2015 Nov 30;60(2):946-54. [4]. Kao YH, et al. Regulation of P-glycoprotein expression in brain capillaries in Huntington's disease and its impact on brain availability of antipsychotic agents risperidone and paliperidone. J Cereb Blood Flow Metab. 2016 Aug;36(8):1412-23. [5]. Matzneller P, et al. Pharmacokinetics of the P-gp Inhibitor Tariquidar in Rats After Intravenous, Oral, and Intraperitoneal Administration. Eur J Drug Metab Pharmacokinet. 2018 Apr 3 |
| Molecular Formula |
C38H38N4O6
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| Molecular Weight |
646.73
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| CAS # |
206873-63-4
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| Related CAS # |
Tariquidar methanesulfonate, hydrate;625375-83-9;Tariquidar dihydrochloride;1992047-62-7
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| SMILES |
O(C([H])([H])[H])C1=C(C([H])=C2C(=C1[H])C([H])([H])N(C([H])([H])C([H])([H])C1C([H])=C([H])C(=C([H])C=1[H])N([H])C(C1=C([H])C(=C(C([H])=C1N([H])C(C1C([H])=NC3=C([H])C([H])=C([H])C([H])=C3C=1[H])=O)OC([H])([H])[H])OC([H])([H])[H])=O)C([H])([H])C2([H])[H])OC([H])([H])[H]
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.5462 mL | 7.7312 mL | 15.4624 mL | |
| 5 mM | 0.3092 mL | 1.5462 mL | 3.0925 mL | |
| 10 mM | 0.1546 mL | 0.7731 mL | 1.5462 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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