产品
编 号：F621280
分子式：C38H40Cl2N4O6
分子量：719.65
分子式：C38H40Cl2N4O6
分子量：719.65
产品类型
规格
价格
是否有货
结构图
CAS No: 1992047-62-7
产品详情
生物活性：
Tariquidar dihydrochloride (XR9576 dihydrochloride) is a potent and specific inhibitor of P-glycoprotein (P-gp) with the high affinity (Kd=5.1 nM).
体内研究：
In mice bearing the intrinsically resistant MC26 colon tumors, coadministration of Tariquidar (XR9576) potentiates the antitumor activity of Doxorubicin without a significant increase in toxicity; maximum potentiation is observed at 2.5-4.0 mg/kg dosed either i.v. or p.o. In addition, coadministration of Tariquidar (6-12 mg/kg p.o.) fully restores the antitumor activity of Paclitaxel, Etoposide, and Vincristine against two highly resistant MDR human tumor xenografts (2780AD, H69/LX4) in nude mice. Tariquidar is found to also significantly potentiate the antitumor activity of doxorubicin against s.c. MC26 tumors in vivo.
体外研究：
Tariquidar (XR9576) is a potent modulator of P-gp mediated [3H]-Vinblastine and [3H]-Paclitaxel transport as it increases the steady-state accumulation of these cytotoxics in CHrB30 cells to levels observed in non-P-gp-expressing AuxB1 cells (EC50=487±50 nM). [3H]-Tariquidar binds to CHrB30 membranes with the highest affinity (Kd=5.1±0.9 nM, n=7) and a binding capacity (Bmax) of 275±15 pmol/mg membrane protein. In contrast to the parental cell line, the accumulation of [3H]-Vinblastine is increased in a dose-dependent fashion by the modulators Tariquidar (EC50=487±50 nM). The MDR modulator Tariquidar is able to inhibit 60-70% of the vanadate-sensitive ATPase activity, with potent IC50 value of 43±9 nM. Tariquidar (XR9576) potentiates the cytotoxicity of several drugs including Doxorubicin, Paclitaxel, Etoposide, and Vincristine; complete reversal of resistance is achieved in the presence of 25-80 nM XR9576. Tariquidar is a potent inhibitor of photoaffinity labeling of P-gp by [3H]Azidopine implying a direct interaction with the protein.
Tariquidar dihydrochloride (XR9576 dihydrochloride) is a potent and specific inhibitor of P-glycoprotein (P-gp) with the high affinity (Kd=5.1 nM).
体内研究：
In mice bearing the intrinsically resistant MC26 colon tumors, coadministration of Tariquidar (XR9576) potentiates the antitumor activity of Doxorubicin without a significant increase in toxicity; maximum potentiation is observed at 2.5-4.0 mg/kg dosed either i.v. or p.o. In addition, coadministration of Tariquidar (6-12 mg/kg p.o.) fully restores the antitumor activity of Paclitaxel, Etoposide, and Vincristine against two highly resistant MDR human tumor xenografts (2780AD, H69/LX4) in nude mice. Tariquidar is found to also significantly potentiate the antitumor activity of doxorubicin against s.c. MC26 tumors in vivo.
体外研究：
Tariquidar (XR9576) is a potent modulator of P-gp mediated [3H]-Vinblastine and [3H]-Paclitaxel transport as it increases the steady-state accumulation of these cytotoxics in CHrB30 cells to levels observed in non-P-gp-expressing AuxB1 cells (EC50=487±50 nM). [3H]-Tariquidar binds to CHrB30 membranes with the highest affinity (Kd=5.1±0.9 nM, n=7) and a binding capacity (Bmax) of 275±15 pmol/mg membrane protein. In contrast to the parental cell line, the accumulation of [3H]-Vinblastine is increased in a dose-dependent fashion by the modulators Tariquidar (EC50=487±50 nM). The MDR modulator Tariquidar is able to inhibit 60-70% of the vanadate-sensitive ATPase activity, with potent IC50 value of 43±9 nM. Tariquidar (XR9576) potentiates the cytotoxicity of several drugs including Doxorubicin, Paclitaxel, Etoposide, and Vincristine; complete reversal of resistance is achieved in the presence of 25-80 nM XR9576. Tariquidar is a potent inhibitor of photoaffinity labeling of P-gp by [3H]Azidopine implying a direct interaction with the protein.
产品资料
Copyright©2015-2024 沪ICP备2022026524号-1
沪公网安备