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    Tariquidar dimesylate
    Tariquidar dimesylate

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1756
    CAS #: 625375-84-0 Purity ≥98%

    Description: Tariquidar dimesylate (also known as XR9576) is a novel potent and selective noncompetitive inhibitor of P-glycoprotein  (P-gp) with Kd of 5.1 nM in CHrB30 cell line, it reverses drug resistance in MDR cell Lines. Tariquidar 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. 

    References: Br J Pharmacol. 1999 Sep;128(2):403-11; Cancer Res. 2001 Jan 15;61(2):749-58.

    Related CAS#206873-63-4 (free base)625375-84-0 (dimesylate); 625375-83-9 (dimesylate hydrate).

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    Molecular Weight (MW)838.94
    FormulaC40H46N4O12S2 
    CAS No. 625375-84-0 (dimesylate)  
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: ≥ 296 mg/mL  
    Water:  < 8.9 mg/mL
    Ethanol: < 8.9 mg/mL
    Solubility (In vivo)O=C(C1=CC2=CC=CC=C2N=C1)NC3=CC(OC)=C(OC)C=C3C(NC4=CC=C(CCN5CC6=C(C=C(OC)C(OC)=C6)CC5)C=C4)=O.OS(=O)(C)=O.OS(=O)(C)=O
    SynonymsXR 9576 dimesylate, XR9576 dimesylate, XR-9576, Tariquidar dimesylate; Tariquidar dimesilate; D06008, D 06008, D-06008 dimesylate


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    In Vitro

    In vitro activity: Tariquidar displays high-affinity binding to P-gp with Bmax of 275 pmol/mg. Tariquidar shows non-competitive interaction with the P-gp substrates vinblastine and paclitaxel. Tariquidar increases the steady-state accumulation of these cytotoxics in CHr<>/supB30 cells to levels observed in non-P-gp-expressing AuxB1 cells with EC50 of 487 nM. Tariquidar is able to inhibit the vanadate-sensitive ATPase activity of P-gp by 60-70%, with potent IC50 values of 43 NM. Tariquidar may inhibit other resistance mechanisms at higher concentrations. 1 μM Tariquidar abrogates ABCG2 (BCRP)-mediated resistance to camptothecins in vitro. Tariquidar potentiates the cyto-toxicity of several drugs including doxorubicin, paclitaxel, etoposide, and vincristine; complete reversal of resistance is achieved in the presence of 25- 80 nM Tariquidar. In MC26, a murine colon carcinoma cell line with intrinsic chemoresistance, the doxorubicin IC50 is fivefold lower in the presence of 0.1 μM Tariquidar (36 vs 7 nM). In murine mammary carcinoma, human small-cell lung carcinoma and human ovarian carcinoma cell lines with acquired chemotherapeutic resistance (EMT6/AR1.0, H69/LX4 and 2780 AD), the in vitro doxorubicin IC50 is 22-150-fold lower in the presence of 0.1 μM Tariquidar. P-gp inhibition persists for 23 h after removal of Tariquidar from the culture system. Tariquidar restored the cyto-toxicity of doxorubicin and vinblastine in the National Cancer Institute (NCI)/ADRRES multicellular tumor spheroid model derived from the MCF7WT breast cancer cell line. 


    Kinase Assay: AuxB1 and CHrB30 cells are grown to confluency in 12-well (24 mm) tissue culture dishes and the steady-state accumulation of [3H]-vinblastine is measured. Accumulation is initiated by the addition of 0.1 μ Ci [3H]-vinblastine and unlabelled vinblastine to a final concentration of 100 nM . The accumulation of [3H]-paclitaxel is measured using 0.1 μ Ci [3H]-paclitaxel and unlabelled drug to a final concentration of 1 μM . Cells are incubated in a reaction volume of 1 mL for 60 min at 37 ℃ under 5% CO2 in order to reach steady-state. The effect of the modulators XR9576 on [3H]-ligand accumulation is investigated in the concentration range 10-9 - 10-6 M. Modulators are added from a DMSO stock giving a final solvent concentration of 0.2 % (v/v). Following cell harvesting, accumulated drug is measured by liquid scintillation counting and normalized for cell protein content. Plots of amount accumulated as a function of modulator concentration are fitted with the general dose-response equation: Y={(a-b)/(1+(X/c)d)}+b Where: Y=response; a=initial response; b=final response; c=EC50 concentration; d=slope value; X=drug concentration.


    Cell Assay: Cells are seeded into 96-well plates at 800/well, in 100 μL of medium and incubated for 4 h at 37 ℃. Varying concentrations of modulator or solvent control (50 μL/well) are subsequently added and incubated for an additional 1 h before the addition of the cytotoxic drug. The cytotoxic drug (50 μL) is added to give a range of final concentrations in quadruplicate wells. After incubation for an additional 4 days, cell proliferation of adherent cells is assessed using the sulforhodamine B assay.

    In VivoTariquidar (2- 8 mg/kg p.o.) is found to significantly potentiate the antitumor activity of doxorubicin (5 mg/kg, i.v.) against MC26 murine colon carcinoma in vivo. In human carcinoma xenografts, coadministration of XR9576 (6 -12 mg/kg p.o.) fully restored the antitumor activity of paclitaxel, etoposide, and vincristine against two highly resistant MDR human tumor xenografts (2780AD, H69/LX4) in nude mice.
    Animal modelMurine colon carcinoma xenografts MC26
    Formulation & DosageDissolved in5% (w/v) D-( 1)-glucose (dextrose) solution; 8 mg/kg ; Coadministration of Tariquidar (p.o.) with doxorubicin (5 mg/kg, i.v.)
    References

    Br J Pharmacol. 1999 Sep;128(2):403-11; Cancer Res. 2001 Jan 15;61(2):749-58.


    These protocols are for reference only. InvivoChem does not independently validate these methods.

    Tariquidar dimesylate

    The effect of modulator on the steady-state accumulation of [3H]-vinblastine (100 nM) and [3H]-paclitaxel (1 μM) was measured in CHrB30 cells at 37°C as described in Methods. Br J Pharmacol. 1999 Sep;128(2):403-11.

    Tariquidar dimesylate

    The effect of XR9576, GF120918, XR9051 and vanadate on the ATPase activity of P-gp-containing CHrB30 membranes (1 μg). Br J Pharmacol. 1999 Sep;128(2):403-11.

    Tariquidar dimesylate

    Saturation isotherms of [3H]-XR9576, [3H]-vinblastine and [3H]-paclitaxel binding to CHrB30 membranes. Br J Pharmacol. 1999 Sep;128(2):403-11.

    Tariquidar dimesylate

    Tariquidar dimesylate

    Tariquidar dimesylate


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