Tariquidar

Catalog No.S8028 Synonyms: XR9576

Tariquidar Chemical Structure

Molecular Weight(MW): 646.73

Tariquidar is a potent and selective noncompetitive inhibitor of P-glycoprotein with Kd of 5.1 nM in CHrB30 cell line, reverses drug resistance in MDR cell Lines. Phase 3.

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In DMSO USD 220 In stock
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USD 470 In stock

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3 Customer Reviews

  • Mutations of the polar residues Y307, Q725 and Y953 to alanine, cysteine and phenylalanine (Y953F only) were tested for their effect on the modulation of basal ATPase activity of P-gp by drugs. Basal activity of cysless WT and mutant P-gps was taken as zero, inhibition was calculated as percentage of the basal activity and shown with downward bars (negative values), while stimulation was calculated as percentage of the basal activity and shown with upward bars (positive values). Bars are colored black for cysless WT or triple A (Y307A/Q725A/Y953A) while they are grey for the single mutants (Y307A/C, Q725A/C, Y953A/C/F). At least three experiments were carried out with duplicate samples for each mutant with indicated compounds, and errors bars denote the standard deviations.

    Biochem Pharmacol, 2016, 101:40-53.. Tariquidar purchased from Selleck.

    Vet Parasitol, 2015, 211(1-2):80-8.. Tariquidar purchased from Selleck.

  • DEX protects L-02 cells from TRAIL-induced apoptosis by upregulating P-gp. Apoptosis was evaluated using a TUNEL assay, and the number of TUNEL-positive cells in each group were counted. (A) Representative photomicrographs of the TUNEL assay. L-02 cells were divided into six groups based on their treatment regimens, (a) control untreated group, (b) pretreated with 10 µM DEX for 24 h, followed by incubation with TRAIL for 24 h, (c) pretreatment with 10 µM DEX for 24 h, followed by incubation with TRAIL and 25 nM TQD for 24 h, (d) pretreated with 10 µM DEX for 24 h, followed by incubation with TRAIL and 50 nM TQD for 24 h, (e) pretreated with 10 µM DEX for 24 h, followed by incubation with TRAIL and 100 nM TQD for 24 h, and (f) incubated with TRAIL for 24 h. All the groups were treated with TRAIL for the induction of apoptosis, with the exception of the control group. Magnification, ×200. (B) Quantitative analysis of the levels of apoptosis. Data are presented as the mean ± standard deviation. *P<0.05. DEX, dexamethasone; TRAIL, tumor necrosis factor-related apoptosis-inducing ligand; TQD, tariquidar; TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labeling.

    Mol Med Rep, 2015, 12(6):8093-100.. Tariquidar purchased from Selleck.

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Notes:

2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.

Biological Activity

Description Tariquidar is a potent and selective noncompetitive inhibitor of P-glycoprotein with Kd of 5.1 nM in CHrB30 cell line, reverses drug resistance in MDR cell Lines. Phase 3.
Targets
P-gp [1]
(CHrB30 cells)
5.1 nM(Kd)
In vitro

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. [1] Tariquidar may inhibit other resistance mechanisms at higher concentrations. 1 μM Tariquidar abrogates ABCG2 (BCRP)-mediated resistance to camptothecins in vitro. [2] 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. [3] 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. [4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
MDCK cells NGf1eGFHfW6ldHnvckBie3OjeR?= NUf2WJM5OzBibXnudy=> M12yT2FkfGm4aYT5JIF1KEKFUmCgLJVvc26xd36gc5Jq\2mwKTDlfJBz\XO|ZXSgbY4hVUSFSzDj[YxteyC3c3nu[{BzcG:mYX3pcoUhOTJ|IHHzJJN2[nO2cnH0[UBqdmO3YnH0[YQh\m:{IEOwJI1qdnNicILpc5IhfG9ic4Xid5Rz[XSnIHHk[Il1cW:wIH3lZZN2emWmIHHmeIVzKDNyIH3pcpMh[nliZnz1c5JwdWW2cnnjJIFv[Wy7c3nzMEBGSzVyPUCuNFEh|ryP M1;GUVI{Ozd2OEey
EMT6/AR1.0 cells NVfr[5YxTnWwY4Tpc44h[XO|YYm= MUKxJIg> MX\Jcohq[mm2aX;uJI9nKG2xdYPlJHBoeCCrbjDFUXQ3N0GUMT6wJINmdGy|IHHmeIVzKDFiaIKgZpkh\GG3bn;yeYJq[2mwIHHjZ5VufWyjdHnvckBie3OjeTygTWM2OD1yLkC2OEDPxE1? Mn;BNVgxQDNyM{S=
human CEM/VLB500 cells NHLLUnhHfW6ldHnvckBie3OjeR?= MnTGN{Bl[Xm| NEToZVNT\X[ncoPhcEBw\iCSLXfwMY1m\GmjdHXkJI12dHSrZIL1[{Bz\XOrc4ThcoNmKHSxII\pcoJt[XO2aX7lJIlvKGi3bXHuJGNGVS:YTFK1NFAh[2WubIOgZYZ1\XJiMzDkZZl{KGK7IILld4F7fXKrbjDhd5NigSxiRVO1NF0xNjB4ODFOwG0> M4ntcVE4Ozl7OUmw
A2780 cells MXfGeY5kfGmxbjDhd5NigQ>? NGLtUm4{OCCvaX7z MnfuTY5pcWKrdHnvckBw\iCqdX3hckBR\3BiaX6gRVI4QDBiY3XscJMh[W[2ZYKgN|AhdWmwczDifUBJd2WlaIP0JFM{OzR{IHHzd4F6NCCLQ{WwQVAvOTJ3OEmg{txO M1q1[|E5ODh|MEO0
human KBV1 cells M1u0fmZ2dmO2aX;uJIF{e2G7 NGTR[GUyOCCvaX7z NILVWW9KdmirYnn0bY9vKG:oIFHCR2IyKGmwIHj1cYFvKEuEVkGgZ4VtdHNiYX\0[ZIhOTBibXnud{BjgSCFYXzj[YlvNUGPIH3pZ5JweGyjdHWgZZN{[XluIFnDOVA:OC5{MkOg{txO MmnhNlQ6ODB4OEO=
human MCF7/Topo cells NWj0eJZZTnWwY4Tpc44h[XO|YYm= NET1UmlKdmirYnn0bY9vKG:oIFHCR2czKGW6cILld5Nm\CCrbjDoeY1idiCPQ1[3M3RweG9iY3XscJMh[nliSH;lZ4h{fCCvaXPyc5Bt[XSnIHHzd4F6NCCLQ{WwQVAvPTJ4IN88US=> MkLDNlE2PzB{OEK=
MCF7 MX cells NI\ZTXdHfW6ldHnvckBie3OjeR?= M2\vZ2lvcGmkaYTpc44hd2ZiQlPSVEBmgHC{ZYPz[YQhcW5iTVPGO{BOYCClZXzsd{BjgSCKb3XjbJN1KDN|M{SyJJN1[WmwaX7nMEBKSzVyPUCuOlgh|ryP NVzLd5BoOTl7M{K5OlA>
human HFE cells NHPrUnNEgXSxdH;4bYPDqGG|c3H5 MXO3NkBp NXS1fHFrS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUE[HIHPlcIx{KGG|c3Xzd4VlKGG|IHPlcIwhfmmjYnnsbZR6KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9NU4zQCEQvF2= MVWyOlE6PzF4MB?=
human HCT116 cells MoDPR5l1d3SxeHnjxsBie3OjeR?= M3fyd|Q5KGh? MU\DfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIR3QyOTZiY3XscJMh[XO|ZYPz[YQh[XNiY3XscEB3cWGkaXzpeJkh[W[2ZYKgOFghcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2xNk42KM7:TR?= Mnf4NlYyQTdzNkC=
human SW620 cells NW\RSG9jS3m2b4TvfIlkyqCjc4PhfS=> NWfWUWZsPDhiaB?= Mn7GR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gV3c3OjBiY3XscJMh[XO|ZYPz[YQh[XNiY3XscEB3cWGkaXzpeJkh[W[2ZYKgOFghcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2yOUDPxE1? NVnU[3JCOjZzOUexOlA>
human SW620/AD300 cells M3vmfWN6fG:2b4jpZ:Kh[XO|YYm= M{XF[FQ5KGh? NWC5Xmx3S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hW1d4MkCvRWQ{ODBiY3XscJMh[XO|ZYPz[YQh[XNiY3XscEB3cWGkaXzpeJkh[W[2ZYKgOFghcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2yOUDPxE1? NHL2S2MzPjF7N{G2NC=>
human CCD-18Co cells MW\DfZRwfG:6aXRCpIF{e2G7 M1Kxb|Q5KGh? Mnf6R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gR2NFNTF6Q3:gZ4VtdHNiYYPz[ZN{\WRiYYOgZ4VtdCC4aXHibYxqfHliYX\0[ZIhPDhiaILzJIJ6KE2WVDDhd5NigSxiSVO1NF0zPSEQvF2= NV\0XnVmOjZzOUexOlA>
human KB-V1 cells NH[xZWdHfW6ldHnvckBie3OjeR?= NH;UOlIzODBibl2= NGGybllKdmirYnn0bY9vKG:oIGCt[5AhcW5iaIXtZY4hU0JvVkGgZ4VtdHNiYYPz[ZN{\WRiYYOgbY5kemWjc3WgbY4hemixZHHtbY5mKDF{MzDhZ4N2dXWuYYTpc44h[XRiMkCwJI5O NIGz[I0zOTZ3N{K3NS=>

... Click to View More Cell Line Experimental Data

In vivo Tariquidar (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. [3]

Protocol

Kinase Assay:[1]
+ Expand

Steady-state drug accumulation 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 Research:[3]
+ Expand
  • Cell lines: Murine mammary carcinoma cell line MDR EMT6/AR1.0
  • Concentrations: ~100 nM Tariquidar
  • Incubation Time: 4 days
  • Method: 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.
    (Only for Reference)
Animal Research:[3]
+ Expand
  • Animal Models: Murine colon carcinoma xenografts MC26
  • Formulation: 5% (w/v) D-( 1)-glucose (dextrose) solution
  • Dosages: 8 mg/kg
  • Administration: Coadministration of Tariquidar (p.o.) with doxorubicin (5 mg/kg, i.v.)
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 52 mg/mL (80.4 mM)
Water <1 mg/mL
Ethanol <1 mg/mL
In vivo 30% propylene glycol, 5% Tween 80, 65% D5W 30 mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 646.73
Formula

C38H38N4O6

CAS No. 206873-63-4
Storage powder
in solvent
Synonyms XR9576

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT00082368 Completed Cancer National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) May 2004 Phase 2
NCT00071058 Completed Adrenal Cortex Neoplasms National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) October 2003 Phase 2
NCT00069160 Completed Lung Neoplasms|Ovarian Neoplasms|Cervix Neoplasms|Renal Neoplasms National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) September 2003 Phase 2
NCT00042315 Terminated Stage IIIb Non-small Cell Lung Cancer|Stage IV Non-small Cell Lung Cancer QLT Inc. June 2002 Phase 3
NCT00042302 Terminated Stage IIIb Non-small Cell Lung Cancer|Stage IV Non-small Cell Lung Cancer QLT Inc. June 2002 Phase 3
NCT00011414 Completed Wilms Tumor|Sarcoma|Adenaocortical Carcinoma|Refractory Cancer|Coldrhood Cancer National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) February 15, 2001 Phase 1

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID