Tariquidar
Catalog No.S8028 Synonyms: XR9576
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.
4 Customer Reviews
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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.
viability of parental and resistant A549 and SW480 cells treated with PU-H71 (PU), puromycin (Puro), tariquidar and combinations of tariquidar with PU-H71 and puromycin for four days.
Oncotarget, 2017, 8(5):7678-7690. Tariquidar purchased from Selleck.
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Effects of LEV alone, or in combination with MDRIs, on the migration of L3 stage H. contortus Kirby (A) and WAL (B) larvae; LEV alone shown with solid lines and closed symbols, IVM plus MDRIs shown as dashed lines and open symbols. The concentration of each MDRI in g/mL is shown as subscript after the MDRI name. Each data point represents mean ± SE, n = 9 (pooled data from three experiments,
each with assays in triplicate); Asc: ascorbic acid, Zq: zosuquidar, Tq: tariquidar.
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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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. | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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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 CHrB30 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] |
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| Cell Data |
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| 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: |
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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)}+bWhere: Y=response; a=initial response; b=final response; c=EC50 concentration; d=slope value; X=drug concentration. |
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Solubility (25°C)
| In vitro | DMSO | 52 mg/mL (80.4 mM) |
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| Water | Insoluble | |
| Ethanol | Insoluble | |
| In vivo | Add solvents to the product individually and in order(Data is from Selleck tests instead of citations): 30% Propylene glycol+5% Tween 80+65% D5W For best results, use promptly after mixing. |
30mg/mL |
* 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 |
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| Formula | C38H38N4O6 |
| CAS No. | 206873-63-4 |
| Storage | powder |
| in solvent | |
| Synonyms | XR9576 |
Bio Calculators
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Clinical Trial Information
| NCT Number | Recruitment | Conditions | Sponsor/Collaborators | Start Date | Phases |
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| 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 |
| NCT00082368 | Completed | Cancer | National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) | May 16 2004 | Phase 2 |
| 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 |
Tech Support
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
Tel: +1-832-582-8158 Ext:3
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Frequently Asked Questions
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Question 1:
Can you please give me more specific and detailed information of how to dissolve and use this compound (S8028) for in vivo studies?
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Answer:
Tariquidar in 30% Propylene glycol, 5% Tween 80, 65% D5W at 30mg/ml will be a suspension or emulsion. If you are going to administrate the compound by oral gavage, it is fine. We also have test some vehicles for Tariquidar for i.p injection, and it is soluble in 5% DMSO+45% PEG 300+ddH2O at 2mg/ml clearly. When preparing the solution, please dissolve the compound in DMSO clearly first, then add PEG. After they mixed well, then dilute with water.
