1. Membrane Transporter/Ion Channel
  2. P-glycoprotein
  3. Elacridar

Elacridar (Synonyms: GF120918; GW0918; GG918; GW120918)

Cat. No.: HY-50879 Purity: 99.80%
Handling Instructions

Elacridar (GF120918) is a potent P-glycoprotein (Pgp) and BCRP inhibitor.

For research use only. We do not sell to patients.

Elacridar Chemical Structure

Elacridar Chemical Structure

CAS No. : 143664-11-3

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Customer Review

Based on 12 publication(s) in Google Scholar

Other Forms of Elacridar:

Top Publications Citing Use of Products

    Elacridar purchased from MCE. Usage Cited in: J Drug Target. 2016;24(5):441-9.

    Cells are co-treated with 5 μM of free LY139481 or an equivalent dose of SMA-LY139481 and either vehicle control (0.01% DMSO), Elacridar (1 μM), KO143 (5 μM), Valspodar (1 μM) or a combination of efflux inhibitors for 6 h.
    • Biological Activity

    • Protocol

    • Purity & Documentation

    • References

    • Customer Review


    Elacridar (GF120918) is a potent P-glycoprotein (Pgp) and BCRP inhibitor[1].

    IC50 & Target

    P-glycoprotein (Pgp), BCRP[1]

    In Vitro

    Elacridar inhibits P-glycoprotein (P-gp) labeling by [3H]azidopine with a IC50 of 0.16 μM[2]. In Caki-1 and ACHN cells, elacridar (2.5 μM) significantly ihibits the cell growth. The P-glycoprotein activity is found to be inhibited by elacridar. The combination of elacridar and SU 11248 lead to a significant reduction in ABC Sub-family B Member 2 (ABCG2) expression in 786-O cells[3].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    In Vivo

    Oral co-administration of elacridar (100 mg/kg, p.o.) and PF-02341066 increases the plasma and brain concentrations and brain-to-plasma ratios of PF-02341066 in wild-type mice, equaling the levels in Abcb1a/1b; Abcg2-/- mice[1]. In friend leukemia virus stain B mice, the brain-to-plasm partition coefficient (Kp, brain) of elacridar is 0.82, 0.43, and 4.31 after intravenous (2.5 mg/kg), intraperitoneal (100 mg/kg), and oral (100 mg/kg) treatment, respectively[4]. In Mrp4(-/-) mice, elacridar fully inhibits P-gp mediated transport of SKF 104864A, without siginificant effects on Bcrp1-mediated transport[5].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Molecular Weight




    CAS No.





    Room temperature in continental US; may vary elsewhere.

    Powder -20°C 3 years
    4°C 2 years
    In solvent -80°C 6 months
    -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    DMSO : 5 mg/mL (8.87 mM; Need ultrasonic)

    H2O : < 0.1 mg/mL (insoluble)

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 1.7742 mL 8.8709 mL 17.7418 mL
    5 mM 0.3548 mL 1.7742 mL 3.5484 mL
    10 mM --- --- ---
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

      Solubility: ≥ 0.5 mg/mL (0.89 mM); Clear solution

    • 2.

      Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

      Solubility: 1.67 mg/mL (2.96 mM); Suspended solution; Need ultrasonic

    *All of the co-solvents are provided by MCE.
    Kinase Assay

    10 μL of unlabeled cell membrane suspension (at 0.4 mg of protein/mL) are aliquoted into each well in 96-well plates. 5 μL of GF120918 are then added to each well. The plate is incubated 25 min at 25°C in the dark. 5 μL of tritiated azidopine (1.8 TBq/mmol) (0.6 μM in HCI 0.2 mM) are added to each well. After 25 min of incubation at 25°C in the dark, samples are simultaneously irradiated for 2 min at 254 nm at 0°C with a thin layer chromatography-designed UV lamp directly in contact with the plate. Samples are solubilized in sodium dodecyl sulfate-polyacrylamide gel electrophoresis sample buffer but not heated. After separation on a 7.5% polyacrylamide gel, the gel is treated for fluorography with Amplify and exposed during 3 days onto a photosensitive film. The fluorography is analysed using a Camag thin layer chromatography Scanner II densitometer.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Cell Assay

    3.0×103 cells per well are seeded in a 96-well plate. After 24 h incubation, an optimum concentration gradient of elacridar is added to each well. After culturing for 48 h, cell viability is assessed using the proliferation reagent, MTT. Control cells are treated with the vehicle only, 0.1% DMSO. After this final incubation, the medium is aspirated and precipitated formazan crystals are dissolved in DMSO (100 μL/well). The absorbance of each well is measured at 540 nm, and a reference wavelength of 650 nm is read with a multiskan JX microplate reader. Cell viability is calculated as percentage of the control value[3].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration

    Mice are fasted for 3 hr before oral administration of either elacridar (100 mg/kg) or elacridar vehicle. Two hours later, PF-02341066 (5 mg/kg) is administered to mice orally. Blood and brains are isolated 4 hr after PF-02341066 oral administration, and processed as described above. The brain concentrations are corrected for the amount of drug in the brain vasculature. Elacridar hydrochloride is dissolved in dimethyl sulfoxide (106 mg/mL) in order to get 100 mg pure elacridar per 1 mL of dimethyl sulfoxide. The stock solution is further diluted with a mixture of Polysorbate 80, ethanol and water [20:13:67 (v/v/v)] to yield a concentration of 10 mg/mL pure elacridar.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.


    Purity: 99.80%

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    ElacridarGF120918 GW0918 GG918 GW120918GF 120918GF-120918GW0918GW 0918GW-0918GG918GG 918GG-918GW120918GW 120918GW-120918P-glycoproteinBCRPP-gpPgpMultidrug resistance protein 1MDR1ATP-binding cassette sub-family B member 1ABCB1Cluster of differentiation 243CD243Breast cancer resistance proteinABCG2Inhibitorinhibitorinhibit

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