2. Membrane Transporter/Ion Channel Apoptosis Autophagy
  3. P-glycoprotein Apoptosis Autophagy
  4. P-gp inhibitor 30

P-gp inhibitor 30 is a potent P-gp inhibitor that reverses multidrug resistance in breast cancer by sensitizing resistant cells to Doxorubicin (ADM) (HY-15142). P-gp inhibitor 30 promotes apoptosis, induces autophagy, and suppresses proliferation, migration, and invasion of drug-resistant breast cancer cells when combined with ADM. P-gp inhibitor 30 inhibits breast tumor growth both in vitro and in vivo. P-gp inhibitor 30 can be used for drug-resistant breast cancer research.

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P-gp inhibitor 30

P-gp inhibitor 30 Chemical Structure

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P-gp inhibitor 30 Related Antibodies

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Description

P-gp inhibitor 30 is a potent P-gp inhibitor that reverses multidrug resistance in breast cancer by sensitizing resistant cells to Doxorubicin (ADM) (HY-15142). P-gp inhibitor 30 promotes apoptosis, induces autophagy, and suppresses proliferation, migration, and invasion of drug-resistant breast cancer cells when combined with ADM. P-gp inhibitor 30 inhibits breast tumor growth both in vitro and in vivo. P-gp inhibitor 30 can be used for drug-resistant breast cancer research[1].

In Vitro

P-gp inhibitor 30 (compound A38) (0.1 μM) reverses ADM resistance in MDA-MB-231/ADM cells, potently reducing the IC50 of ADM from 785.46 μM to 2.05 μM[1].
P-gp inhibitor 30 (0.125-4 μM) significantly inhibits P-gp ATPase activity at different concentrations in a concentration-dependent manner[1].
P-gp inhibitor 30 interacts with P-gp to inhibit its function without downregulating its expression, and stabilizes the protein, thereby reducing its degradation in MCF7/ADM cells upon increasing temperature[1].
P-gp inhibitor 30 (6 h) significantly increases Rh123 intensity in MCF7/ADM cells and increases the accumulation of ADM and inhibits the efflux of Rh123 in MDA-MB-231/ADM cells[1].
P-gp inhibitor 30 (0.1-1 μM, 24 h-15 days) promotes apoptosis, inhibits cell proliferation, and suppresses the migration and invasion of breast cancer drug-resistant cells (MCF7/ADM and MDA-MB-231/ADM cells), when combined with ADM, demonstrating that it sensitizes these cells to ADM[1].
P-gp inhibitor 30 (0.1 μM) leads to the accumulation of autophagosomes and significantly increases the expression of autophagy-related proteins in MCF7/ADM and MDA-MB-231/ADM cells when combined with ADM, thereby inducing cell death[1].
P-gp inhibitor 30 (1-10 days) significantly reduces the tumor volume of both MCF7/ADM and MDA-MB-231/ADM cells when combined with ADM in a 3D tumor spheroid model[1].

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

P-gp inhibitor 30 Related Antibodies

Western Blot Analysis[1]

Cell Line: MCF7/ADM and MDA-MB-231/ADM cells
Concentration: 0.1 μM
Incubation Time: 24 h
Result: Significantly increases the expression level of LC3 when combined with ADM.

Apoptosis Analysis[1]

Cell Line: MCF7/ADM and MDA-MB-231/ADM cells
Concentration: 0.1, 0.5 and 1 μM
Incubation Time: 48 h
Result: Significantly increased ADM-induced apoptosis in a dose-dependent manner compared to the MCF7/ADM control group.
Significantly increased ADM-induced apoptosis on MDA-MB-231/ADM cells.

Cell Proliferation Assay[1]

Cell Line: MCF7/ADM and MDA-MB-231/ADM cells
Concentration: 0.1, 0.5 and 1 μM
Incubation Time: 15 days
Result: Significantly inhibited the proliferation of MCF7/ADM cells in a dose-dependent manner compared to the MCF7/ ADM control group when combined with ADM.
Resulted in only a few cells survived at a concentration of 1 μM.
Markedly inhibited the proliferation of drug-resistant breast cancer cells when combined with ADM.

Cell Migration Assay [1]

Cell Line: MCF7/ADM and MDA-MB-231/ADM cells
Concentration: 0.1 μM
Incubation Time: 36 h
Result: Suppressed the migration ability of breast cancer drug- resistant cells when combined with ADM.

Cell Invasion Assay[1]

Cell Line: MCF7/ADM and MDA-MB-231/ADM cells
Concentration: 0.1 μM
Incubation Time: 24 h
Result: Suppressed the invasion ability of breast cancer drug- resistant cells when combined with ADM.
In Vivo

P-gp inhibitor 30 (2 mg/kg, i.p., every 2 days for 14 days) shows antitumor effects when combined with ADM in MCF-7/ADM mouse model[1].

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

Animal Model: Female BALB/c nude mice (4-5 weeks old) subcutaneously injected with MCF-7/ADM cells[1]
Dosage: 2 mg/kg
Administration: i.p., every 2 days for 14 days
Result: Significantly reduced tumor size when combined with ADM (10 mg/kg), with efficacy comparable to Tariquidar (HY-10550).
Showed significantly lower tumor weight than that of other groups.
Showed no significant loss compared to control.
Caused no significant tissue cell necrosis.
Molecular Weight

386.38

Formula

C22H15FN4O2
SMILES

N#CC1=CC(NC(C2=NNC3=C2C=CC=C3)=O)=CC=C1OCC4=C(C=CC=C4)F
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

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P-gp inhibitor 30 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

P-gp inhibitor 30P-glycoproteinApoptosisAutophagyP-gpPgpMultidrug resistance protein 1MDR1ATP-binding cassette sub-family B member 1ABCB1Cluster of differentiation 243CD243drug-resistant breast cancerADMMCF7/ADMMDA-MB-231/ADMInhibitorinhibitorinhibit

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