EGFR T790M/FAK-IN-2

Name: EGFR T790M/FAK-IN-2
Brand: MedChemExpress
SKU: HY-183120

Cat. No.: HY-183120: Data Sheet Handling Instructions
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EGFR T790M/FAK-IN-2 is an orally active dual FAK and EGFR^T790M kinase inhibitor, with an IC₅₀ of 1.03 nM against FAK and an IC₅₀ of 3.89 nM against EGFR^T790M. EGFR T790M/FAK-IN-2 exerts antiproliferative effects in drug-resistant cancer cells overexpressing FAK, inducing apoptosis and cell cycle arrest. EGFR T790M/FAK-IN-2 exhibits antitumor activity in a pancreatic cancer xenograft mouse model. EGFR T790M/FAK-IN-2 can be used for the research of pancreatic cancer, breast cancer and non-small cell lung cancer.

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EGFR T790M/FAK-IN-2 화학구조

CAS No. : 2143104-11-2

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Biological Activity
순도&문서
References
고객리뷰

제품 설명

Cellular Effect

Cell Line	Type	Value	Description	References
NCI-H1975	IC₅₀	0.333 μM Compound: 8	Antiproliferative activity against human NCI-H1975 cells harboring EGFR L858R/T790M mutant assessed as reduction in cell viability incubated for 72 hrs by CCK8 assay Antiproliferative activity against human NCI-H1975 cells harboring EGFR L858R/T790M mutant assessed as reduction in cell viability incubated for 72 hrs by CCK8 assay	[PMID: 34218082]

In Vitro

EGFR T790M/FAK-IN-2 (Compound 9a) (1.25-40 μM; 72 h) inhibits the proliferation of AsPC-1, BxPC-3, Panc-1, Hpde6-c7, MCF-7/adr and H1975 cells, with IC₅₀ values ranging from 0.333 μM to 1.347 μM^[1].
EGFR T790M/FAK-IN-2 (0.5-8 μM; 24-72 h) reduces the viability of AsPC-1 and Panc-1 cells in a dose- and time-dependent manner^[1].
EGFR T790M/FAK-IN-2 (0-1 μM; 72 h) induces apoptosis in AsPC-1 cells in a dose-dependent manner in vitro^[1].
EGFR T790M/FAK-IN-2 (0.25-1.0 μM; 72 h) dose-dependently arrests AsPC-1 cells at the G2/M phase^[1].

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

Cell Proliferation Assay^[1]

Cell Line:	AsPC-1, BxPC-3, Panc-1, Hpde6-c7, MCF-7/adr, H1975 human cancer cell lines
Concentration:	1.25-40 μM
Incubation Time:	72 h
Result:	Inhibited proliferation of AsPC-1 cells with an IC₅₀ of 0.909 μM. Inhibited proliferation of BxPC-3 cells with an IC₅₀ of 0.761 μM. Inhibited proliferation of Panc-1 cells with an IC₅₀ of 1.218 μM. Inhibited proliferation of Hpde6-c7 cells with an IC₅₀ of 1.347 μM. Inhibited proliferation of MCF-7/adr cells with an IC₅₀ of 0.892 μM. Inhibited proliferation of H1975 cells with an IC₅₀ of 0.333 μM.

Cell Viability Assay^[1]

Cell Line:	AsPC-1, Panc-1 human cancer cell lines
Concentration:	0.5 μM, 4 μM, 8 μM (AsPC-1); 0.5 μM, 2 μM, 8 μM (Panc-1)
Incubation Time:	24 h, 48 h, 72 h
Result:	Decreased cell viability of AsPC-1 cells in a dose- and time-dependent manner: 0.5 μM reduced viability to 62.6% (24 h), 58.3% (48 h), 44.5% (72 h); 4 μM reduced viability to 10.1% (24 h), 5.1% (48 h), 0% (72 h); 8 μM reduced viability to 3.4% (24 h), 38.6% (48 h), 2.4% (72 h). Decreased cell viability of Panc-1 cells in a dose- and time-dependent manner: 0.5 μM reduced viability to 88.7% (24 h), 82.6% (48 h), 33.2% (72 h); 2 μM reduced viability to 60% (24 h), 9.8% (48 h), 9.5% (72 h); 8 μM reduced viability to 3.7% (24 h), 36.5% (48 h), 0.71% (72 h).

Apoptosis Analysis^[1]

Cell Line:	AsPC-1 human cancer cell line
Concentration:	0, 0.25, 0.5, 1 μM
Incubation Time:	72 h
Result:	Induced apoptosis in a dose-dependent manner, with the percentage of apoptotic cells increasing from 52.9% to 90.4% with higher inhibitor concentrations after 72 h treatment, compared to the control group.

Cell Cycle Analysis^[1]

Cell Line:	AsPC-1 human cancer cell line
Concentration:	0, 0.25, 0.5, 1 μM
Incubation Time:	72 h
Result:	Arrested cells in the G2/M phase in a dose-dependent manner: 0.25 μM increased G2/M phase cells to 5.72% and decreased G0/G1 phase cells to 63.89%; 0.5 μM increased G2/M phase cells to 15.42% and decreased G0/G1 phase cells to 57.38%; 1.0 μM increased G2/M phase cells to 27.19% and decreased G0/G1 phase cells to 39.90%. Showed minor changes in the percentage of cells in S phase.

In Vivo

EGFR T790M/FAK-IN-2 (30-60 mg/kg; p.o.; once daily; 10 days) inhibits the growth of pancreatic cancer tumors in BALB/c nude mice in a dose-dependent manner^[1].

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

Animal Model:	BALB/cJNju-Foxn1nu/Nju (nude) (female, 5-6 weeks old, 20-25 g, subcutaneous xenograft with human AsPC-1 cells)^[1]
Dosage:	30 mg/kg; 60 mg/kg
Administration:	p.o.; daily; 10 days
Result:	Achieved tumor growth inhibition (TGI) rate of 24.45% at 30 mg/kg dose. Achieved tumor growth inhibition (TGI) rate of 36.6% at 60 mg/kg dose. Exhibited dose-dependent reduction in tumor weight and volume relative to controls.

분자량

510.00

화학식

C₂₅H₂₈ClN₇O₃

CAS No.

2143104-11-2

SMILES

O=C(NC)C=1C=CC=CC1NC2=NC(=NC=C2Cl)NC3=CC=C(NC(=O)CN4CCOCC4)C(=C3)C

선적

Room temperature in continental US; may vary elsewhere.

보관

Please store the product under the recommended conditions in the Certificate of Analysis.

순도&문서

Handling Instructions (2659 KB)

References

[1]. Ai M, Wang C, Tang Z, Liu K, Sun X, Ma T, Li Y, Ma X, Li L, Chen L. Design and synthesis of diphenylpyrimidine derivatives (DPPYs) as potential dual EGFR T790M and FAK inhibitors against a diverse range of cancer cell lines. Bioorg Chem. 2020 Jan;94:103408. [Content Brief]