VEGFR-2/P-gp-IN-2
VEGFR-2/P-gp-IN-2 is a VEGFR-2 inhibitor (IC50 = 126.4 nM) and P-glycoprotein inhibitor. VEGFR-2/P-gp-IN-2 induces G1 phase cell cycle arrest and Apoptosis. VEGFR-2/P-gp-IN-2 can be used for research on cervical cancer.
For research use only. We do not sell to patients.
- Formula: C26H20F3N3O3
- Molecular Weight:479.45
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All VEGFR Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
VEGFR2 126.4 nM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HeLa | IC50 |
1.21 μM
|
Antiproliferative activity against human HeLa cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay.
Antiproliferative activity against human HeLa cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay.
|
42623911 |
| Ca-Ski | IC50 |
1.67 μM
|
Antiproliferative activity against human CaSki cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay.
Antiproliferative activity against human CaSki cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay.
|
42623911 |
| SiHa | IC50 |
1.72 μM
|
Antiproliferative activity against human SiHa cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay.
Antiproliferative activity against human SiHa cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay.
|
42623911 |
In Vitro
VEGFR-2/P-gp-IN-2 (Compound 5N) (0.78125-100 μM; 48 h) exhibits potent antiproliferative activity against HeLa, CaSki, SiHa, and HeLa/DDP cell lines with an SI of 53.0[1].
VEGFR-2/P-gp-IN-2 (5 μM; 1 h) strongly inhibits VEGFR-2 kinase activity in cell-free assays with an IC50 of 126.4 nM[1].
VEGFR-2/P-gp-IN-2 (1-4 μM; 24 h) effectively blocks VEGFR-2 phosphorylation in HeLa and HeLa/DDP cells in a concentration-dependent manner[1].
VEGFR-2/P-gp-IN-2 (1-4 μM) effectively inhibits endothelial tube formation in HUVECs in a concentration-dependent manner, demonstrating potent anti-angiogenic potential[1].
VEGFR-2/P-gp-IN-2 (1-4 μM; 24 h) effectively blocks cell cycle progression at the G1 checkpoint in a concentration-dependent manner in HeLa and HeLa/DDP cells[1].
VEGFR-2/P-gp-IN-2 (1-4 μM; 24 h) inhibits the proliferation of HeLa and HeLa/DDP cells by triggering robust apoptosis in a concentration-dependent manner[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HeLa, CaSki, SiHa, HeLa/DDP, H8
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Concentration:0.78125-100 μM
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Incubation Time:48 h
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Result:Displayed IC50 values of 1.21 μM (HeLa), 1.67 μM (CaSki), 1.72 μM (SiHa), and 1.88 μM (HeLa/DDP).
Exhibited low toxicity toward normal H8 cells with an IC50 of 64.17 μM.
Achieved a selectivity index (SI) of 53.0.
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Cell Line:HeLa, HeLa/DDP
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Concentration:1-4 μM
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Incubation Time:24 h
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Result:Robustly downregulated p-VEGFR-2 levels in a concentration-dependent manner compared with the vehicle control group.
At 4 μM, the inhibitory efficacy on VEGFR-2 phosphorylation was comparable or slightly superior to that of sorafenib (2 μM).
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Cell Line:HeLa, HeLa/DDP
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Concentration:1-4 μM
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Incubation Time:24 h
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Result:Induced a robust, concentration-dependent accumulation of cells in the G1 phase.
In HeLa cells, increased the G1 population to 30.03%, 41.42%, and 54.09%, respectively, compared with 20.38% in the vehicle control.
In HeLa/DDP cells, the G1 proportion shifted from 23.89% (control) to 33.16%, 37.95%, and 52.61%, respectively.
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Cell Line:HeLa, HeLa/DDP
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Concentration:1-4 μM
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Incubation Time:24 h
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Result:In HeLa cells, the total percentage of apoptotic cells increased to 29.86%, 66.60%, and 86.90% following treatment with 1, 2, and 4 μM, respectively, compared to 3.63% in the vehicle control group.
In HeLa/DDP cells, drove the total apoptotic population up to 25.67%, 54.30%, and 73.90% at the corresponding concentrations, compared with a mere 3.27% in the control group.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wild-type AB strain[1]
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Dosage:6.25, 12.5, 25, 50, 100, 200, 400 μM
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Administration:Incubation; 96 h
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Result:Exhibited no observable mortality at concentrations up to 100 μM.
Increased mortality rate to 57.14% at 200 μM.
Induced 100.00% mortality at 400 μM.
Caused no malformations at any concentration tested.
Chemical Information
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Molecular Weight 479.45
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Formula C26H20F3N3O3
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SMILES
O=C(/C=C/C1=CC=C(NC2=NC=NC3=C2C=C(OC)C(OC)=C3)C=C1)C4=CC(C(F)(F)F)=CC=C4
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)