2. Protein Tyrosine Kinase/RTK PI3K/Akt/mTOR Stem Cell/Wnt MAPK/ERK Pathway
  3. VEGFR FGFR FLT3 PDGFR RET Akt ERK c-Kit
  4. VEGFR2-IN-84

VEGFR2-IN-84 is an orally active, multi-targeted tyrosine kinase inhibitor based on a naphthalene ring scaffold. VEGFR2-IN-84 inhibits VEGFR2 with sub-nanomolar affinity and broadly targets kinases including Kit, FGFR, PDGFR, and Ret. By competitively binding to the ATP-binding pocket, VEGFR2-IN-84 blocks the phosphorylation of VEGFR2 and its downstream AKT/ERK signaling pathway, thereby significantly inhibiting endothelial cell proliferation, migration, and tumor angiogenesis. VEGFR2-IN-84 exhibits broad-spectrum antiproliferative activity against various solid tumors such as liver cancer, lung cancer, and renal cancer, shows weak toxicity to normal cells, and has superior potency to Lenvatinib (HY-10981). VEGFR2-IN-84 possesses favorable pharmacokinetic properties and high safety (LD50>2000 mg/kg), and can be used in related studies of various malignant tumors.

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

VEGFR2-IN-84

VEGFR2-IN-84 Chemical Structure

CAS No. : 861877-12-5

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VEGFR2-IN-84 Related Antibodies

Top Publications Citing Use of Products

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VEGFR1/Flt-1 VEGFR2/KDR/Flk-1 VEGFR3/Flt-4

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PDGFR PDGFRβ PDGFRα

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Akt Akt1 Akt2 Akt3

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ERK ERK1 ERK2 ERK5 ERK8

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Description

VEGFR2-IN-84 is an orally active, multi-targeted tyrosine kinase inhibitor based on a naphthalene ring scaffold. VEGFR2-IN-84 inhibits VEGFR2 with sub-nanomolar affinity and broadly targets kinases including Kit, FGFR, PDGFR, and Ret. By competitively binding to the ATP-binding pocket, VEGFR2-IN-84 blocks the phosphorylation of VEGFR2 and its downstream AKT/ERK signaling pathway, thereby significantly inhibiting endothelial cell proliferation, migration, and tumor angiogenesis. VEGFR2-IN-84 exhibits broad-spectrum antiproliferative activity against various solid tumors such as liver cancer, lung cancer, and renal cancer, shows weak toxicity to normal cells, and has superior potency to Lenvatinib (HY-10981). VEGFR2-IN-84 possesses favorable pharmacokinetic properties and high safety (LD50>2000 mg/kg), and can be used in related studies of various malignant tumors[1].

IC50 & Target

VEGFR2

0.303 nM (EC50)

PDGFRα

0.742 nM (EC50)

PDGFRβ

2.12 nM (EC50)

Flt-4

1.35 nM (EC50)

FGFR1

195 nM (EC50)

FGFR2

4.43 nM (EC50)

FGFR3

28.7 nM (EC50)

Flt-1

1.61 nM (EC50)

In Vitro

VEGFR2-IN-84 (E20) (4.92 nM; 96 h) significantly inhibits VEGF-induced proliferation of HUVEC cells, with approximately 10-fold the activity of Lenvatinib (HY-10981)[1].
VEGFR2-IN-84 (10-1000 nM; 48 h) dose-dependently inhibits the phosphorylation of VEGFR2 and its downstream molecules AKT and ERK in HUVEC, A549 and HepG2 cells, and exhibits superior activity to Lenvatinib[1].
VEGFR2-IN-84 (8.53-14.1 μM; 72 h) exhibits weak inhibitory activity against normal cells LO2, HEK293T and BEAS-2B, showing favorable tumor cell selectivity[1].

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

VEGFR2-IN-84 Related Antibodies

Cell Proliferation Assay[1]

Cell Line: Human umbilical vein endothelial cells (HUVECs)
Concentration: IC50
Incubation Time: 96 h
Result: Significantly inhibited hVEGF-165 (20 ng/mL)-induced proliferation of HUVECs with an IC50 value of 4.92 nM, which was over 10-fold more potent than lenvatinib (IC50=51.2 nM).

Western Blot Analysis[1]

Cell Line: HUVECs, A549 cells, HepG2 cells
Concentration: 10 nM, 1000 nM
Incubation Time: 48 h
Result: Dose-dependently suppressed hVEGF-165 (50 ng/mL)-induced phosphorylation of VEGFR2 (Tyr1175), AKT (Ser473), and ERK1/2 (Thr202/Tyr204) in HUVECs.
Significantly reduced p-VEGFR2 and p-ERK levels.
Dose-dependently inhibited the phosphorylation of VEGFR2, AKT, and ERK in A549 and HepG2 cells, and exhibited more potent inhibitory effects than lenvatinib at the same concentrations.
In Vivo

VEGFR2-IN-84 (E20) (50 mg/kg; p.o.; once daily; 21 days) significantly inhibits tumor growth in a male BALB/c nude mouse HepG2 hepatocellular carcinoma xenograft model, with efficacy superior to that of Lenvatinib (HY-10981) at the same dose, and causes no obvious body weight loss[1].
VEGFR2-IN-84 (30-60 mg/kg; p.o.; once daily; 20-30 days) dose-dependently inhibits tumor growth in male BALB/c nude mouse xenograft models of A549 lung cancer, 786-O renal cell carcinoma, and 8305C thyroid carcinoma, respectively, and exhibits superior efficacy over Lenvatinib at the same dose[1].
VEGFR2-IN-84 (2 mg/kg; tail vein injection; single dose; 24 h) exhibits a moderate elimination half-life (T1/2=5.05 h) and plasma exposure (AUC0-∞=1970 ng?h/mL) in healthy ICR mice[1].

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

Animal Model: Male BALB/c nude mice (4-5 weeks old, 15-17 g), HepG2 hepatocellular carcinoma subcutaneous xenograft model[1]
Dosage: 50 mg/kg
Administration: Intragastric (p.o.) administration, once daily (qd)
Result: Significantly inhibited the growth of HepG2 xenografts with a tumor growth inhibition (TGI) rate of 94.3%, which was superior to lenvatinib (TGI=83.6%) at the same dose.
No significant body weight loss or overt signs of toxicity were observed throughout the experimental period.
Animal Model: Male BALB/c nude mice (4-5 weeks old, 15-17 g), A549 non-small cell lung cancer subcutaneous xenograft model[1]
Dosage: 30 mg/kg or 60 mg/kg
Administration: Intragastric (p.o.) administration, once daily (qd)
Result: Exhibited dose-dependent antitumor activity.
At 30 mg/kg, the TGI rate was 76.9%, which was superior to lenvatinib (TGI=61.3%) at the same dose.
At 60 mg/kg, achieved a TGI rate of 95.7%, significantly outperforming lenvatinib (TGI=84.6%).
No significant body weight loss was observed.
Molecular Weight

470.50

Formula

C25H18N4O4S
CAS No.
SMILES

NC(C1=C(C=C(C2=C1)N=CC=C2OC3=CC4=C(C=C3)C(C(NC5=NC=CS5)=O)=CC=C4)OC)=O
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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VEGFR2-IN-84 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:

VEGFR2-IN-84861877-12-5VEGFRFGFRFLT3PDGFRRETAktERKc-KitVascular endothelial growth factor receptorFibroblast growth factor receptorCluster of differentiation antigen 135CD135Fms like tyrosine kinase 3Platelet-derived growth factor receptorPKBProtein kinase BExtracellular signal regulated kinasesSCFRCD117VEGFR2FGFR2KitPDGFRαFlt4RetFlt1PDGFRβAKTFGFR3Inhibitorinhibitorinhibit

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