2. Protein Tyrosine Kinase/RTK Apoptosis
  3. VEGFR Apoptosis Caspase MDM-2/p53 Bcl-2 Family
  4. VEGFR-2-IN-70

VEGFR-2-IN-70 is a potent VEGFR-2 inhibitor with an IC50 of 18.04 nM. VEGFR-2-IN-70 exhibits cytotoxicity against A549 and MCF-7 cancer cells with IC50 values of 0.43 μM and 3.8 μM, respectively. VEGFR-2-IN-70 induces G1 cell cycle arrest and apoptosis in lung cancer cells. VEGFR-2-IN-70 is useful in cancer research.

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

VEGFR-2-IN-70 Chemical Structure

VEGFR-2-IN-70 Chemical Structure

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VEGFR-2-IN-70 Related Antibodies

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Bcl-2 Bcl-xL Bcl-W Mcl-1 Bfl-1 Bcl-B Bax Bak Bim BNIP3

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Description

VEGFR-2-IN-70 is a potent VEGFR-2 inhibitor with an IC50 of 18.04 nM. VEGFR-2-IN-70 exhibits cytotoxicity against A549 and MCF-7 cancer cells with IC50 values of 0.43 μM and 3.8 μM, respectively. VEGFR-2-IN-70 induces G1 cell cycle arrest and apoptosis in lung cancer cells. VEGFR-2-IN-70 is useful in cancer research[1].

IC50 & Target[1]

VEGFR2

18.04 nM (IC50)

Bax

 

Caspase-8

 

Caspase-9

 

Caspase 3

 

In Vitro

VEGFR-2-IN-70 (Compound 12g) (0.01-100 μM, 48 h) inhibits cell growth against A549 and MCF-7 cancer cells, with IC50s of 0.43 μM and 3.86 μM[1].

VEGFR-2-IN-70 (0.43 μM; 0-72 h) inhibits cell migration in A549 cells[1].

VEGFR-2-IN-70 (0.43 μM, 48 h) increases cell apoptosis, induces increased expression of pro-apoptotic genes and inhibits growth by causing cell cycle arrest at the G1 phase in A549 cells[1].

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

VEGFR-2-IN-70 Related Antibodies

Apoptosis Analysis[1]

Cell Line: A549 cells
Concentration: 0.43 μM
Incubation Time: 48 h
Result: Increased apoptosis, resulting in an overall apoptotic cell death rate of 23.12% (including 19.21% early apoptosis and 3.91% late apoptosis) .
Caused a slight increase in necrotic cell death (4.84%).

Cell Cycle Analysis[1]

Cell Line: A549 cells
Concentration: 0.43 μM
Incubation Time: 48 h
Result: Inhibited growth by causing cell cycle arrest at the G₁ phase, increased the percentage of cells in the G₁ phase to 76.53% and decreased the proportions of cells in the S phase and G₂/M phase to 19.36% and 4.11%, respectively.

RT-PCR[1]

Cell Line: A549 cells
Concentration: 0.43 μM
Incubation Time: 48 h
Result: Induced an increased in the expression of pro-apoptotic genes, such as P53 (fold change = 10.8), Bax (fold change = 8.7), and Caspase-3 (fold change = 9.6), Caspase-8 (fold change = 1.2), and Caspase-9 (fold change = 8.7) .
Suppressed the expression of anti-apoptotic genes Bcl-2 with 0.13-fold change.
Molecular Weight

440.91

Formula

C20H17ClN6O2S
SMILES

CC1=C(C(NNC(NC2=C(C)N(C3=CC=C(Cl)C=C3)N=N2)=O)=O)SC4=C1C=CC=C4
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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VEGFR-2-IN-70 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:

VEGFR-2-IN-70VEGFRApoptosisCaspaseMDM-2/p53Bcl-2 FamilyVascular endothelial growth factor receptorInhibitorA549 cellsMCF-7 cellsAnti-cancerinhibitorinhibit

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