product name Axitinib
Description: Axitinib, also known as AG013736, is a potent, orally bioavailable, multi-targeted inhibitor of VEGFR1, VEGFR2, VEGFR3, PDGFRβ and c-Kit with IC50 of 0.1 nM, 0.2 nM, 0.1-0.3 nM, 1.6 nM and 1.7 nM in Porcine aorta endothelial cells, respectively. Axitinib inhibits the proangiogenic cytokines VEGF and PDGF, thereby exerting an anti-angiogenic effect.
References: Int J Cancer. 2011 Jun 1;128(11):2748-58; Magn Reson Imaging. 2007 Apr;25(3):319-27.
386.47
Formula
C22H18N4OS
CAS No.
319460-85-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 35 mg/mL (90.5 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
0.5% CMC: 30 mg/mL
Synonyms
AG013736
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19401437
| In Vitro |
In vitro activity: Axitinib could block the cellular autophosphorylation of VEGFR and VEGF-mediated endothelial cell viability, tube formation, and downstream signaling. Axitinib inhibits the proliferation of variable cell lines with IC50 of >10,000 nM (IGR-N91), 849 nM (IGR-NB8), 274 nM (SH-SY5Y) and 573 nM (non-VEGF stimulated HUVEC). Kinase Assay: Porcine aorta endothelial (PAE) cells, which overexpress full-length VEGFR2, PDGFRβ, Kit, and NIH-3T3, which overexpress murine VEGFR2 (Flk-1) or PDGFRα, are generated. The 96-well plates are coated with 100 μL/well of 2.5 μg/mL anti-VEGFR2 antibody, 0.75 μg/mL anti-PDGFRβ antibody, 0.25 μg/mL anti-PDGFRα antibody, 0.5 μg/mL anti-KIT antibody, or 1.20 μg/mL anti-Flk-1 antibody to prepare ELISA capture plates. Then phosphorylation of RTK is measured by ELISA. Cell Assay: Cells (HUVEC, SH-SY5Y, IGR-N91 and IGR-NB8 cells) are seeded in a 96-well plate at a density of 5 × 104 and cultured for 24 hours. Axitinib is added to the cells at concentrations ranging from 1 nM to 10 μM. Cell viability is measured after 72 hours by MTS tetrazolium substrate and IC50 values are calculated. |
|---|---|
| In Vivo | Axitinib exhibits primary inhibition to orthotopically transplanted models such as M24met (melanoma), HCT-116 (colorectal cancer), and SN12C (renal cell carcinoma). Axitinib delays the tumor growth with 11.4 days compared to the controls (p.o. 30 mg/kg) and decreases the Mean Vessels Density (MVD) to 21, compared to 49 in controls, in IGR-N91 flank xenografts. Axitinib significantly inhibits growth and disrupts tumor microvasculature in BT474 breast cancer model at 10-100 mg/kg. Axitinib has shown single-agent activity in variable tumors, including renal cell carcinoma, thyroid cancer, non-small cell lung cancer, and melanoma. |
| Animal model | BT474 breast cancer cells are implanted subcutaneously into Immune-deficient female mice (Nu/nu; age 8-12 weeks). |
| Formulation & Dosage | Dissolved in 0.5% carboxymethylcellulose (CMC); 10, 30 or 100 mg/kg; Oral gavage |
| References | Int J Cancer. 2011 Jun 1;128(11):2748-58; Magn Reson Imaging. 2007 Apr;25(3):319-27. |
Related Posts
product name Axitinib
Description: Axitinib, also known as AG013736, is a potent, orally bioavailable, multi-targeted inhibitor of VEGFR1, VEGFR2, VEGFR3, PDGFRβ and c-Kit with IC50 of 0.1 nM, 0.2 nM, 0.1-0.3 nM, 1.6 nM and 1.7 nM in Porcine aorta endothelial cells, respectively. Axitinib inhibits the proangiogenic cytokines VEGF and PDGF, thereby exerting an anti-angiogenic effect.
References: Int J Cancer. 2011 Jun 1;128(11):2748-58; Magn Reson Imaging. 2007 Apr;25(3):319-27.
386.47
Formula
C22H18N4OS
CAS No.
319460-85-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 35 mg/mL (90.5 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
0.5% CMC: 30 mg/mL
Synonyms
AG013736
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19401437
| In Vitro |
In vitro activity: Axitinib could block the cellular autophosphorylation of VEGFR and VEGF-mediated endothelial cell viability, tube formation, and downstream signaling. Axitinib inhibits the proliferation of variable cell lines with IC50 of >10,000 nM (IGR-N91), 849 nM (IGR-NB8), 274 nM (SH-SY5Y) and 573 nM (non-VEGF stimulated HUVEC). Kinase Assay: Porcine aorta endothelial (PAE) cells, which overexpress full-length VEGFR2, PDGFRβ, Kit, and NIH-3T3, which overexpress murine VEGFR2 (Flk-1) or PDGFRα, are generated. The 96-well plates are coated with 100 μL/well of 2.5 μg/mL anti-VEGFR2 antibody, 0.75 μg/mL anti-PDGFRβ antibody, 0.25 μg/mL anti-PDGFRα antibody, 0.5 μg/mL anti-KIT antibody, or 1.20 μg/mL anti-Flk-1 antibody to prepare ELISA capture plates. Then phosphorylation of RTK is measured by ELISA. Cell Assay: Cells (HUVEC, SH-SY5Y, IGR-N91 and IGR-NB8 cells) are seeded in a 96-well plate at a density of 5 × 104 and cultured for 24 hours. Axitinib is added to the cells at concentrations ranging from 1 nM to 10 μM. Cell viability is measured after 72 hours by MTS tetrazolium substrate and IC50 values are calculated. |
|---|---|
| In Vivo | Axitinib exhibits primary inhibition to orthotopically transplanted models such as M24met (melanoma), HCT-116 (colorectal cancer), and SN12C (renal cell carcinoma). Axitinib delays the tumor growth with 11.4 days compared to the controls (p.o. 30 mg/kg) and decreases the Mean Vessels Density (MVD) to 21, compared to 49 in controls, in IGR-N91 flank xenografts. Axitinib significantly inhibits growth and disrupts tumor microvasculature in BT474 breast cancer model at 10-100 mg/kg. Axitinib has shown single-agent activity in variable tumors, including renal cell carcinoma, thyroid cancer, non-small cell lung cancer, and melanoma. |
| Animal model | BT474 breast cancer cells are implanted subcutaneously into Immune-deficient female mice (Nu/nu; age 8-12 weeks). |
| Formulation & Dosage | Dissolved in 0.5% carboxymethylcellulose (CMC); 10, 30 or 100 mg/kg; Oral gavage |
| References | Int J Cancer. 2011 Jun 1;128(11):2748-58; Magn Reson Imaging. 2007 Apr;25(3):319-27. |