Axitinib

Information	Axitinib (AG-013736) is a multiple receptor kinase inhibitor of VEGFR-1, VEGFR-2, VEGFR-3, PDGFR-β and c-KIT with IC50 of 0.1 nM, 0.2 nM, 0.1-0.3 nM, 1.6 nM and 1.7 nM, respectively.
Targets	VEGFR-1	VEGFR-2	VEGFR-3	PDGFR-β	c-KIT
IC50	0.1 nM	0.2 nM	0.1-0.3 nM	1.6 nM	1.7 nM ^[1]
In vitro	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). ^[2]
In vivo	Axitinib exhibits primary inhibition to orthotopically transplanted models such as M24met (melanoma), HCT-116 (colorectal cancer), and SN12C (renal cell carcinoma). ^[1] 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. ^[2] Axitinib significantly inhibits growth and disrupts tumor microvasculature in BT474 breast cancer model at 10–100 mg/kg. ^[3] Axitinib has shown single-agent activity in variable tumors, including renal cell carcinoma, thyroid cancer, non-small cell lung cancer, and melanoma.
Clinical Trials	Axitinib is currently in Phase III clinical trial in advanced hepatocellular carcinoma.
Features	Axitinib is superior as second-line therapy compared with sorafenib, the current standard of care.

Information

Axitinib (AG-013736) is a multiple receptor kinase inhibitor of VEGFR-1, VEGFR-2, VEGFR-3, PDGFR-β and c-KIT with IC50 of 0.1 nM, 0.2 nM, 0.1-0.3 nM, 1.6 nM and 1.7 nM, respectively.

Targets

VEGFR-1

VEGFR-2

VEGFR-3

PDGFR-β

c-KIT

IC50

0.1 nM

0.2 nM

0.1-0.3 nM

1.6 nM

1.7 nM ^[1]

In vitro

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). ^[2]

In vivo

Axitinib exhibits primary inhibition to orthotopically transplanted models such as M24met (melanoma), HCT-116 (colorectal cancer), and SN12C (renal cell carcinoma). ^[1] 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. ^[2] Axitinib significantly inhibits growth and disrupts tumor microvasculature in BT474 breast cancer model at 10–100 mg/kg. ^[3] Axitinib has shown single-agent activity in variable tumors, including renal cell carcinoma, thyroid cancer, non-small cell lung cancer, and melanoma.

Clinical Trials

Axitinib is currently in Phase III clinical trial in advanced hepatocellular carcinoma.

Features

Axitinib is superior as second-line therapy compared with sorafenib, the current standard of care.

Cellular receptor kinase phosphorylation assay	Porcine aorta endothelial (PAE) cells, which overexpress full-length VEGFR-2, PDGFR-β, KIT, and NIH-3T3, which overexpress murine VEGFR-2 (Flk-1) or PDGFR-α, are generated. The 96-well plates are coated with 100 μL/well of 2.5 μg/mL anti-VEGFR-2 antibody, 0.75 μg/mL anti-PDGFR-β antibody, 0.25 μg/mL anti-PDGFR-α 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 lines:	HUVEC, SH-SY5Y, IGR-N91 and IGR-NB8 cells
Concentrations:	1 nM to 10 μM
Incubation Time:	72 hours
Method:	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.

Cell lines:

HUVEC, SH-SY5Y, IGR-N91 and IGR-NB8 cells

Concentrations:

1 nM to 10 μM

Incubation Time:

72 hours

Method:

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.

Animal Models:	BT474 breast cancer cells are implanted subcutaneously into Immune-deficient female mice (Nu/nu; age 8–12 weeks).
Formulation:	0.5% carboxymethylcellulose (CMC)
Dosages:	10, 30 or 100 mg/kg
Administration:	Oral daily

Animal Models:

BT474 breast cancer cells are implanted subcutaneously into Immune-deficient female mice (Nu/nu; age 8–12 weeks).

Formulation:

0.5% carboxymethylcellulose (CMC)

Dosages:

10, 30 or 100 mg/kg

Administration:

Oral daily

Molecular Weight (WM):	386.47
Formula:	C₂₂H₁₈N₄OS
CAS No.:	319460-85-0
Synonyms:	AG 013736

Molecular Weight (WM):

386.47

Formula:

C₂₂H₁₈N₄OS

CAS No.:

319460-85-0

Synonyms:

AG 013736

Dissolve in (25°C):	DMSO <1mg/mL
	Water <1mg/mL
	Ethanol <1mg/mL
Storage:	2 years-20°CPowder
	1 week-4°Cin DMSO
	1 month-80°in DMSO

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Biological Activity

Protocol (Only for Reference)

Kinase Assay: [1]

Cell Assay: [2]

Animal Study:[3]

References

Product Information

Quality Control & MSDS

Research Area

Related Inhibitors

Secondary Antibodies

Loading Control Antibodies

Recommended Screening Libraries

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Kinase Assay: ^[1]

Cell Assay: ^[2]

Animal Study:^[3]

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