VEGFR

Vascular endothelial growth factor (VEGF) is an important signaling protein involved in both vasculogenesis (the formation of the circulatory system) and angiogenesis (the growth of blood vessels from pre-existing vasculature).

B0084-429717
TG 100572
867334-05-2
B0084-463666
Toceranib phosphate
874819-74-6
B0084-153700
MGCD-265
875337-44-3
B0084-462772
R1530
882531-87-5
B0084-463669
AZD2932
883986-34-3
B0084-119097
(E)-FeCP-oxindole
884338-18-5
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ZK-261991
886563-25-3
B0084-267744
BFH772
890128-81-1
B0084-474893
BIBF 1202
894783-71-2
B0084-474894
Flumatinib
895519-90-1
B0084-462546
JI-101
900573-88-8
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RAF265
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B0084-460626
Golvatinib
928037-13-2
B0084-156198
ENMD-2076
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ACTB-1003
939805-30-8

Background


An overview of VEGFR

Vascular endothelial growth factor (VEGF) is an important signaling protein. Combined with the corresponding vascular endothelial growth factor receptor (VEGFR), it can stimulate the proliferation and migration of endothelial cells through specific signaling pathways, thus facilitating angiogenesis. Therefore, VEGF, VEGFR and their associated downstream signaling pathways can be used as targets for anti-tumor drug action.

Major types of VEGFR

VEGFR can be divided into three types, including VEGFR1, VEGFR2 and VEGFR3. Human VEGFR2 is a receptor containing kinase insertion region expressed on the surface of vascular endothelial cells, whose structure can be divided into three parts, including extracellular region, intracellular region and one transmembrane region.

Inhibition of VEGFR

Afibercept , which is a potent VEGFR blocker, has obtained positive results in clinical Ⅲ study of the second-line regimen for non-small cell lung cancer (NSCLC), which is associated with docetaxel.

VEGFR and diseases

When the tumor has just occurred, and the volume is less than 2 ~ 3 mm, there is no need for angiogenesis, because oxygen and other nutrients can reach the tumor tissue by penetrating the blood vessels that are located next to the tumor tissue. When its volume exceeds 3 mm, the tumor is in anoxic condition. Hypoxia and oncogene can raise the expression of VEGF in tumor cells, and VEGF and hypoxia could further improve the expression of VEGFR-1 and kinase inserted domain containing receptor (KDR). Thus, the tumors induce angiogenesis through VEGF-VEGFR signaling pathways. And the expression of VEGF and VEGFR in many tumor tissues has been found to be higher than normal tissues by using in situ hybridization and immunohistochemical methods, and they are positively correlated with the vascular density of tumor tissue. This shows that the VEGF-VEGFR signal transduction pathway is closely related to tumor angiogenesis and tumor growth. In addition, animal experiments have confirmed that specific VEGF neutralizing antibodies can inhibit new angiogenesis and tumor growth in mouse transplanted tumors, and this antibody has no direct inhibitory effect on tumor cells.