VEGFR3/Flt-4
VEGFR3/Flt-4 is a receptor tyrosine kinase whose expression becomes mainly restricted to lymphatic endothelium during development, defining it as a core regulator of lymphatic vessel biology[1]. Its ligands VEGF-C and VEGF-D activate VEGFR3, and VEGF-C induces VEGFR3 autophosphorylation and lymphangiogenesis in experimental systems[2][3]. Mechanistically, VEGFC/FLT4 signaling can promote endothelial sprouting through ERK-linked cell-cycle control in venous and lymphatic endothelial cells[4]. In tumor models, VEGFR3 signaling supports tumor lymphangiogenesis and regional lymph-node metastasis, making the VEGF-C/VEGFR3 axis relevant for metastasis-focused experimental design[5]. Compared with VEGFR2-driven angiogenic signaling, VEGFR3 ligand-binding and kinase activity are required for lymphangiogenesis but not angiogenesis, while VEGFR3 can modulate VEGFR2-mediated vascular permeability signaling[6][7]. For isoform-specific studies, VEGF-C Cys156Ser functions as a selective VEGFR3 agonist that binds and activates VEGFR3 without activating VEGFR2, supporting receptor-selective pathway analysis[8]. - VEGFR3/Flt-4 primarily supports lymphatic endothelial signaling, lymphangiogenesis, and metastasis-relevant vascular remodeling. - VEGF-C Cys156Ser enables VEGFR3-selective activation, separating lymphatic signaling from VEGFR2 permeability effects.
References:
- [1]. Kaipainen A, et al. Expression of the fms-like tyrosine kinase 4 gene becomes restricted to lymphatic endothelium during development. Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3566-70. [Content Brief]
- [2]. Jiang R, et al. Effectiveness of exercise on perinatal depression and anxiety symptoms: A network meta-analysis and dose-response analysis. Int J Gynaecol Obstet. 2026 Jun;173(3):1308-1324. [Content Brief]
- [3]. Veikkola T, et al. Signalling via vascular endothelial growth factor receptor-3 is sufficient for lymphangiogenesis in transgenic mice. EMBO J. 2001 Mar 15;20(6):1223-31. [Content Brief]
- [4]. Jerafi-Vider A, et al. VEGFC/FLT4-induced cell-cycle arrest mediates sprouting and differentiation of venous and lymphatic endothelial cells. Cell Rep. 2021 Jun 15;35(11):109255. [Content Brief]
- [5]. He Y, et al. Suppression of tumor lymphangiogenesis and lymph node metastasis by blocking vascular endothelial growth factor receptor 3 signaling. J Natl Cancer Inst. 2002 Jun 5;94(11):819-25. [Content Brief]
- [6]. Zhang L, et al. VEGFR-3 ligand-binding and kinase activity are required for lymphangiogenesis but not for angiogenesis. Cell Res. 2010 Dec;20(12):1319-31. [Content Brief]
- [7]. Heinolainen K, et al. VEGFR3 Modulates Vascular Permeability by Controlling VEGF/VEGFR2 Signaling. Circ Res. 2017 Apr 28;120(9):1414-1425. [Content Brief]
- [8]. Joukov V, et al. A recombinant mutant vascular endothelial growth factor-C that has lost vascular endothelial growth factor receptor-2 binding, activation, and vascular permeability activities. J Biol Chem. 1998 Mar 20;273(12):6599-602. [Content Brief]
All Product Categories
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VEGFR3/Flt-4 Related Products (69)
Related Products (69)
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Recombinant Proteins (7)
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Sorafenib
0 ImagesSynonyms: Bay 43-9006Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.
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Lenvatinib
0 ImagesSynonyms: E7080
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Nintedanib
0 ImagesSynonyms: BIBF 1120Nintedanib (BIBF 1120) is a potent triple angiokinase inhibitor for VEGFR1/2/3, FGFR1/2/3 and PDGFRα/β with IC50s of 34 nM/13 nM/13 nM, 69 nM/37 nM/108 nM and 59 nM/65 nM, respectively.
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Regorafenib
0 ImagesSynonyms: BAY 73-4506
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Cabozantinib
0 ImagesSynonyms: XL184; BMS-907351Cabozantinib is a potent and orally active inhibitor of VEGFR2 and MET, with IC50 values of 0.035, and 1.3 nM, respectively. Cabozantinib displays strong inhibition of KIT, RET, AXL, TIE2, and FLT3 (IC50=4.6, 5.2, 7, 14.3, and 11.3 nM, respectively). Cabozantinib shows antiangiogenic activity. Cabozantinib disrupts tumor vasculature and promotes tumor and endothelial cell apoptosis.
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Sorafenib tosylate
0 ImagesSynonyms: Bay 43-9006 tosylateSorafenib (Bay 43-9006) tosylate is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib tosylate induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib tosylate inhibits tumor growth and metastasis in mouse and rat models. Sorafenib tosylate can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.
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VEGFR2-IN-84
0 ImagesCat. No.: HY-182354CAS No.: 861877-12-5VEGFR2-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.
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Nintedanib esylate
0 ImagesSynonyms: BIBF 1120 esylateNintedanib esylate (BIBF 1120 esylate) is a potent triple angiokinase inhibitor for VEGFR1/2/3, FGFR1/2/3 and PDGFRα/β with IC50s of 34 nM/13 nM/13 nM, 69 nM/37 nM/108 nM and 59 nM/65 nM, respectively.
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Lenvatinib mesylate
0 ImagesSynonyms: E7080 mesylate
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Vandetanib
0 ImagesSynonyms: ZD6474Vandetanib (D6474) is a potent, orally active, and blood-brain-barrier penetrate inhibitor of VEGFR2/KDR tyrosine kinase activity (IC50=40 nM). Vandetanib also has activity versus the tyrosine kinase activity of VEGFR3/FLT4 (IC50=110 nM) and EGFR/HER1 (IC50=500 nM).
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MAZ51
0 ImagesMAZ51 is a selective inhibitor of VEGFR-3 (Flt-4) tyrosine kinase. MAZ51 inhibits VEGF-C-induced activation of VEGFR-3 without blocking VEGF-C-mediated stimulation of VEGFR2. MAZ51 had no effect on ligand-induced autophosphorylation of EGFR, IGF-1R and PDGFRβ. MAZ51 blocks proliferation and induces apoptosis in a wide variety of tumor cells. Antitumor activity.
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SAR131675
0 ImagesSAR131675 is a potent and selective VEGFR3 inhibitor with an IC50 of 23 nM. SAR131675 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
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Sorafenib-d3
0 ImagesSynonyms: Donafenib; Bay 43-9006-d3Sorafenib-d3 (Donafenib) is the deuterated-labeled Sorafenib (HY-10201). Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.
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Sitravatinib
0 ImagesSynonyms: MGCD516; MG-516Sitravatinib (MGCD516) is an orally bioavailable receptor tyrosine kinase (RTK) inhibitor with IC50s of 1.5 nM, 2 nM, 2 nM, 5 nM, 6 nM, 6 nM, 8 nM, 0.5 nM, 29 nM, 5 nM, and 9 nM for Axl, MER, VEGFR3, VEGFR2, VEGFR1, KIT, FLT3, DDR2, DDR1, TRKA, TRKB, respectively. Sitravatinib shows potent single-agent antitumor efficacy and enhances the activity of PD-1 blockade through promoting an antitumor immune microenvironment.
