Taurocholic acid sodium (Sodium taurocholate; N-Choloyltaurine sodium) has marked bioactive effects such as an inhibitory potential against hepatic artery ligation induced biliary damage by upregulation of VEGF-A expression. Immunoregulation effect[1].
Ponatinib (AP24534) hydrochloride is a hydrochloride of ponatinib. Ponatinib is an orally active multi-targeted kinase inhibitor with IC50s of 0.37 nM, 1.1 nM, 1.5 nM, 2.2 nM, and 5.4 nM for Abl, PDGFRα, VEGFR2, FGFR1, and Src, respectively[1].
Cabozantinib is a potent multiple receptor tyrosine kinases inhibitor that inhibits VEGFR2, c-Met, Kit, Axl and Flt3 with IC50s of 0.035, 1.3, 4.6, 7 and 11.3 nM, respectively.
AG-13958 (AG-013958), a potent VEGFR tyrosine kinase inhibitor, is used for treatment of choroidal neovascularization associated with age-related macular degeneration (AMD)[1].
Tivozanib hydrochloride hydrate is a potent and selective and orally active VEGFR tyrosine kinase inhibitor with IC50是of 0.21, 0.16, 0.24 nM for VEGFR-1, VEGFR-2, VEGFR-3, respectively. Tivozanib hydrochloride hydrate inhibits angiogenesis and vascular permeability in tumor tissues and shows antitumor activity. Tivozanib hydrochloride hydrate has the potential for the research of metastatic renal cell carcinoma (RCC) [1][2][3].
AT-533 is a potent Hsp90 and HSV inhibitor. AT-533 suppresses tumor growth and angiogenesis by blocking the HIF-1α/VEGF/VEGFR-2 signaling pathway. AT-533 also inhibits the activation of the downstream pathways, including Akt/mTOR/p70S6K, Erk1/2 and FAK. AT-533 inhibits the tube formation, cell migration, and invasion of human umbilical vein endothelial cells (HUVECs)[1][2][3].
PF 477736 is a potent, selective ATP-competitive inhibitor of Chk1, with a Ki of 0.49 nM, 100-fold selectivity versus Chk2 (Ki, 47 nM).
Sorafenib tosylate is a potent multikinase inhibitor, with IC50s of 6 nM, 20 nM, and 22 nM for Raf-1, B-Raf, and VEGFR-3, respectively.
Foretinib is a multi-target tyrosine kinase inhibitor with IC50s of 0.4 nM and 0.9 nM for Met and KDR.
MAZ51 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[1][2].
Naphazoline (Naphthazoline) is a potent α-adrenergic receptor agonist. Naphazoline reduces vascular hyperpermeability and promotes vasoconstriction. Naphazoline reduces the levels of inflammatory factors (TNF-α, IL-1β and IL-6), cytokines (IFN-γ and IL-4), IgE, GMCSF, and NGF。Naphazoline can be used for non-bacterial conjunctivitis research[1][2].
Ivonescimab (AK112) is a PD-1/VEGF Bispecific Antibody. Ivonescimab can be used for cancer research[1][2][3].
VEGFR-2-IN-21 (Compound 5d) is a potent VEGFR-2 inhibitor with an IC50 of 0.10 μM. VEGFR-2-IN-21 shows anticancer activity[1].
AZD8601 is an mRNA designed to produce vascular endothelial growth factor A (VEGF-A). AZD8601 accelerates diabetic wound healing[1][2].
EGFR-IN-26 is a EGFR inhibitor extracted from patent WO2019162323A1 compound I-028. EGFR-IN-26 can be used for the research of cancer[1].
HSP90-IN-13 (compound 5k) is a highly potent HSP90 pan inhibitor with an IC50 value of 25.07 nM. HSP90-IN-13 has multi-target activity against EGFR, VEGFR-2 and Topoisomerase-2. HSP90-IN-13 causes cell cycle arrest at G2/M phase and induces apoptosis of MCF-7 cells through mitochondrial-mediated pathway[1].
Pegaptanib sodium is an RNA aptamer directed against vascular endothelial growth factor (VEGF)-165. Pegaptanib could be used for the study of neovascular age-related macular degeneration (AMD) [1].
Henatinib is an orally active small-molecule multikinase inhibitor that has demonstrated broad and potent antitumor activities. Henatinib inhibits the activity of VEGFR-2, c-kit, PDGFR with IC50 values of 0.6 nM, 3.3 nM and 41.5 nM, respectively. Henatinib significantly inhibits VEGFR-2 phosphorylation and its downstream signal pathway in human umbilical vein endothelial cells (HUVECs)[1].
Tafetinib (SIM010603) is an oral multi-targets receptor tyrosine kinases inhibitor. Tafetinib inhibitsstem cell factor receptor (Kit),vascular endothelial growth factor receptor-2 (VEGFR-2),platelet-derived growth factor receptor-β (PDGFR-β),glial cell line-derived neurotrophic factor receptor (Rearranged during Transfection; RET), andFms-like tyrosine kinase-3 (FLT3)withIC50values between 5.0 and 68.1 nmol/l. Tafetinib inhibits the phosphorylation ofPDGFR-βandVEGFR-2. Tafetinib inhibits endothelial cell proliferation, endothelial cells chemotaxis, and corneal angiogenesis[1].
Tarcocimab (OG1953) is a humanized anti-VEGFA monoclonal antibody (IgG1 type). Tarcocimab is available for research in retinal vein occlusion (RVO) and wet age-related macular degeneration (AMD).
Dilpacimab (ABT165) is a potent dual-variable domain immunoglobulin, targets both delta-like ligand 4 (DLL4) and VEGF pathways.. Dilpacimab can be used in research of cancer[1].
Vulinacimab (HLX-06) is an anti-VEGFR-2 monoclonal antibody (mAb). Vulinacimab can be used in the research of cancers. VEGFR-2, overexpressed in certain tumors, is critical in angiogenesis and the proliferation, survival, migration and differentiation of endothelial cells[1].
Regorafenib (BAY 73-4506) mesylate is an orally active and potent multi-targeted receptor tyrosine kinase inhibitor, with IC50 values of 13/4.2/46, 22, 7, 1.5 and 2.5 nM for VEGFR1/2/3, PDGFRβ, Kit, RET and Raf-1, respectively. Regorafenib mesylate shows very robust antitumor and antiangiogenic activity[1].
Coibamide A, an N-methyl-stabilized cytotoxic depsipeptide, shows potent antiproliferative activity. Coibamide A induces autophagosome accumulation via an mTOR-independent mechanism. Coibamide A induces apoptosis. Coibamide A inhibits VEGFA/VEGFR2 expression and suppresses tumor growth in glioblastoma xenografts[1][2].
Z-guggulsterone, a constituent of Indian Ayurvedic medicinal plant Commiphora mukul, inhibits the growth of human prostate cancer cells by causing apoptosis. Z-guggulsterone inhibits angiogenesis by suppressing the VEGF–VEGF-R2–Akt signaling axis[1].
TIE-2/VEGFR-2 kinase-IN-1 is used for the synthesis of TIE-2 and/or VEGFR-2 inhibitors, extracted from patent WO2003022852, example 14. TIE-2/VEGFR-2 kinase-IN-1 is used for the study of diseases associated with inappropriate angiogenesis[1].
TIE-2/VEGFR-2 kinase-IN-4, benzimidazole, is a potent TIE-2 and VEGFR-2 tyrosine kinase receptors inhibitors with IC50 values of 5.2 nM and 5.1 nM, respectively. TIE-2/VEGFR-2 kinase-IN-4 can be used for the research of angiogenesis[1].
Tinengotinib is the modulator of one or more protein kinases such as Aurora kinase and VEGFR kinase. Tinengotinib has the potential for the research of these kinase abnormalities diseases mediated, especially cancer-related diseases (extracted from patent WO2018108079A1)[1].
Takeda-6D (compound 6d) is an orally active and potent BRAF/VEGFR2 inhibitor, with IC50 values of 7.0 and 2.2 nM, respectively. Takeda-6D shows antiangiogenesis by suppressing the VEGFR2 pathway in 293/KDR and VEGF-stimulated HUVEC cells.Takeda-6D shows significant suppression of ERK1/2 phosphorylation. Takeda-6D shows antitumor activity[1].