corneal neovascularization/tyrosine

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Inhibitory effects of SU5416, a selective vascular endothelial growth factor receptor tyrosine kinase inhibitor, on experimental corneal neovascularization.

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OBJECTIVE Treatment of neovascularization in ocular diseases with vascular endothelial growth factor (VEGF) inhibition shows promising results. SU5416 is a low-molecular-weight tyrosine kinase inhibitor. It selectively inhibits the membrane-bound tyrosine kinase activity of VEGF-2 receptor

Role of protein tyrosine phosphorylation in rat corneal neovascularization.

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BACKGROUND Recent studies have suggested that tyrosine kinase pathways that are activated by angiogenic growth factors may play a role in corneal neovascularization. METHODS Corneal neovascularization was induced in rat corneas by chemical cauterization. At 6, 24, 48, 96, and 168 h after chemical

Inhibitory effects of regorafenib, a multiple tyrosine kinase inhibitor, on corneal neovascularization.

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OBJECTIVE To evaluate the inhibitory effects of regorafenib (BAY 73-4506), a multikinase inhibitor, on corneal neovascularization (NV). METHODS Thirty adult male Sprague-Dawley rats weighing 250-300 g, were used. Corneal NV was induced by NaOH in the left eyes of each rat. Following the

Preclinical activity of ABT-869, a multitargeted receptor tyrosine kinase inhibitor.

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ABT-869 is a structurally novel, receptor tyrosine kinase (RTK) inhibitor that is a potent inhibitor of members of the vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) receptor families (e.g., KDR IC50 = 4 nmol/L) but has much less activity (IC50s > 1 micromol/L)

Pharmacological Potential of Small Molecules for Treating Corneal Neovascularization

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Under healthy conditions, the cornea is an avascular structure which allows for transparency and optimal visual acuity. Its avascular nature is maintained by a balance of proangiogenic and antiangiogenic factors. An imbalance of these factors can result in abnormal blood vessel proliferation into

TLR9 agonist regulates angiogenesis and inhibits corneal neovascularization.

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Myeloid cells are highly adaptable and may positively or negatively regulate angiogenesis dependent on the cognate and soluble signals they receive. Toll-like receptors (TLRs) initiate immune responses, orchestrate adaptive immune responses, and regulate vascular endothelial growth factor

Src tyrosine kinase inhibition suppresses lymphangiogenesis in vitro and in vivo.

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OBJECTIVE The close association of lymphatic and blood vessels and their coordinated development in vivo suggest that there are parallel mechanisms regulating hemangiogenesis and lymphangiogenesis. Here, we hypothesize that inhibition of the Src tyrosine kinase, apart from anti-hemangiogenic

Proangiogenic role of ephrinB1/EphB1 in basic fibroblast growth factor-induced corneal angiogenesis.

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Corneal neovascularization is a vision-threatening condition caused by various ocular pathological conditions. The aim of this study was to evaluate the function of the ephrin ligands and Eph receptors in vitro and in vivo in corneal angiogenesis in a mouse model. The Eph tyrosine kinase receptors

Comparison of the Effects of Dovitinib and Bevacizumab on Reducing Neovascularization in an Experimental Rat Corneal Neovascularization Model.

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To compare the inhibitory effects of dovitinib and bevacizumab for treatment of corneal neovascularization (CNV).Thirty-nine adult female Sprague Dawley rats weighing 180 to 250 g were used. CNV was induced by silver nitrate in the right eye of each rat.

Corneal neovascularization: an anti-VEGF therapy review.

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Corneal neovascularization is a serious condition that can lead to a profound decline in vision. The abnormal vessels block light, cause corneal scarring, compromise visual acuity, and may lead to inflammation and edema. Corneal neovascularization occurs when the balance between angiogenic and

Development of Mucoadhesive Cationic Polypeptide Micelles for Sustained Cabozantinib Release and Inhibition of Corneal Neovascularization

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Corneal neovascularization (CNV) is one of the leading risk factors for vision loss. Anti-angiogenic drugs can theoretically be extended to the treatment of CNV. However, the application of these drugs is often hindered by traditional administration methods, e.g., eye drops, which is ascribed to the

Sunitinib malate-loaded biodegradable microspheres for the prevention of corneal neovascularization in rats

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Corneal neovascularization (NV) predisposes patients to compromised corneal transparency and visional acuity. Sunitinib malate (Sunb-malate) targeting against multiple receptor tyrosine kinases, exerts potent antiangiogenesis. However, the rapid clearance of Sunb-malate eye drops administered

Preclinical anti-angiogenesis and anti-tumor activity of SIM010603, an oral, multi-targets receptor tyrosine kinases inhibitor.

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OBJECTIVE SIM010603 is a structurally novel, oral, multi-targeted receptor tyrosine kinase inhibitor. This study investigated the anti-angiogenic and anti-tumor effects of SIM010603. METHODS A radiometric protein kinase assay was used for measuring the kinase activity of the 32 protein kinases.

Pharmacological characterization of CP-547,632, a novel vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for cancer therapy.

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Signaling through vascular endothelial growth factor (VEGF) receptors (VEGFRs) is a key pathway initiating endothelial cell proliferation and migration resulting in angiogenesis, a requirement for human tumor growth and metastasis. Abrogation of signaling through VEGFR by a variety of approaches has

Topical axitinib is a potent inhibitor of corneal neovascularization.

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BACKGROUND This study evaluated the effects of topically applied axitinib, a tyrosine kinase inhibitor, in an experimental model of corneal neovascularization (CNV). METHODS A total of 48 New Zealand rabbits were used. CNV was induced by placing five silk sutures in the upper cornea of one eye per

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