摘要:
The invention is directed to a method of prophylactically or therapeutically treating choroidal neovascularization, wherein the method comprises directly administering to the eye a therapeutic factor or a nucleic acid sequence that encodes a therapeutic factor, which he expressed to produce the therapeutic factor, to selectively induce apoptosis of endothelial cells associated with neovascularization of the choroid such that choroidal neovascularization is treated prophylactically or therapeutically. The invention also provides a method of prophylactically or therapeutically treating ocular neovascularization, wherein the method comprises directly administering to the eye a nucleic acid sequence encoding a therapeutic factor to promote apoptosis of endothelial cells associated with neovascularization, such that the nucleic acid is expressed thereby producing the therapeutic factor to treat ocular neovascularization prophylactically or therapeutically.
摘要:
The invention is directed to a method of prophylactically or therapeutically treating choroidal neovascularization, wherein the method comprises directly administering to the eye a therapeutic factor or a nucleic acid sequence that encodes a therapeutic factor, which he expressed to produce the therapeutic factor, to selectively induce apoptosis of endothelial cells associated with neovascularization of the choroid such that choroidal neovascularization is treated prophylactically or therapeutically. The invention also provides a method of prophylactically or therapeutically treating ocular neovascularization, wherein the method comprises directly administering to the eye a nucleic acid sequence encoding a therapeutic factor to promote apoptosis of endothelial cells associated with neovascularization, such that the nucleic acid is expressed thereby producing the therapeutic factor to treat ocular neovascularization prophylactically or therapeutically.
摘要:
Proliferation of retinal pigment epithelium following surgery or trauma or resulting in ocular diseases associated with choroidal neovascularization, such as age related macular degeneration and histoplasmosis syndrome, is prevented by contacting retinal pigment epithelium cells with a therapeutic amount of a retinoic acid receptor (RAR agonist, preferably one with specific activity for retinoic acid receptors. Preferably the RAR agonist is also a potent antagonist of AP1-dependent gene expression. Alternatively, the proliferation of retinal pigment epithelium is ameliorated with a therapeutic amount of an AP-1 antagonist, alone or in combination with an RAR agonist. The drug can be administered by bolus injection into the vitreous cavity using a dosage from about 50 to 150 &mgr;g. Or by slow release from liposomes or an oil tamponade injected into the vitreous cavity. Formulations for preventing proliferation of retinal pigment epithelium are also provided.
摘要:
The invention provides for therapeutic compositions as well as a method of blocking blood vessel growth, a method of promoting neovascularization, a method of promoting the growth or differentiation of a cell expressing the TIE-2 receptor, a method of blocking the growth or differentiation of a cell expressing the TIE-2 receptor and a method of attenuating or preventing tumor growth in a human.
摘要:
Proliferation of retinal pigment epithelium following surgery or trauma or resulting in ocular diseases associated with choroidal neovascularization, such as age related macular degeneration and histoplasmosis syndrome, is prevented by contacting retinal pigment epithelium cells with a therapeutic amount of a retinoic acid receptor (RAR agonist, preferably one with specific activity for retinoic acid receptors. Preferably the RAR agonist is also a potent antagonist of AP1-dependent gene expression. Alternatively, the proliferation of retinal pigment epithelium is ameliorated with a therapeutic amount of an AP-1 antagonist, alone or in combination with an RAR agonist. The drug can be administered by bolus injection into the vitreous cavity using a dosage from about 50 to 150 .mu.g. Or by slow release from liposomes or an oil tamponade injected into the vitreous cavity. Formulations for preventing proliferation of retinal pigment epithelium are also provided.
摘要:
Transgenic mammals are provided which develop neovascularization of the retina, similar to that found in a variety of disease states, including diabetes, age related macular degeneration, retinopathy of prematurity, sickle cell retinopathy. These mammals can be used as test systems to evaluate potential prophylactic and therapeutic regimens. The effect of a regimen on the neovascularization is indicative of its beneficial effect in a disease state which is associated with neovascularization.
摘要:
Proliferation of retinal pigment epithelium following surgery or trauma is prevented by contacting retinal pigment epithelium cells with a therapeutic amount of a retinoic acid receptor (RAR) agonist, preferably one with specific activity for retinoic acid receptors. Preferably the RAR agonist is also a potent antagonist of AP1-dependent gene expression. Alternatively, the proliferation of retinal pigment epitelium is ameliorated witha therapeutic amount of an AP-1 antagonist, alone or in combination with an RAR agonist. The drug can be administered by bolus injection into the vitreous cavity using a dosage from about 50 to 150 .mu.g, or by slow release from liposomes or an oil tamponade injected into the vitreous cavity. Formulations for preventing proliferation of retinal pigment epithelium are also provided.
摘要:
Proliferation of retinal pigment epithelium following surgery or trauma or resulting in ocular diseases associated with choroidal neovascularization, such as age related macular degeneration and histoplasmosis syndrome, is prevented by contacting retinal pigment epithelium cells with a therapeutic amount of a retinoic acid receptor (RAR agonist, preferably one with specific activity for retinoic acid receptors. Preferably the RAR agonist is also a potent antagonist of AP1-dependent gene expression. Alternatively, the proliferation of retinal pigment epithelium is ameliorated with a therapeutic amount of an AP-1 antagonist, alone or in combination with an RAR agonist. The drug can be administered by bolus injection into the vitreous cavity using a dosage from about 50 to 150 &mgr;g. Or by slow release from liposomes or an oil tamponade injected into the vitreous cavity. Formulations for preventing proliferation of retinal pigment epithelium are also provided.
摘要:
Oxidative damage contributes to cone cell death in retinitis pigmentosa and death of rods, cones, and retinal pigmented epithelial (RPE) cells in ocular oxidative stress related diseases including age-related macular degeneration and retinitis pigmentosa. Oral antioxidants may provide modest benefits, but more efficient ways of preventing oxidative damage are needed. Compositions and methods are provided herein for the prevention, amelioration, and/or treatment of early or late stage ocular disease by increasing the expression or activity of one or more peroxidases in cells of the eye, particularly retinal cells, and further optionally increasing the expression or activity of one or more superoxide dismuatases in the same cells.
摘要:
A method for treating a subject suffering from epiretinal membrane formation or retinal detachment due to epiretinal membrane formation is disclosed. The method comprises administering a compound of the formula: wherein n is 0 to 2, R is H or lower alkyl; X is imino, oxa, or thia; Y is aryl; and Z is unsubstituted or substituted pyridyl, an N-oxide thereof, wherein 1 or more N atoms carry an oxygen atom, or a salt thereof.