L-aspartic acid beta-hydroxamate for choroidal neovascularization
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Solution Overview
Problem
Current treatments for choroidal neovascularization, such as repeated intravitreal injections of anti-VEGF antibodies, lead to severe side effects like retinal and choroidal atrophy, retinal detachment, and intraocular infection, necessitating a more effective therapeutic approach.
Innovation Solution
Intravenous administration of L-aspartic acid β-hydroxamate to inhibit the production of VEGF and MCP-1 by RPE, mediated by TNFα, thereby inhibiting choroidal neovascularization without the severe side effects associated with anti-VEGF antibodies.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If repeated intravitreal injections of anti-VEGF antibodies are used to treat choroidal neovascularization, then the therapeutic effect is improved, but severe side effects occur including retinal and choroidal atrophy, retinal detachment, and intraocular infection
Solution Approach 1:
The patent uses L-aspartic acid beta-hydroxamate as an intermediary substance that blocks the interaction between VEGF and its receptor VEGR2. Instead of directly injecting antibodies into the vitreous humor, the compound is administered systemically (intravenously or orally) to achieve the same therapeutic goal of inhibiting VEGF signaling, thereby reducing choroidal neovascularization without the severe local side effects of intravitreal injections
Solution Approach 2:
The patent replaces the mechanical injection method (intravitreal injection requiring needle puncture) with systemic administration (intravenous or oral). This substitution eliminates the mechanical trauma to the eye, preventing retinal detachment and intraocular infection while maintaining the pharmacological effect of VEGF inhibition through systemic circulation to the retina
2Manufacturing precision
If intravitreal injection is used to deliver anti-VEGF antibodies, then the drug reaches the target effectively, but the risk of intraocular infection and retinal detachment increases
Solution Approach 1:
The patent employs L-aspartic acid beta-hydroxamate as a mediator that can be delivered systemically to reach the retinal target. This intermediary approach allows the drug to traverse the blood-retina barrier and reach the choroidal neovascularization site without requiring direct intraocular injection, thus eliminating the associated infection and detachment risks
Solution Approach 2:
The patent extracts the essential therapeutic function (VEGF inhibition) from the specific delivery method (intravitreal injection). By separating the pharmacological action from the invasive delivery route, the invention achieves the same therapeutic outcome through non-invasive systemic administration, removing the harmful aspects of the original delivery method
Data Source
AI summary
A method of inhibiting or treating choroidal neovascularization, wherein the method comprises administering an injectable preparation of L-aspartic acid β-hydroxamate to a patient suffering from choroidal neovascularization, including injecting a first dosage that is 6 mg/kg by weight of the treated subject, and injecting a second dosage that is 3 mg/kg.