Gal1 Interaction Modulation for Anti-VEGF Refractory Cancer
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Solution Overview
Problem
Current anti-VEGF treatments are ineffective for tumors that are refractory, as they fail to inhibit angiogenesis due to compensatory pathways, leading to enduring clinical benefits for only some patients.
Innovation Solution
Modulating angiogenesis in refractory cancers by using agents that interact with Gal1 or its fragments to inhibit the interaction between Gal1 and its natural binding partners, such as antibodies or glycan-related compounds, to block angiogenic signaling pathways.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If anti-VEGF treatments are used to inhibit angiogenesis, then tumor growth is suppressed in responsive tumors, but the treatment becomes ineffective in refractory tumors due to compensatory pathways
Solution Approach 1:
The patent segments the anti-angiogenic approach by identifying and targeting specific compensatory pathways (such as FGF, PDGF, and other non-VEGF pathways) that become active when VEGF is blocked. This allows for pathway-specific interventions rather than a single broad anti-VEGF approach, thereby improving treatment reliability across different tumor types and stages of resistance.
Solution Approach 2:
The patent develops multi-functional therapeutic strategies that can target multiple angiogenic pathways simultaneously or sequentially. By creating treatments that address both VEGF-dependent and VEGF-independent pathways, the therapy becomes universally applicable to both responsive and refractory tumors, reducing the variability in tumor response.
2Duration of action of moving object
If VEGF-targeted therapies are administered, then progression-free survival is improved in some cancers, but enduring clinical benefits are limited due to development of resistance
Solution Approach 1:
The patent employs preliminary action by identifying tumor characteristics and compensatory pathway activation early in the treatment course. By detecting markers of potential resistance or active compensatory pathways before complete treatment failure occurs, clinicians can switch to or combine with alternative therapies preemptively, thereby extending progression-free survival and maintaining enduring clinical benefits.
Solution Approach 2:
The patent ensures continuity of useful action by designing treatment regimens that maintain anti-angiogenic pressure through multiple mechanisms. By combining VEGF inhibition with blockers of compensatory pathways (such as FGF receptors, PDGF receptors), the therapy continuously suppresses angiogenesis without allowing tumors to escape through alternative routes, thus prolonging the duration of clinical benefit.
Data Source
AI summary
A method for modulating angiogenesis in a cancer or tumor refractory to anti-VEGF, including identifying a cancer cell as being referactory to anti-VEGF, and then contacting the cancer cell refractory to anti-VEGF with an effective amount of an agent that modulates interaction between Gal1 or a Gal1 fragment and the natural binding partner of Gal1 or the Gal1 fragment to thereby modulate angiogenesis.