Mechanism

VEGF-A / FGF-2 (dual blockade)

Assets acting on this target.

Class
Recombinant chimeric decoy-receptor trap fusion protein (bispecific VEGF/FGF-2 blocker)
Pathway
VEGF/VEGFR and FGF/FGFR angiogenic signaling

VEGF-A (vascular endothelial growth factor A) and FGF-2 (basic fibroblast growth factor) are signaling proteins that drive angiogenesis, the growth of new blood vessels from existing ones. Both work by binding receptors on the surface of endothelial cells lining blood vessels, triggering proliferation, migration, and vessel formation. In many diseases, excessive or poorly regulated angiogenesis contributes to pathology, most notably in neovascular eye diseases such as wet age-related macular degeneration and diabetic eye disease, where abnormal, leaky vessels can grow into the retina or vitreous and cause vision loss. Blocking VEGF-A alone is an established strategy, but tumors and diseased tissue can partially compensate by upregulating alternative angiogenic drivers, including FGF-2, sustaining vessel growth despite VEGF suppression. A dual blockade approach uses a single engineered molecule, a decoy-receptor fusion protein, that presents receptor fragments capable of capturing both VEGF-A and FGF-2 before they reach their natural receptors. The rationale is that neutralizing two independent but converging angiogenic pathways simultaneously may produce a more complete and durable suppression of pathological vessel growth than targeting either factor alone, addressing a known limitation of single-pathway inhibition.

Research

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