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In normal physiology, the majority of circulating IGF-1 is bound to IGFBP-3, forming a large ternary complex with the acid-labile subunit that prevents rapid clearance and buffers free IGF-1 within a tightly controlled range

Malaria infection , particularly with Plasmodium falciparum, compromises RBC deformability through multiple mechanisms, including parasite digestion of hemoglobin and oxidative damage to cell membranes [2]

A key supporting study was retracted due to data fabrication, and the related prodrug fosgonimeton saw adverse events in clinical trials