2) The binding of ivonescimab to PD-1 reciprocally augments its affinity for VEGF, by effectively sequestering VEGF-A and VEGF-B, ivonescimab inhibits their interaction with VEGFR, and this inhibition disrupts the downstream PI3K/AKT/mTOR signaling cascade, suppressing the proliferation of tumor cells and vascular endothelial cells, and attenuating neovascularization. Here, KDR is linked to neoplasm.