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Summit Therapeutics just slapped the face of Keytruda

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Summit's drug ivonescimab is a PD-1/VEGF inhibitor. PD-1 and VEGF inhibition (downregulates angiogenesis) would definitely be better than PD-1 alone. Their recent trial was for EGFR-mutated nonsquamous non-small cell lung cancer. Keytruda's trial in the same indication showed no statistically significant improvement. Which is no surprise since no PD1/PD-L1 inhibitor has shown improvement in the EGFR variant. So certainly ivonescimab's very good improvement* is due to the VEGF side of the drug. Leronlimab downregulates PD-L1 and VEGF and EGF/EGFR and so much more than ivonescimab so you have to wonder what leronlimab's progression free survival would be.

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Leronlimab's MOAs for cancer - Leronlimab elicits an NKT cell response - promoting tumor cell death , upregulates CD8+ T cells, Inhibits angiogenesis, shuts down cancer reappearing through collagen downregulation, Stops the recruitment of Tregs to tumor sites (Tregs promote tumor immunity), inhibits tumor cell dna repair via GRP78 downregulation, inhibits IL-13 a tumor protectant, downregulates IL-4 (IL-4 promotes tumor immunity), upregulates IFN-gamma promoting tumor cell death, downregulates PD-1 -PD-L1's receptor, polarization of macrophages - promoting tumor cell death , downregulates calcium channel signaling, blocks CCL5 shutting down pathways for CTCs and downregulates EGF/EGFRs .

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*The PFS showed significant improvements in patients receiving ivonescimab plus chemotherapy (hazard ratio [HR], 0.46; P<.0001), with a median PFS per IRRC of 7.06 months in the patients receiving ivonescimab plus chemotherapy, compared with a median PFS of 4.80 months in those receiving chemotherapy plus placebo.https://docwirenews.com/post/investigators-pr...ni-a-trial

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