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Mechanistically, PYC inhibits NF-B activation, leading to decreased transcription of pro-inflammatory mediators such as TNF-, ICAM-1, and vascular cell adhesion molecule-1, thereby modulating cytokine-driven inflammatory responses and endothelial activation ( Network pharmacology and protein-protein interaction analyses have identified IL-6, TNF, IL-1B, prostaglandin endoperoxide synthase 2, and NF-B1 as core molecular targets of PYC, with Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment highlighting the IL-17 and TNF signaling pathways as key anti-inflammatory mechanisms

Timing Optional Monitoring guidance is pathway-based, with copper and liver context added for repeated systemic exposure discussions

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Although ponatinib is an FDA-approved TKI that directly targets T315I-Bcr-Abl leukemia, its association with cardiovascular toxicity is a significant concern in clinical therapy

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