Pronounced tumour cell abnormalities underscore their potential as anticancer drugs, with Nassar and El-Sayed highlighting the critical role of the 1,3,4-thiadiazole nucleus.52 Docking studies revealed that 56b binds thymidine phosphorylase (TP) or EGFR (Kd ∼ 2–5 μM) with β-d-glucose, forming H-bonds (for example, His85 and Lys721) and a furfuryl-oxadiazole core, enabling π–π stacking with Phe210 or Tyr residues. The gene discussed is TYMP; the disease is neoplasm.