New Drug Turns Cancer’s Sugar Hunger Into Its Achilles’ Heel
UT Austin researchers report a two-part drug that forces cancer cells to burn more sugar while blocking their fatty-acid energy source, killing many cancer cells in mice and in several human cancer cell lines. The compound binds the glycolysis enzyme PFKL to accelerate sugar use and then releases a second payload that inhibits CPT2, disrupting fatty acid metabolism. This covalent “electrophile-drug conjugate” approach could be easier to manufacture than antibody-drug conjugates, with potential applicability beyond cancer, but human testing remains years away.