Abstract

Kojin Therapeutics has launched with $60 million to develop drugs that exploit the plasticity of cells, and in particular their tendency to become vulnerable to an iron-dependent process called ferroptosis. Common wisdom in the field of oncology holds that when a drug stops working it’s because tumor cells have mutated to evade it. But cancers have other sneaky ways of resisting our pharmacopeia, one of which is morphing into a state in which they’re vulnerable to a different kind of cell death. All our current oncology drugs push tumors to their demise through a process called apoptosis, but some cancer cells alter their gene expression to become reliant on ferroptosis, explains Stuart Schreiber , cofounder of Kojin and a chemical biologist at Harvard University and Broad Institute of MIT and Harvard. “Every cell in our body also has an inherent plasticity, an ability to switch,” Schreiber says. That switch is

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