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CIL56 (also known as CIL-56) is a small molecule inducer of ferroptosis, a form of regulated, iron-dependent non-apoptotic cell death. Identified through high-throughput screening, CIL56 is distinguished from other ferroptosis inducers (such as erastin or RSL3) by its specific dependency on the activity of the lipid biosynthetic enzyme acetyl-CoA carboxylase 1 (ACC1). The compound promotes the accumulation of lethal lipid peroxides, a process that requires functional fatty acid synthesis pathways to provide the substrates for lipid peroxidation. Recent research has explored CIL56 as a potential therapeutic agent for glioblastoma (GBM), particularly in overcoming resistance to standard-of-care apoptosis-inducing therapies. Studies indicate that bone morphogenic protein (BMP) signaling can sensitize GBM cells to CIL56-induced ferroptosis, suggesting a novel combinatorial approach for treating aggressive, treatment-resistant brain tumors.
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