dACSL4

dACSL4: sourced facts only. name: "dACSL4 selectively degrades acyl-CoA synthetase long-chain family member 4 (ACSL4) while concurrently activating peroxisome proliferator-activated receptor γ (PPARγ), thereby coordinating lipid metabolism and oxidative stress to suppress neuronal ferroptosis." [PMID:42480533]; target: "dACSL4 selectively degrades acyl-CoA synthetase long-chain family member 4 (ACSL4) while concurrently activating peroxisome proliferator-activated receptor γ (PPARγ), thereby coordinating lipid metabolism and oxidative stress to suppress neuronal ferroptosis." [PMID:42480533]; developer: "Beijing National Laboratory for Molecular Science, CAS Key Laboratory of Analytical Chemistry for Living Biosystems, Institute of Chemistry, Chinese Academy of Sciences, Beijing 100190, China; University of Chinese Academy of Sciences, Beijing 100049, China." [PMID:42480533]; modality: "Herein, we report a dual-function PROTAC, dACSL4, and its nose-to-brain delivery for brain-preferred protein degradation and therapeutic suppression of ferroptosis in neurodegeneration." [PMID:42480533]; stage: "Intranasal delivery of dACSL4 using biodegradable lipid nanoparticles (BAmP-TK12) enabled brain-preferred ACSL4 degradation and PPARγ activation, reducing lipid peroxidation and preserving dopaminergic neurons in a Parkinson's disease model, ultimately improving motor function." [PMID:42480533]