Abstract
Two complementary PROTAC classesbenzimidazole-anchored degraders of LRRK2 and pyrrolopyridine-based scaffolds for tau and α-synuclein clearancedemonstrate subnanomolar degradation potency, improved SAR over phthalimide comparators, and translational positioning for Parkinson's disease and tauopathies. Together, they highlight the therapeutic convergence of chemically differentiated anchors and robust degradation assays in advancing CNS-targeted protein degradation modalities.