Leucine Rich Repeat Kinase 2 (LRRK2) is one of the most promising targets for Parkinson’s Disease. LRRK2 targeting strategies have primarily focused on Type 1 kinase inhibitors, which however have limitations as the inhibited protein can interfere with natural mechanisms and lead to undesirable side effects. Herein, we report the development of LRRK2 Proteolysis Targeting Chimeras (PROTACs), culminating in the discovery of degrader XL01126, as an alternative LRRK2 targeting strategy XL01126 induces degradation of LRRK2 by 80-90% in wildtype (WT) mouse embryonic fibroblasts (MEFs), G2019S LRRK2 MEFs, R1441C LRRK2 MEFs, bone barrow-derived macrophages, and human peripheral blood mononuclear cells (PBMCs) with DC50s consistently within 15-72 nM, and degradation half-lives of 0.6-2.4 h. XL01126 forms a positively cooperative ternary complex with VHL and LRRK2 (α=5.7), which compensates for a substantial loss of binary binding affinities to VHL and LRRK2, underscoring its strong degradation performance in cells. Remarkably, XL01126 is orally bioavailable (F=15%) and can penetrate the blood brain barrier after either oral or parenteral dosing in mice. Taken together, these experiments qualify XL01126 as a suitable degrader probe to study non-catalytic and scaffolding functions of LRRK2 in vitro and in vivo and offer an attractive starting point for future drug development.