Adel-Y01
ADEL-Y01 is an anti-Tau mAb (monoclonal antibody) that selectively targets disease-specific pathological tau, rather than normal tau, using the acetylated K280 (acK280) epitope.
DEVELOPMENT STAGE
Phase 1b — Completed in patients with early-stage AD
Commercialized
AT A GLANCE
Target
pathological Tau
Disease-specific pathological tau
INDICATION
Alzheimer’s disease
Early-stage AD, including MCI due to AD and mild AD dementia
MODALITY
mAb
Targets pathological tau via the acK280 epitope
Pathological tau remains a key therapeutic gap beyond amyloid
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by worsening memory and cognitive function. Recently approved anti-amyloid antibodies have introduced disease-modifying treatment for early AD by reducing amyloid burden and slowing clinical decline. However, these therapies do not stop disease progression, require careful patient selection and monitoring, and primarily address amyloid pathology. Tau pathology is more closely linked to neuronal dysfunction, disease stage, and cognitive decline, highlighting tau as an important complementary therapeutic target. Acetylation of tau at lysine 280 (acK280) is associated with pathological tau aggregation, seeding, and intercellular propagation, providing a rationale for selectively targeting disease-associated tau species. There remains a significant unmet need for therapies that can selectively disrupt pathogenic tau propagation while minimizing interaction with physiological tau.
Selective targeting of acK280-modified pathological tau
ADEL-Y01 differentiates itself from other tau antibodies under development by selectively targeting disease-specific pathological tau, rather than normal tau, through the acetylated K280 (acK280) epitope. This disease-selective approach is designed to minimize unnecessary engagement of normal tau while focusing antibody activity on tau species associated with pathological seeding and propagation. By binding extracellular acK280-containing tau, ADEL-Y01 is designed to neutralize seeding-competent tau, limit its aggregation and spread between neurons, and promote the uptake and clearance of antibody-bound pathological tau by microglia. ADEL-Y01 demonstrated superior inhibition of tau aggregation compared with competing programs targeting normal tau. Moreover, unlike approved anti-amyloid antibodies, which primarily target amyloid pathology important for disease initiation, anti-tau antibodies directly address tau accumulation, which is more closely correlated with clinical symptoms, and may therefore offer a more direct approach to slowing tau-driven disease progression.
Co-developed with ADEL - Licensed to SANOFI
Exclusive global license · December 2025
