Alzheimer's Disease is a devastating global health crisis affecting over 50 million people, with cases projected to double by 2050 without a medical breakthrough. The disease is driven by a complex pathological cascade, including the buildup of amyloid-β and tau proteins, which leads to inflammation, synaptic dysfunction, and irreversible neurodegeneration.
Built on greater understanding of Alzheimer’s Disease pathology our lead candidate RN-077 is a small molecule therapy that targets both amyloid-β and tau pathologies simultaneously. It does this by inhibiting a key kinase implicated in multiple disease mechanisms and demonstrated to ameliorate learning and memory deficits in animal models. This differentiated mechanism has been shown in preclinical models to not only reduce the hallmark tau and amyloid-β pathologies but also to modulate inflammation and synaptic dysfunction.
By intervening at this early, pivotal point in the disease cascade, RN-077 offers a rare opportunity to modify disease at its roots, not just manage symptoms for a truly disease-modifying therapy, a significant departure from single-target, downstream treatments.
Preclinical candidate RN-077 nominated based on:
Excellent Oral Drug-like Properties
First-in-Class Potential
Excellent Selectivity
Dose Dependent Inhibition of Tau Phosphorylation