Our Alzheimer’s program (OLX07010) is a small molecule inhibitor of tau self-association which has demonstrated in vivo efficacy in two transgenic mouse models of tauopathy, htau and JNPL3, representing tau aggregation in AD and inherited tauopathies, respectively.
The mice were treated using a prevention paradigm and the recently published htau study demonstrated reduction of insoluble tau with statistical significance (Davidowitz EJ et al., 2020). A similar preventive study was performed using the JNPL3 mice in which mutated tau is more prone to misfold and aggregate and develop tau pathology more aggressively than what is observed in non-mutated tau. Even so, OLX07010 showed similar results to our studies in htau (manuscript in preparation)
Therapeutic studies dosed JNPL3 mice for five months (from 7 to 12 months of age) and showed similar results as our studies in preventive paradigm (manuscript in preparation)
The activity in these two models translated from in vitro and cellular assays to an in vivo model of tau aggregation validating our screening approach and showing that targeting tau-self association can inhibit the entire tau aggregation pathway.
Our lead program is poised to transition into Phase 1.
As an oral, small molecule targeting tau-self association (the beginning stages of the tau aggregation cascade), OLX-07010 has the potential to be easily administered to improve patient compliance, accessible on a global scale and manufactured at lower costs compared to other approaches. Additionally, OLX-07010 could complement both tau and beta-amyloid antibody treatment.
