Interim Phase 2 Findings for Enrupatinib
Elixiron Immunotherapeutics (TPEx:7871) issued a press release on 11 June 2026 announcing interim results from its ongoing open‑label Phase 2 study of enrupatinib, an oral colony‑stimulating factor 1 receptor inhibitor intended to modulate microglial‑driven neuroinflammation in Alzheimer’s disease. The trial enrolled participants with mild‑to‑severe Alzheimer’s disease who received enrupatinib at a dose of 448.2 mg taken orally twice daily for a 28‑day treatment period. The study is financially supported by the Alzheimer’s Association through its Part the Cloud programme.
Safety Profile
Among the seven evaluable participants, the company reported no drug‑related serious adverse events and no clinically significant hepatotoxicity, a safety distinction the firm highlighted relative to earlier drugs in the same class.
Biomarker and Imaging Outcomes
In a biomarker‑defined subgroup, 80 % of participants achieved reductions exceeding 30 % in TSPO‑PET imaging signals across multiple brain regions, with a statistically significant reduction observed specifically in the Posterior Cingulate/Precuneus region. Across the broader PET‑evaluable population, 57 % of participants demonstrated reductions in neuroinflammation signals from baseline.
Cognitive Signal
One participant who exhibited a TSPO‑PET response also showed an 8‑point increase in Mini‑Mental State Examination (MMSE) score from baseline. The company emphasized that the study was not designed or powered to evaluate cognitive efficacy at this interim stage.
Future Development
Preliminary analyses identified a candidate predictive biomarker, and Elixiron plans to launch a placebo‑controlled study that will use this biomarker to select participants. The interim findings are based on a limited number of subjects; the company cautioned that final results may differ and provided no assurance that the observed findings will be replicated in larger studies.
Drug Mechanism
Enrupatinib is described as an investigational oral inhibitor of colony‑stimulating factor 1 receptor, aimed at reducing microglial‑driven neuroinflammation, a hypothesised driver of Alzheimer’s pathology.