Experimental treatment reduces toxic heart protein in ATTR-CM trial

Long-term treatment with the experimental therapy candidate cliramitug safely and effectively reduces toxic clumps of the transthyretin (TTR) protein and heart damage markers in adults with transthyretin amyloid cardiomyopathy (ATTR-CM).

That’s according to nearly three years of data from the Phase 1 NI006-101 clinical trial (NCT04360434), which confirmed the therapy’s favorable safety and efficacy profiles seen in the study’s first year. Cliramitug works by binding to toxic TTR aggregates — the underlying cause of ATTR-CM — and marking them for destruction.