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Cliramitug is an investigational, fully human recombinant monoclonal antibody that selectively targets misfolded and fibrillar transthyretin (TTR) deposits in transthyretin amyloid cardiomyopathy (ATTR-CM), promoting immune-mediated clearance of cardiac amyloid and subsequent improvement in cardiac structure and function.[3][10][13][16] Discovered by Neurimmune and being co-developed with Alexion AstraZeneca Rare Disease, cliramitug (formerly NI006, ALXN2220) is administered by intravenous infusion and is in Phase 3 clinical development (DepleTTR-CM, NCT06183931) following Phase 1 data showing favorable safety, tolerability, and signals of cardiac benefit in patients with wild-type and variant ATTR-CM.[2][5][10][11][13][16] Its mechanism is based on high-affinity binding to TTR amyloid fibrils in the myocardium, engaging phagocytic immune cells to deplete pathogenic deposits without directly altering native TTR production, positioning it as a fibril-depleting complement to TTR stabilizers and silencers in systemic ATTR therapies.[3][10][13][16]
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