Neurimmune expands collaboration with AstraZeneca to develop and commercialize fibril depleter NI009 for AL amyloidosis
ZURICH, Dec. 4, 2025 /PRNewswire/ -- Neurimmune today announced that it has expanded on its transthyretin amyloid cardiomyopathy (ATTR-CM) collaboration with Alexion, AstraZeneca Rare Disease by entering into an exclusive global collaboration and license agreement to develop NI009, a preclinical human monoclonal antibody designed to target and deplete lambda light chain fibrils and deposits from affected tissues and organs in light chain (AL) amyloidosis.
Neurimmune is a clinical stage biopharmaceutical company building next generation therapeutics to address protein aggregation diseases with extensive experience in amyloid depletion. The collaboration stands to leverage Alexion's expertise in AL amyloidosis and strengths in late-stage rare disease drug development and expands upon the two companies' existing Phase III development of cliramitug, an investigational human monoclonal antibody designed to deplete amyloid deposits in ATTR-CM.
"We are very pleased to build upon our collaboration with Alexion by adding this targeted fibril depleter program in AL amyloidosis. By leveraging our expertise in designing therapeutics that trigger immune-mediated clearance of disease-causing protein aggregates, we have developed a novel antibody that can, potentially, efficiently deplete amyloid light chain deposits. NI009 exhibits broad activity against amyloids of diverse lambda light chain subtypes across patients despite the high clonal heterogeneity of the disease," said Roger M. Nitsch, President & CEO of Neurimmune.
"This announcement follows the high-level results from Alexion's CARES Phase III clinical program which demonstrated anselamimab's potential as a first-in-class fibril depleter to improve survival and cardiac outcomes in patients living with advanced AL-kappa amyloidosis, a debilitating progressive rare disease. In expanding our collaboration with Neurimmune, we aim to apply key learnings from the CARES program to develop NI009 as a complementary fibril depleter to potentially benefit more patients living with AL amyloidosis," said Gianluca Pirozzi, SVP, Head of Development, Regulatory and Safety, Alexion.
AL amyloidosis is a rare, systemic and progressive disorder caused by defective plasma cells in the bone marrow. In AL amyloidosis, abnormal kappa (κ) or lambda (λ) light chain proteins produced by these plasma cells misfold, aggregate and form amyloid fibrils that deposit in tissues and organs. Left untreated, the accumulation of these toxic amyloid deposits, particularly in the heart and kidneys, can cause progressive organ damage and dysfunction and may lead to premature death, most commonly due to cardiac failure.
Under the agreement, Alexion will be granted an exclusive, worldwide license to research, develop, manufacture and commercialize Neurimmune's antibodies targeting amyloid light chains. The lead candidate NI009 is currently in advanced preclinical development. Neurimmune will receive an undisclosed upfront payment and potential additional contingent milestone payments of up to $780 million payable upon achievement of certain development, regulatory and commercial milestones, as well as tiered royalties on net sales of any approved medicine resulting from the collaboration. Neurimmune will continue to be responsible for preclinical development, initial manufacturing activities and conducting the first-in-human clinical study. Alexion will be responsible for further clinical development, manufacturing, and commercialization.
About Neurimmune
Neurimmune is a clinical-stage biopharmaceutical company building next generation antibody therapeutics. The company pioneers amyloid depletion as a novel therapeutic mechanism to treat CNS and related protein aggregation diseases including Alzheimer's disease, amyotrophic lateral sclerosis and ATTR cardiomyopathy. Neurimmune discovered the anti-ATTR antibody cliramitug (formerly NI006, ALXN2220, Phase 3) for ATTR cardiomyopathy, the anti-misfolded SOD1 antibody AP-101 (Phase 2) for ALS, the anti-NogoA antibody NG004 (Phase 1) for spinal cord injury and the anti-amyloid light chain antibody NI009 (preclinical) for AL amyloidosis.
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SOURCE Neurimmune
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