Neurimmune today announced that three poster presentations related to ALXN2220 (formerly NI006) for the treatment of transthyretin amyloid cardiomyopathy (ATTR-CM) will be presented by Neurimmune, our partners Alexion, AstraZeneca Rare Disease and our clinical investigators in Rochester, Minnesota at the XIX International Symposium on Amyloidosis, a scientific congress of the International Society of Amyloidosis (ISA).
ALXN2220 is an investigational human monoclonal antibody designed to deplete amyloid deposits in ATTR-CM as add-on to standard of care.1,2 High-resolution live-cell imaging data presented will offer new insight into the underlying cellular mechanism of antibody-mediated amyloid removal with ALXN2220. Results will show the addition of ALXN2220 to ATTR patient-derived cardiac tissue triggered phagocytosis, including recruitment of macrophages to amyloid deposits, detachment, internalization and degradation of ATTR amyloid.
An encore poster presentation will report results from the first-in-human study of ALXN2220. Initial treatment with ALXN2220 was well tolerated with a transient increase in C-reactive proteins, suggesting initial targeted immune activation and recruitment of phagocytic immune cells. Additionally, an encore poster presentation will describe the pharmacokinetic and pharmacodynamic (PK/PD) model used for the selection of the dose range, dose escalation, dosing interval and study duration.
Presentation Details
Title: ALXN2220: high-resolution live-cell imaging of antibody-mediated cardiac ATTR amyloid depletion
Presenter: Aubin Michalon, Director Amyloidosis & Preclinical Development, Neurimmune
Date: May 28, 2024
Poster ID: PBI (#226)
Title: ALXN2220: targeted immune activation in patients undergoing antibody-mediated cardiac ATTR amyloid depletion
Presenter: Fabian aus dem Siepen, University Hospital Heidelberg
Date: May 29, 2024
Poster ID: PC116 (#227)
Title: Prediction of cardiac ATTR depletion by NI006 using mechanistic PK/PD modeling
Presenter: Aubin Michalon, Director Amyloidosis & Preclinical Development, Neurimmune
Date: May 29, 2024
Poster ID: PC123 (#291)
Amyloid transthyretin cardiomyopathy (ATTR-CM) is an underdiagnosed, systemic condition that leads to progressive heart failure and high rate of fatality within four years from diagnosis.3,4 Progressive ATTR amyloid depositions characterize the disease, causing heart failure and death. Despite recent advances and approved therapies, there remains significant unmet medical need in treating moderate to severe ATTR-CM, and amyloid depletion may constitute an important new mechanism to achieve further effectiveness.
In 2022, Neurimmune entered into an exclusive global collaboration and license agreement with Alexion, AstraZeneca Rare Disease, for ALXN2220. Neurimmune is responsible for completion of the Phase 1b clinical study on behalf of Alexion, with Alexion incurring certain trial costs. Aside from the Phase 1b trial, Alexion is responsible for further clinical development, manufacturing, and commercialization of ALXN2220. In 2024, Alexion initiated the Phase 3 DepleTTR-CM clinical study to assess the efficacy and safety of ALXN2220 for the treatment of ATTR-CM.
1Garcia-Pavia et al., N Engl J Med 2023; 389(3):239.
2Michalon et al., Nat Commun 2021; 12(1):3142.
3 Lauppe RE, et al. Open Heart. 2021 Oct;8(2):e001755.
4 González-Duarte A, et al. Neurol Ther. 2020;9(1):135-149.
About Neurimmune
Neurimmune is a biopharmaceutical company translating human immune memory into antibody therapeutics. Neurimmune develops drug candidates for CNS and related protein aggregation diseases including Alzheimer’s disease, amyotrophic lateral sclerosis, frontotemporal dementia and ATTR cardiomyopathy. Neurimmune discovered NI101SQ, a human monoclonal antibody to deplete brain amyloid of patients with Alzheimer’s disease. With its Reverse Translational MedicineTM technology, Neurimmune discovered the anti-SOD1 antibody AP-101 for ALS and the anti-ATTR antibody NI006 for ATTR cardiomyopathy, programs being currently evaluated in clinical trials.
Contact for Media
John Capodanno (US)
john.capodanno@dentonsglobaladvisors.com
Martin Meier-Pfister (Switzerland)
media@neurimmune.com
