Company: PRTA
Filing Date: 2025-11-06
Form Type: 10-Q
Source: 0001559053-25-000044
Chunk: 32

Company: PROTHENA CORP PUBLIC LTD CO
Filing Date: 2025-11-06
Form: 10-Q
Item: Part I, Item 2
Chunk 32
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.23 billion. We have earned approximately $100 million to date.

Phase 3 CLEOPATTRA Clinical Trial

In September 2025, Novo Nordisk initiated the Phase 3 CLEOPATTRA clinical trial evaluating coramitug as a potential treatment for ATTR-CM. CLEOPATTRA is a randomized, double-blind, placebo-controlled, multicenter clinical trial in approximately 1,280 participants with ATTR-CM. Primary endpoint is the number of occurrences of composite endpoint of cardiovascular (CV) deaths and recurrent CV events (CV hospitalizations and urgent heart failure visits) in a timeframe to end of study up to approximately four years.

Phase 2 Clinical Trial

A Phase 2 clinical trial of coramitug in 105 patients with ATTR amyloidosis with cardiomyopathy was conducted by Novo Nordisk (NCT05442047). Results are planned to be presented at the American Heart Association Scientific Sessions in November 2025.

BMS-986446 (formerlyPRX005) for the Potential Treatment of Alzheimer’s Disease

BMS-986446 is a humanized monoclonal antibody that targets multiple domains of the microtubule binding region of tau, a highly pathogenic tau fragment associated with neurofibrillary tangle formation and cognitive decline in Alzheimer’s disease. BMS-986446 binds to specific regions of the tau protein (R1 - R3 within the microtubule-binding domain) to prevent the cell-to-cell spread of tau and tau uptake into cells. It also activates microglia - the brain’s immune cells - through its Fc receptor function, promoting the clearance of tau via phagocytosis. Neurofibrillary tangles composed of misfolded tau proteins, along with amyloid beta plaques, are pathological hallmarks of Alzheimer’s disease. Cell-to-cell transmission of pathogenic extracellular tau and the accumulation of pathogenic tau also correlate with the progression of symptomatology and clinical decline in patients with Alzheimer’s disease. Recent publications suggest that during the course of Alzheimer’s disease progression, tau appears to spread throughout the brain via synaptically-connected pathways; this propagation of pathology is thought to be mediated by tau “seeds” containing the MTBR of tau. Additionally, it has been recently reported that the presence of MTBR fragments in cerebrospinal fluid correlate with dementia stages and tau tangles in Alzheimer’s disease to a higher degree than fragments of other tau regions. In preclinical research, antibodies targeting this region of