Neuraltus’ programs focus on novel drug molecules with promising mechanisms of action representing first-in-class approaches to treating the Company’s target disease indications.
| Clinical Pipeline | ||||
|---|---|---|---|---|
| Preclinical | Phase 1 | Phase 2 | Phase 3 | |
| NP001 | Macrophage regulation |
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| NP002 | Nicotinic receptor agonism |
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| NP003 | Undisclosed |
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NP001, a novel, proprietary approach that regulates macrophage activation, targets diseases including ALS, Parkinson’s disease, Alzheimer’s disease and multiple sclerosis. NP001 is designed to transform select immune cells (macrophages) from a neurotoxic state to a neuroprotective state, normalizing the cellular environment of critical nerve cells.
Neuraltus’ focus on macrophages is based on the recent understanding of the fundamental role of inflammation and macrophages in neurological diseases. Runaway inflammation has been associated with many of the symptoms seen in severe neurological diseases and is believed to play a major role in the progression of these diseases. Treating inflammation of the central nervous system (neuroinflammation) provides a robust platform for addressing upstream disease mechanisms associated with the most severe neurodegenerative diseases
NP002, a small molecule, nicotinic receptor agonist, is designed to reduce dyski nesi as (muscle movement disorders) that are a primary side effect of L-dopa treatment of Parkinson’s disease. Of the 500,000 - 1.5 million Parkinson’s patients in the United States, more than 50% experience L-dopa-induced dyskinesias (LIDs). Preclinical in vivo research has shown NP002 reduces LIDs without affecting Parkinsonian symptoms on or off L-dopa treatment. Link to Dyskinesias Trial.
NP003 is an orally bioavailable, small molecule designed to treat lysosomal storage disorders such as Fabry's disease and Gaucher's disease. NP003 works by limiting the ability of harmful lipids to collect in the cells of lysosomal storage disorder patients. NP003 is expected to be synergistic with current enzyme replacement therapies. In addition, because it crosses the blood-brain barrier, NP003 is expected to provide central nervous system protection from abnormal lipid accumulation. NP003 may also inhibit glycolipid-induced aggregation in the brain of α-synuclein protein, believed to be a primary cause of Parkinson's disease.