Advancing First-in-Class Therapies across Neurotraumatic and Neurologic Conditions with Significant Unmet Need.
Candidate
Indications
Preclinical
Phase 1
Proof of Concept
Registrational
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Chronic Spinal Cord Injury
NVG-291
Additional Neurotraumatic and Neurodegenerative Conditions
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NVG-300
Additional Neurotraumatic and Neurodegenerative Conditions
Select Additional Conditions with NVG-291 Preclinical Efficacy
Stroke
Stroke occurs when blood flow to part of the brain is interrupted by a clot or a ruptured vessel, depriving brain tissue of oxygen and causing cell death that can leave lasting motor, sensory, and cognitive disability. More than 795,000 people in the United States experience a stroke each year, and there is currently no approved pharmacologic therapy that repairs the resulting brain damage. As the brain forms a glial scar around the injured region, CSPGs are upregulated and inhibit the sprouting of new connections and the migration of newly born neurons needed for recovery. In a peer-reviewed preclinical study published in Cell Reports, NVG-291-R drove significant improvement in motor function, sensory function, and memory even when treatment began seven days after stroke onset.
Multiple Sclerosis
Multiple Sclerosis (MS) is a chronic, immune-mediated disease in which the protective myelin coating of nerve fibers in the brain and spinal cord is progressively damaged, disrupting the signals that travel between the brain and the body. Approximately one million adults in the United States live with MS, with most diagnosed between the ages of 20 and 50 and women affected at roughly three times the rate of men. In MS lesions, CSPGs accumulate and create an environment that blocks oligodendrocyte precursor cells from maturing and rebuilding myelin, leaving demyelinated areas unable to repair even when inflammation subsides. In preclinical models of MS, NVG-291-R promoted remyelination and functional recovery, supporting the rationale for a repair-focused approach that complements existing therapies aimed at suppressing the immune response.
Traumatic Brain Injury (TBI)
Traumatic Brain Injury (TBI) results from a sudden blow, jolt, or blast to the head that disrupts normal brain function and can produce lasting impairments in movement, cognition, and behavior. TBI is a leading cause of long-term disability, with millions of Americans living with its lasting effects and a disproportionate burden among military service members and veterans. As with other forms of central nervous system trauma, CSPGs are upregulated at the site of injury, forming an inhibitory environment that limits the brain’s capacity to rewire and repair. Preclinical development of NVG-291 in TBI is being funded and conducted by the U.S. Department of Defense through the Walter Reed Army Institute of Research.
Sensorineural Hearing Loss
Sensorineural Hearing Loss arises from damage to the sensory structures and neural pathways of the inner ear, including the effects of blast exposure, and is among the most common and persistent service-connected conditions affecting military personnel. There are currently no approved therapies that repair the underlying neural damage responsible for this form of hearing loss. CSPGs are present in the perineuronal nets surrounding auditory neurons and contribute to the inhibitory environment that limits recovery after injury. In a Department of Defense-sponsored preclinical study of blast-induced hearing loss, NVG-291-R promoted significant restoration of hearing function.
Peripheral Nerve Injury (PNI)
Peripheral Nerve Injury (PNI) involves damage to the nerves outside the brain and spinal cord, often from trauma, and can cause muscle weakness, loss of sensation, and impaired function that may persist long after the initial injury. Severe peripheral nerve injuries frequently recover incompletely, leaving lasting disability and a significant burden on both civilian and military populations. Following injury, CSPGs are upregulated along the damaged nerve and surrounding tissue, where they impede the axonal regrowth required to restore function. In Department of Defense-sponsored preclinical models of moderate and severe peripheral nerve injury, daily treatment with NVG-291-R produced statistically significant improvements in neuromuscular function and axonal regeneration.
Alzheimer's Disease (AD)
Alzheimer’s Disease (AD) is a progressive neurodegenerative disease and the most common cause of dementia, characterized by the gradual loss of memory, reasoning, and the ability to carry out daily activities. An estimated 7 million Americans are living with Alzheimer’s today, a number projected to rise sharply as the population ages. CSPGs are a principal component of perineuronal nets, the specialized structures surrounding neurons that regulate synaptic plasticity, and their dysregulation is increasingly implicated in the cognitive decline seen in AD. In preclinical work, NVG-291-R produced improvements in memory and spatial learning, raising the possibility of an approach that supports cognitive function rather than only slowing its decline.
Optic Neuritis
Optic Neuritis is inflammation of the optic nerve that disrupts the transmission of visual signals to the brain, causing sudden vision loss, pain with eye movement, and impaired color perception. It is frequently the first clinical sign of multiple sclerosis and occurs in roughly half of people with MS over the course of their disease, with acute episodes also arising on their own or in association with other neuroinflammatory conditions. Because the optic nerve is part of the central nervous system, recovery is constrained by the same biology seen elsewhere: CSPGs are upregulated in the inflamed and demyelinated nerve, where they inhibit remyelination and the regrowth of damaged axons. In a preclinical model of optic neuritis, NVG-291-R promoted nervous system repair and recovery of visual function, reinforcing the breadth of the underlying mechanism.
Frontotemporal Dementia and ALS (C9ORF72)
Frontotemporal Dementia and ALS (C9ORF72) sit on a shared disease spectrum, and a repeat expansion in the C9ORF72 gene is the most common genetic cause of both. The mutation produces toxic dipeptide repeat proteins that impair the endosomal and lysosomal systems neurons rely on to clear damaged material and stay alive. In a study published in Neuron, NVG-291-R restored this cellular machinery and improved the survival of neurons derived from C9ORF72 patients. In a mouse model of the disease, NVG-291-R preserved neurons and improved motor function, activity, and memory. These findings extend the rationale for PTPσ modulation beyond tissue repair into genetic neurodegeneration, through a distinct cellular mechanism.
The Future of Neurorepair Has Begun. Be Part of What Comes Next.
