Dedicated to reversing the permanence of neurological damage
Our approach
LDL receptors, and LRP1 in particular, have been implicated as promising therapeutic targets in a variety of diseases. LRP1 in particular has shown significant promise in terms of its potential for regenerative or disease-modifying benefits in disease or damage of the CNS. Novoron has developed proprietary tools and unique expertise fundamental to exploiting LRP1 and related proteins for their maximal therapeutic potential while avoiding the potential pitfalls associated with off-target, or within-target unwanted interactions that can lead to negative consequences that threaten to offset therapeutic benefit.
ALZHEIMER’S & TAUOPATHIES
Tau is a naturally occurring protein in the brain. When too much is produced or altered, it can contribute to neurodegenerative diseases such as Alzheimer’s or chronic traumatic encephalopathy (CTE). One of the hallmarks of tauopathies is the spread of tau from parts of the brain with abnormal production to other brain regions.
Research into the causes of and effective treatments for tauopathies and Alzheimer’s has been ongoing for decades, with frustratingly few results. Recently, research has shown that LRP1 is a critical factor in the spread of tau. We’re currently working to develop molecules that stop the spread of tau in the brain.
SPINAL CORD INJURY (SCI)
Nerves damaged after a spinal cord injury attempt to regenerate, but are blocked from doing so by inhibitory molecules at the site of damage. We’ve developed a molecule that shuts down the signals that confuse neurons and suppress regeneration.
In animal models of injury, our approach promotes the growth of nerve cells and leads to significant recovery of motor function. We’re currently working to explore the therapeutic potential of our molecule and inform preclinical studies to set our drug up for success in clinical trials.
MULTIPLE SCLEROSIS (MS)
In multiple sclerosis, the immune system attacks the protective coating on nerves called myelin. Once the myelin is removed, nerves become dysfunctional and eventually die. While therapies today can reduce the number and severity of MS attacks, no treatment exists to repair damage after an attack has occurred.
Repairing myelin—a process called remyelination—is our best chance for reversing the effects of MS. Our technology has shown promise in promoting myelin repair in MS lesions and we’re now working to optimize the administration and dosing.