Independent Mouse Study Reinforces Remyelinating Potential of ISP Therapy

A new study demonstrates that intracellular sigma peptide (ISP) can promote remyelination in a mouse model of multiple sclerosis (MS). Importantly, this study was independent of NervGen, a pharmaceutical company that is developing an ISP-like compound — NVG-291 — for the treatment of nerve injury and MS.

The study, “Modulating proteoglycan receptor PTPσ using intracellular sigma peptide improves remyelination and functional recovery in mice with demyelinated optic chiasm,” was published in the journal Molecular and Cellular Neuroscience.

ISP is an inhibitor of the protein tyrosine phosphatase sigma (PTPσ), which slows the healing process when there is inflammation in the central nervous system. By blocking this healing-preventing receptor, ISP can promote nervous system healing and remyelination — the repair of myelin, the nerve cell “sheath” that becomes damaged in MS.

ISP was first developed by the laboratory of Jerry Silver, PhD, a professor at Case Western Reserve University and scientific co-founder of NervGen. Silver and colleagues have published several studies demonstrating ISP’s nerve repair-inducing properties in several animal models, including those with MS.

The newest study was undertaken by scientists at Tarbiat Modares University, Tehran, Iran, who are unaffiliated with Silver or NervGen. The team used a MS mouse model, and the results showed that ISP treatment increased remyelination, decreased observable nerve damage, and led to animals getting more normal results on behavior tests.

Furthermore, ISP treatment led to increased generation of oligodendrocyte cells, which are responsible for the production of myelin.

“Our results demonstrated the possibility of using ISP as a new strategy to inhibit PTPσ for myelin protection, myelin repair in demyelinated axons, and functional neural pathway conductivity restoration in patients suffering from MS,” the researchers wrote.

“The findings from this independent study are consistent with the remyelination observed by my research group in two previous animal model studies, one in multiple sclerosis and the other in spinal cord injury. The body of data supporting the remyelination mechanism of action continues to grow,” Silver said in a press release from NervGen.

Ernest Wong, president and CEO of NervGen, added: “A cornerstone of our technology is the validation of our science in different preclinical models by independent research groups around the world. The publication of this latest dataset, generated in a MS relevant animal model completely independent from that of Dr. Silver’s group, further validates the potential of our technology to address demyelination in multiple sclerosis.”

NervGen plans to submit to the U.S. Food and Drug Administration (FDA) an investigational new drug application for NVG-291, in order to launch a Phase 1 clinical trial in early 2020. The company is advancing NVG-291 for the treatment of spinal cord injury and MS.