Science’s Long March Toward Healing: How Two Experimental Compounds Could Rewrite the Story of Multiple Sclerosis

By Viviana Cetola

With Life News Today — October 2025

For generations, multiple sclerosis has been a disease of frustration, a slow unraveling of the nervous system where the body turns against itself. But in two university labs separated by 1,700 miles, a pair of molecules may be writing a new chapter in how we think about healing.

At the University of California, Riverside, neuroscientist Seema Tiwari-Woodruff and her team have spent years asking one question: Can damaged nerves be coaxed to heal themselves? Her collaborators at the University of Illinois Urbana-Champaign, including chemist John Katzenellenbogen, believed the answer might be hidden in the structure of a forgotten compound. Together, they found it, or rather, they built it.

Their discovery began with a molecule known as indazole chloride, an old laboratory curiosity that showed flashes of promise in repairing the protective coating around nerves. That coating, called myelin, works like the insulation around an electrical wire. When the immune system mistakes it for an invader and attacks it, nerve signals slow, falter, and sometimes stop altogether. The result is multiple sclerosis, a chronic autoimmune disorder that affects more than 2.9 million people worldwide.

Existing drugs can dial down inflammation and ease flare-ups, but none have ever rebuilt what was lost. That limitation turned a generation of neurologists into firefighters, able to contain damage but never truly restore function. Tiwari-Woodruff wanted to change that. “We weren’t interested in just slowing the fire,” she said in a recent release. “We wanted to rebuild the house.”

Working with Katzenellenbogen’s chemistry group, the researchers re-engineered indazole chloride into dozens of variations, more than 60 in all. Each tweak adjusted stability, potency, and safety. Under the direction of UC Riverside researcher Micah Feri, two compounds stood out: K102 and K110. Both promoted remyelination, the process of restoring that crucial protective sheath, and both calmed the overactive immune response that drives MS. Of the two, K102 became the star performer. In mouse models and human cell cultures, it not only repaired myelin but also appeared to normalize immune signaling. “A dual-action therapy,” Katzenellenbogen called it, “the kind of compound we’ve been looking for.”

This is not science fiction. It’s early-stage, yes, but solid. The results, published in Scientific Reports and highlighted by ScienceDaily and UC Riverside News, outline a carefully built bridge from laboratory theory to preclinical reality.

Behind every medical breakthrough lies paperwork, and plenty of it. The patents for K102 and K110 are now jointly held by UC Riverside and UIUC, with exclusive licensing rights granted to Cadenza Bio, an Oklahoma-based biotechnology firm that specializes in neurological disorders. The agreement was shepherded through by UC Riverside’s Office of Technology Commercialization, which matched university discovery with private-sector urgency.

Cadenza Bio’s chief operating officer, Elaine Hamm, said the company saw immediate promise: “We were impressed by the shift from slowing degeneration to actually repairing it. That’s a fundamental leap.”

The company has launched toxicology and pharmacokinetics studies, the safety hurdles every potential drug must clear before reaching human trials. Early data, according to the research team, show improved nerve conduction and visual recovery in animal models, without toxic side effects. If those results hold, first-in-human trials could be proposed to the FDA within the next development phase.

The story of K102 is also a lesson in how science now works. No single lab or even a single university could have pushed this research so far so quickly. The National Multiple Sclerosis Society funded the early studies through two programs: its Investigator-Initiated Grant and Fast Forward, a venture-style initiative that accelerates promising academic discoveries toward commercialization. That partnership connected Tiwari-Woodruff’s neuroscience with Katzenellenbogen’s chemistry and Cadenza Bio’s development expertise.

“Fast Forward was instrumental,” Tiwari-Woodruff said. “It gave us the resources and visibility to move from discovery to something that can actually reach patients.”

At the molecular level, the research also drew in scientists from The Scripps Research Institute in Florida, including Kendall Nettles and Jerome Nwachukwu, who analyzed how the new compounds bind to estrogen-receptor β, an interaction thought to promote myelin repair. Additional team members—Flavio Cardenas, Alyssa Anderson, Brandon Poole, Devang Deshpande, Kelley Atkinson, Stephanie Peterson, and Martin Garcia-Castro—helped refine testing and data.

To understand why this matters, imagine the nervous system as a country of interconnected highways. In MS, those roads are riddled with potholes and blockades. For decades, medicine has focused on reducing new potholes, lessening inflammation, but the roads already damaged remained broken. K102 aims to fill those potholes. In animal studies, it repaired the myelin and restored nerve function, allowing signals to flow more efficiently. In human cell experiments, the compound prompted oligodendrocytes, the body’s natural myelin producers, to start rebuilding. That’s why researchers and patients alike see this as more than incremental progress. It hints at regeneration, not just remission.

Interestingly, the researchers say K110 might prove even more useful in conditions beyond multiple sclerosis. Its chemical structure interacts differently within the central nervous system, possibly aiding recovery from spinal-cord injuries, stroke, or traumatic brain injury, any disorder where myelin loss plays a role. Such versatility could open new doors in neuroregenerative medicine, a field long starved for success. “The idea that we can actually rebuild parts of the nervous system once thought irreparable is thrilling,” said Cadenza Bio co-founder David Martin.

Hope is not the same as hype, and everyone involved knows it. Translating a discovery from Petri dish to pharmacy shelf can take a decade or more. Safety trials, dose testing, and regulatory review form a gauntlet that only a handful of experimental drugs survive. But even cautious optimism matters. For people living with MS, it is the difference between managing decline and envisioning recovery.

At UC Riverside, Iqbal Pittalwala, senior public information officer who first reported the university’s breakthrough, put it simply: “It’s the result of years of perseverance, collaboration, and trust.”

Tiwari-Woodruff echoed that sentiment. Since establishing her lab in 2014, she has mentored dozens of young scientists and built a research culture defined by persistence. “This work isn’t driven by profit,” she said. “It’s driven by the desire to restore health and hope.”

The K102 story also reflects how modern science has evolved. The myth of the lone genius in the lab coat has given way to networks of collaboration—universities, nonprofits, and private startups woven together by shared purpose. In this model, public funding lights the spark, philanthropy fans the flame, and biotech carries the torch to the marketplace. Without any one of those, the chain breaks.

For patients, that chain now represents something precious: a line connecting the distant world of laboratory mice to the very real world of human healing.

If clinical trials confirm what early research suggests, K102 and K110 could represent the first true remyelination therapy, medicine that not only halts damage but rebuilds the nervous system itself. That’s a bold promise. But so was the idea of electricity running through copper wire, or a man walking on the moon. Science moves forward not by certainty, but by conviction, by people willing to test impossible ideas until they work.

And somewhere in Riverside, California, that conviction hums quietly in a lab, where scientists are still watching nerves heal under the microscope, believing that one day, what they see there might change the world.

Sources: University of California, Riverside News (by Iqbal Pittalwala); ScienceDaily; Scientific Reports (October 2025).