Multiple Sclerosis is a chronic condition that impacts over 2.8 million people worldwide. In the United States alone, one in 300 people is affected by MS, with a high incidence among women. Although there’s a lot we don’t know about this condition, most experts believe MS is an autoimmune disorder. MS causes a wide range of symptoms that impact brain, optic nerve, and spinal cord function.

At its core, MS is a neuroinflammatory disease that causes a spike in tumor necrosis factor-α (TNF-alpha), which plays a significant role in the body’s inflammatory response against invading pathogens. TNF-alpha is one type of proinflammatory cytokine produced in the body. Chronic or excessive production of TNF-alpha has been implicated in Multiple Sclerosis.

This is a large part of what makes the potential for our first-in-class drug, MYMD-1, to address the TNF-alpha phenomenon via its plant alkaloids component so compelling. MYMD-1 is an alkaloid derived from the tobacco plant with anti-inflammatory cytokines, which inhibit the production of TNF-alpha. MYMD-1 targets these response receptors at the source where damaging inflammation leading to MS can occur, rather than simply treating the symptoms.

MYMD-1 also has the unique and impressive ability to cross the blood-brain barrier. Tightly packed cells in the brain’s capillaries constitute the blood-brain barrier. This barrier or filter prevents substances that can do harm from entering the brain. The challenge, of course, is that this wall of cells also prevents beneficial medications designed to treat brain conditions from reaching their destination. With a condition like MS, the ability to cross the blood-brain barrier is essential to the efficacy of any medication treatment.

TNF-alpha, inflammation and Multiple Sclerosis

Drugs that act as TNF inhibitors and work to address inflammatory responses in the wide variety of autoimmune diseases and conditions is a $16 billion a year market. Before 1993, there were zero treatments for MS, and older treatments decreased the number of lesions by 30 percent. Now we have treatments that double or triple that as far as the ability to block exacerbations. Over time, those treatments have gotten more aggressive and have been fraught with side effects, including death. While these treatments offer up a good chance at preventing the inflammatory component, there’s also evidence that suggests that beneficial healing of the central nervous system (CNS) is also blocked.

As importantly, none of the existing medications developed in the last decade cross the vital blood-brain barrier. In fact, existing TNF-alpha inhibitor medications do something very peculiar — they can cause symptoms that look like MS. Dr. Kaplin, MyMD’s Chief Scientific Officer, specializes in the neuropsychiatry of MS and spoke to his experience witnessing patients being diagnosed with MS in this way. He shared that once these peripheral TNF-alpha inhibitors were stopped, the patients’ symptoms disappeared immediately. This is what makes MYMD-1 distinct in its ability to be selective. It targets the adaptive immune system where B and T cells learn to recognize invaders.

Going forward, as we examine what our best approach to treating MS over the long term will be over traditional strategies, aggressive treatment early on that targets TNF-alpha receptors may be one course of action. At MyMD, we hope that by getting more at the cause rather than the symptoms, we’ll be able to prevent MS, including its progressive form, which can gradually erode the quality of life for people afflicted in this way. Primary-progressive Multiple Sclerosis (PPMS) accounts for about 10 percent of patients diagnosed with MS, which tend to be older than those that have relapsing MS. PPMS symptoms and the development of the disease gradually get worse over time. It’s a particularly dreadful medical condition with no good treatment options available today.

Because MYMD-1 is a TNF-α inhibitor, not just a blocker, TNF-alpha inhibition also stands a chance to block the inflammatory components that lead to attacks — perhaps even allowing for CNS healing processes to take place. The idea of being able to prevent the progressive aspects of MS through “the combination of not only stopping inflammation (presumably through TNF-α inhibition) but also the very nature of [the source] — IL-6 and IL-17 inhibition — could really be a game-changer,” says Dr. Kaplin. He strongly believes in the possibility that just the TNF-alpha inhibition in the CNS might make a big difference in the brain’s ability to finally start healing itself. With more effective treatments, Dr. Kaplin reports that people have described experiencing an improvement in their cognition.

Addressing Depression in Patients with Multiple Sclerosis

MS has the highest rate of depression among any neurological and neurosurgical disease. 50 percent of people with MS will have clinical depression at some point in their life. Suicide rates for people with MS battling depression are seven and a half times higher than in the general population, and it’s a major cause of morbidity and mortality. As a reference point, roughly 15 percent of a cross-section of people will be clinically depressed at any time.

Backed by our research, it’s clear that inflammation causes depression and that anti-inflammatory drugs — Anti-IL 12, Anti-IL 6 — have antidepressant activity. Since there is still no treatment in double-blind studies that has been shown to be beneficial for MS and depression, we’re researching the treatment of immune-mediated depression. We are also in the process of looking into a possible orphan drug designation of MYMD-1 for depression in MS.

Hope for the Future

The implications of targeting TNF-alpha receptors as the source of damaging inflammation for a condition like MS is very profound and an evolving area of research. But with MYMD-1’s unique chemistry, ability to cross the blood-brain barrier, and successful mechanism in suppressing TNF-alpha, we are very hopeful for the opportunity to better treat MS in the future.

“Based on our observations, we haven’t solved the problem but I think that there’s enough data out there to suggest that [the problem] is ongoing inflammation and if we can really effectively turn it off, we might be able to really make a difference,” said Dr. Kaplin.

Follow us along our journey through the FDA and learn more about our other drug candidate, Supera-CBD, targeting anxiety, chronic pain and seizures.

 

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