Do recent advancements in immunology provide hope for those suffering from autoimmune diseases such as Multiple Sclerosis? 

Imbalances in the immune system cause an increase in pro-inflammatory status, which is a hallmark of aging and fuels overactive immune responses in patients with autoimmune diseases. MYMD-1, our novel immuno-metabolic regulator, has been developed to target the underlying source of inflammation associated with a range of age-related and autoimmune diseases. In the context of treating immunometabolic dysfunction, MYMD-1 has the potential to offer unmatched benefits where current immunotherapy treatments fall short. 

The main target of our first-in-class drug is tumor necrosis factor-α (TNF-α), which plays a significant role in the body’s inflammatory response against invading pathogens. Unlike other TNF-alpha therapies on the market, MYMD-1 can cross the blood-brain barrier, which should offer a valuable immunomodulatory effect against TNF-alpha. MYMD-1 is a specific TNF-α blocker compared to some of the current FDA-approved TNF-α blockers on the market that are non-specific.

To truly appreciate MYMD-1’s innovative approach, as well as its potential to treat such large patient populations, it’s important to understand the intricacies of central nervous system diseases like Multiple Sclerosis (MS).

Using Novel Plant Alkaloids to Combat Autoimmune Diseases

TNF-alphas play a significant role in the body’s inflammatory response against invading pathogens. Produced by a variety of immune cells, TNF-α is one of the many cytokines that cells secrete in recognition of the invading pathogens and activates other immune cells until the invading organism has been cleared. 

Patients with autoimmune diseases like diabetes and rheumatoid arthritis have elevated levels of inflammatory cytokines and typically have a surplus of tumor necrosis factor-α. Although it can be unclear what causes an autoimmune response, regulating the release of inflammatory cytokines including TNF-α is necessary to prevent damage caused by an unwanted surplus of TNF-α. 

MYMD-1 is a novel plant alkaloid that is an analogue of nicotine. Nicotine and other alkaloids are known to suppress the immune response, which is key to managing an autoimmune disease. MYMD-1 draws from the same positive effects as nicotine, suppressing TNF-alpha but without the carcinogenic effects. This produces an immunomodulatory effect that makes it a promising candidate to treat complex autoimmune diseases like Multiple Sclerosis.

The Biologic Mechanism of Multiple Sclerosis

Affecting more than two million people worldwide, Multiple Sclerosis is a complicated disease and follows a variable clinical course. The etiology has yet to be fully understood, but there is curiosity around the likelihood that MS is developed due to a combination of genetic susceptibility and environmental influences. 

When an autoreactive event occurs, it occurs in a large area with multiple cell types in the central nervous system. Neurons in the CNS are coated with a myelin sheath made by oligodendrocytes which attach themselves to the axons of those neurons. If there is any damage that occurs between these elements from an attack on the brain and spinal cord from the immune system, it disrupts signals to and from the brain. The symptoms that arise from this disconnect are unique to the individual. Some people have debilitating, intermittent attacks but only have mild disability and others present severe symptoms and experience a rapid decline in functionality, resulting in a severe disability. 

Looking to Future Immunotherapies

New immunotherapy research has stirred a recent interest in leveraging neuroprotection and neurorepair to develop future therapies for MS. The recent emphasis on these mechanisms for therapy is supported by historical evidence showing that signals sent through nicotinic acetylcholine receptors could offer neuroprotection, as this could send growth signals to neurons. As an analogue of nicotine, the theory is that MYMD-1 should attach to the nicotinic acetylcholine receptor in the brain without causing addiction. 

Current MS treatments are immune modular modulators and are not capable of crossing the blood-brain barrier, which is why they have not been proven to be effective in treating progressive MS. Additionally, the majority of these therapies are offered as injectables which don’t provide an ideal patient experience and could cause a range of side effects like headaches and allergic reactions. More potent immune suppressants actually make patients more vulnerable to infections as well. 

Not only has MYMD-1 shown to have no significant toxicity in Phase 1 clinical trials, it is also believed to be the only drug with an issued patent for altering programmed cell death and extending cell life that can be administered as a pharmaceutical salt. Treatments delivered as pharmaceutical salts allow them to be taken orally and increases the chemical stability of the product. At only 146 daltons, we believe that MYMD-1 is the first TNF-alpha oral regulator capable of crossing the blood-brain barrier. 

In essence, we believe that MYMD-1 seems to meet all the necessary requirements for an effective immunotherapy to address MS in the central nervous system: 

  • A small molecule that can cross the blood-brain barrier to potentially deliver a immunomodulatory effect
  • An easily administered treatment that should not have toxic side effects (based on Phase 1 results) 
  • An immuno-metabolic regulator that targets the cause of inflammation, not the symptoms

Potential Breakthrough Treatment for Autoimmune Diseases

As we continue our journey through the FDA, we look forward to the potential opportunity that MYMD-1 has to provide a local immunomodulation within the CNS, possibly serving as an effective immunotherapy for more progressive forms of MS. Learn more about MYMD-1 in our candidate pipeline.

 

Sources:

  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737409/
  • https://www.news-medical.net/health/
  • https://pubmed.ncbi.nlm.nih.gov/27531077/
  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5880159/

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