According to Census Bureau estimates, there are over 52 million Americans over the age of 65 now and that number will increase steadily as baby-boomers age. Two-thirds of these older Americans suffer from multiple degenerative diseases. Along with the growing aging population, autoimmune diseases like rheumatoid arthritis and inflammatory bowel disease are becoming more prevalent. Out of the 56 million Americans dealing with immunometabolic diseases, 24 million are suffering from autoimmune diseases. Unfortunately, these patient populations do not have access to existing drugs that are both effective and treat underlying causes, rather than symptoms. Our clinical-stage pharmaceutical company has been developing a therapeutic platform that aims to fill the need for an alternative to current medications on the market.
Extending Healthy Lifespan
In pursuit of our mission to extend healthy lifespan, our first-in-class drug, MYMD-1, targets three primary inflammatory cytokines linked to aging and autoimmune diseases, including tumor necrosis factor alpha or TNF-α. Cutting inflammation off at the source, MYMD-1 is a TNF-α inhibitor, suppressing chronic runaway inflammation before symptoms begin.
As our platform’s main target, we’re exploring the impactful role that TNF-alpha plays in the body’s response to inflammation and how the selective control and reduction of this cytokine could be the key to treating chronic inflammatory and autoimmune diseases, giving people the opportunity to age in good health.
Having a holistic understanding of the TNF-alpha function – as well as the inefficiencies in traditional therapies utilizing TNF blockers – is vital to grasping the significance of this drug candidate.
What is TNF-alpha?
TNF-alpha is one type of proinflammatory cytokine produced in the body. It is produced primarily by certain white blood cells, acting as a chemical messenger throughout the body to regulate many aspects of the immune system. Its function can have both positive and negative effects on the body. TNF-α is responsible for a range of signals within cells, leading to necrosis—defined as the death of most or all of the cells in an organ or tissue—but also important for resistance to infection and cancers. It exerts many of its effects by binding to specific cell membrane receptors.
How does TNF-α impact inflammation and autoimmune diseases?
TNF-α is essential to mounting an inflammatory response to defend the body against disease and infection; however, chronic or excessive production of TNF-α has been implicated in a number of acute and chronic inflammatory and autoimmune diseases such as diabetes, rheumatoid arthritis, multiple sclerosis and sarcopenia. These and other autoimmune diseases result from a hyperactive immune response in which the immune system starts producing antibodies that attack the body’s own healthy cells, tissues, and organs instead of fighting infections.
What are traditional therapies for autoimmune diseases?
Traditional therapies for the majority of diseases caused by immune system dysfunction include anti-inflammatory drugs and immunosuppressive agents such as TNF blockers. A TNF blocker (sometimes called a TNF inhibitor) is a pharmaceutical drug that suppresses the physiologic response to tumor necrosis factor (TNF). These therapies often fail to achieve significant clinical benefits and can cause serious side effects such as severe drops in certain blood component counts, liver toxicity, osteoporosis, teratogenicity and various endocrine abnormalities.
MyMD Pharmaceuticals’ research into TNF immunology
In order to characterize the function of MYMD-1, we performed a BioMAP Diversity analysis in a panel of 12 human primary cell-based systems. The BioMAP system represents in vitro disease models consisting of quality-assured human primary cell cultures or co-cultures with standardized stimulation to model specific disease states, validating both clinically approved and investigative test agents. The results of the BioMAP Diversity analysis show that MYMD-1 was active in 11 of the 12 systems in the panel.
Overall, MYMD-1 demonstrated a robust inhibition pattern that included decreased biomarker levels in several physiological and pathological categories. MYMD-1 inhibited multiple inﬂammation-related biomarkers, which is indicative of broad anti-inﬂammatory potential. These biomarkers included decreased levels of Eotaxin 3, E-selectin, MCP-1, SAA, sTNFα, MIP-1α, P-selectin, and IL-6 levels, with modulated VCAM-1 and IL-8.
Our research and development team is working to learn more about MYMD-1, as well as other synthetic therapeutics for treatment of autoimmune disease, aging and anxiety. As we look forward to beginning our Phase 2 clinical trials this year, we are hopeful for the potential impact that this new approach could have on healthcare outcomes.
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