MYMD-1, MyMD Pharmaceuticals’ lead candidate for the treatment of several autoimmune and age-related disorders, showed promising efficacy in targeting the root causes of inflammation in idiopathic pulmonary fibrosis (IPF), according to data from a recent study.
The therapy reduced the activity of molecules that are known drivers of inflammation and tissue scarring (fibrosis).
Findings from the study, carried out by Eurofins Discovery, a global leader in food and pharmaceutical product testing, support the future development of MYMD-1 as a therapy for several fibrotic disorders.
“MYMD-1 continues to demonstrate broad utility and capability to inhibit inflammation in preclinical data, which is linked to myriad diseases including IPF,” Chris Chapman, MD, president and chief medical officer of MyMD, said in a press release.
“This study stirs hope for those affected by the disease and gives MYMD-1 an additional path forward,” Chapman said.
A man-made plant compound, MYMD-1 can control the release of several pro-inflammatory cytokines — molecules that mediate the body’s immune and inflammatory responses. These cytokines include interleukin-6 (IL-6), interleukin-17A (IL-17A), and tumor necrosis factor alpha (TNF-alpha).
Due to that ability, MYMD-1 is currently being investigated as a potential treatment for several autoimmune diseases in which these pro-inflammatory molecules are usually found in excess, such as multiple sclerosis and rheumatoid arthritis.
Now, a new study found evidence that MYMD-1 might be valuable to help reduce inflammation and scarring in IPF.
This study found that MYMD-1 was able to inhibit the activity of pro-inflammatory TNF and transforming growth factor-beta (TGF-beta), a known key driver of lung tissue scarring in IPF. According to Eurofins, this dual mechanism of action supports the future development of MYMD-1 as a new treatment candidate for IPF and other fibrotic disorders.
“We have learned over the years from testing both approved fibrosis drugs and failed candidates, that efficacy requires not only anti-fibrotic impacts, but also anti-inflammatory activities,” said Alison O’Mahony, PhD, vice president of Translational Biology at Eurofins.
“During the study, MYMD-1 inhibited both aspects of fibrosis biology. We were also able to determine well-tolerated treatment concentrations as part of the study,” O’Mahony said.
Eurofins conducted the study using its proprietary BioMAP Phenotypic Screening and Profiling Platform, which combines the use of cell-based disease models, protein biomarkers, and bioinformatic tools to evaluate the safety, efficacy, and mode of action of new therapeutic compounds.
“We selected Eurofins to run the study knowing the credibility and breadth of their platform, and were pleased to see the readouts specifically showed inhibition of disease biology among key biomarkers associated with IPF, especially through Eurofins’ human phenotypic screening platform, allowing us to see patient-specific cell activity,” said Adam Kaplin, MD, PhD, chief scientific officer of MyMD.
The company is now planning to move forward and start exploring the effects of combining MyMD-1 with other approved anti-fibrotic therapies for the treatment of IPF.
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