HUMAN-CENTERED
HUMAN-CENTERED
IL-10
Immune Modulation by Targeting a Master Regulator
Enter Interleukin-10 (IL-10): a master regulator and modulator of the immune response. A potent cytokine with anti-inflammatory properties, it plays a critical, upstream role in maintaining cytokine homeostasis across a broad range of complex chronic inflammatory diseases. IL-10 acts to modulate inflammation through multiple pathways including: suppressing transcription, translation, processing and release of certain cytokines such as TNF- α, IL-1α, IL-1β, IL-6, IL-12 and GM-CSF; down-regulating cytokine receptors and up-regulating antagonists; and inhibiting hydrogen peroxide and nitric oxide production. IL-10 deficiency is associated with chronic inflammatory and autoimmune diseases.
OUR NON-VIRAL GENE THERAPY APPROACH
Our research and deep understanding of IL-10 biology is converging with recent technology advancements, notably in non-viral gene therapy platforms. Using this method, we are now poised to make a breakthrough in delivering scalable solutions that can be effective, safe and provide longer duration of relief for the millions affected by these devastating conditions, including osteoarthritis, neuropathic pain, facet joint syndrome, multiple sclerosis and countless others.
Our lead therapeutic candidate, XT-150, combats pathologic inflammation through expression of IL-10 locally at the sites of inflammation. XT-150 is a locally injectable plasmid DNA gene therapy expressing IL-10v, a proprietary modified variant of IL-10, to address pathologic inflammation and pain. We have designed XT-150 to have an optimized regimen, dosing and formulation – significantly increasing the duration of its effects compared to current standard of care and staying within the site of injection. Because XT-150 is non-viral, there is also the potential for redosing. We are currently evaluating XT-150 in a range of chronic inflammatory disease indications addressing over 300 million patients on a global scale, which can be viewed on our Pipeline page.