Autoimmune Disease

The Sofra™ technology platform includes preclinical product candidates for the treatment of autoimmune disease.

Autoimmune diseases, including systemic lupus erythematosus (SLE), psoriasis, type 1 diabetes, rheumatoid arthritis, and multiple sclerosis affect as many as 5% of Australians. These conditions are characterised by uncontrolled inflammation that contributes to many chronic health issues and has an enormous impact on longevity and quality of life.

Hudson Institute of Medical Research has developed a novel strategy that utilises oligonucleotides to block the receptors that are overactivated in those diseases, known as pattern recognition receptors. Noxopharm via its subsidiary Pharmorage has licenced these oligonucleotides.

The most advanced oligonucleotide Noxopharm and Hudson Institute have in development is a preclinical drug candidate, SOF-SKN, that targets an inflammatory receptor called Toll-like receptor 7 (TLR7). Researchers have identified a direct link between overactivation of TLR7 and lupus or SLE, validating the importance of this target.

The Victorian government has recently awarded a grant to Hudson Institute to support the ongoing investigation of TLR7 inhibitors, targeting the common autoimmune disease SLE. Noxopharm is co-investing in this research and holds Composition of Matter patents with a view to progressing high potential drug candidates into the Noxopharm and Pharmorage drug development program.

Download the Sofra Autoimmune and Inflammatory Fact Sheet pdf here

Noxopharm recently presented findings from the SOF-SKN preclinical development program to world experts in SLE at a major medical conference, the 15th International Congress on Systemic Lupus Erythematosus (LUPUS 2023).

In order to create a TLR7-driven model for skin inflammation that mimics cutaneous (skin) manifestations of SLE, Aldara^® cream containing 5% imiquimod (a TLR7 agonist) was applied topically to the back and ear of mice over several days. SOF-SKN was also applied topically to the same areas.

Mice were scored daily for the appearance and severity of skin inflammation i.e., skin scaling, redness, and thickening of skin of the ear. SOF-SKN treated mice showed fewer signs of skin inflammation, as illustrated below.

Ear thickness, indicating an inflammatory response, was decreased in mice treated with SOF-SKN (blue line) compared with mice that received no SOF-SKN (vehicle – red line).		Redness of the ear skin in the SOF-SKN treated mice was negligible (blue line) compared with mice that received no SOF-SKN (vehicle – red line).
Redness of the back skin of the SOF-SKN treated mice (blue line) was negligible compared with mice that received no SOF-SKN (vehicle – red line).		Scaliness of the back skin of the SOF-SKN treated mice (blue line) was negligible compared with mice that received no SOF-SKN (vehicle – red line).