Lead Pharma has launched a research collaboration with Sanofi to discover, develop, and commercialize its lead program, focused on small molecule therapies directed against the nuclear receptors known as retinoic acid receptor-related orphan receptor gamma (RORγt).

The value of the collaboration was not disclosed. Lead Pharma did say it will receive from Sanofi an upfront payment, and will be eligible for payments tied to research, development, regulatory, and commercial milestones. Lead Pharma is also entitled to receive royalty payments on global sales from any such products.

In return, Sanofi agreed to oversee clinical development and will have worldwide marketing and commercialization rights to any products that may be developed as a result of the collaboration.

Sanofi said in a separate statement the companies will collaborate during the early phase of R&D, with a goal of identifying drug candidates and beginning human trials within three to four years.

Both companies said their partnership was aimed at creating treatments for a broad range of autoimmune disorders, including rheumatoid arthritis, psoriasis, and inflammatory bowel disease.

“With an estimated 25 million people in the U.S. alone affected by such a broad range of autoimmune disorders, a significant unmet medical need exists in the area, and anti-ROR gamma (t) therapies represent a ground-breaking opportunity that we are eager and motivated to pursue through our collaboration with Lead Pharma,” said Christian Antoni, vp and head of the immunology and inflammation franchise, R&D, Sanofi.

Lead Pharma says it has identified new potential inhibitors of RORγt, a target that regulates the production of key pro-inflammatory proteins, including interleukin (IL)-17A, IL-17F, and the receptor for IL-23. Because the IL-17 pathway has a critical role in chronic autoimmune-related inflammation, Lead Pharma reasons, a modulation of RORγt by small molecules bears great potential for the treatment of autoimmune diseases.

Sanofi cited recent research showing that the biological function of RORγt can be moderated with small molecules.

In a study published last year in the journal Immunity, a research team identified three RORγt-specific inhibitors that suppress T helper 17 (Th17) cell responses, including Th17-cell-mediated autoimmune disease. The three inhibitors modulated the RORγt-dependent transcriptional network to varying extents and through distinct mechanisms: One inhibitor displaced RORγt from its target loci, while the other two inhibitors affected transcription predominantly without removing DNA binding.

The team systemically characterized RORγt binding in the presence and absence of drugs with corresponding whole-genome transcriptome sequencing, concluding: “Our work illustrates the power of a system-scale analysis of transcriptional regulation to characterize potential therapeutic compounds that inhibit pathogenic Th17 cells and suppress autoimmunity.”








This site uses Akismet to reduce spam. Learn how your comment data is processed.