Data demonstrates the potential of ‘1805 to reset the immune system through its unique mechanism of action across various autoimmune diseases, including inflammatory bowel disease and rheumatoid arthritis
NEW ORLEANS and CAMBRIDGE, UK, June 5, 2023 – Revolo Biotherapeutics (“Revolo” or the “Company”), a company developing therapies that reset the immune system to achieve superior long-term remission for patients with autoimmune and allergic diseases, today announced new pre-clinical and ex-vivo data in an oral presentation at the 5th Treg Directed Therapies Summit, showcasing the ability of its immune-resetting drug candidate ‘1805 to alter the T regulatory cell (Treg) phenotype, gene expression and inflammation in human gut tissue with inflammatory bowel disease (IBD) as well as selectively alter transcripts in macrophages harvested from rheumatoid arthritis (RA) subjects.
“This compelling data shows that ‘1805 enhances CD69+ and CD39+ Tregs in human tissue afflicted with IBD and improves anti-inflammatory gene transcription. This further illustrates ‘1805 unique mechanism of action as it resets the immune system to restore immune system balance,” said Jonathan Rigby, Chief Executive Officer of Revolo. “Additional data for ‘1805 in immune cells harvested from patients with RA showcases the selective alteration of RA cell transcripts compared to controls. Altogether, this data supports our upcoming Phase 2 trial in RA as well as future efforts in ulcerative colitis and other IBD indications. We are eager to continue exploring the broad potential of ‘1805 in various indications with the goal of providing long-term disease remission in patients living with autoimmune diseases.”
Data highlights include:
Inflammatory Bowel Disease
- Enhanced generation of double positive CD69+/CD39+ FoxP3 Tregs in the inflamed lamina propria of gut biopsies from IBD patients following treatment with ‘1805 while non-inflamed tissue biopsies did not.
- In mononuclear cultures, ‘1805 sustains an increase in CD69 expression on Tregs as well as that of its ligands, galectin-1, and S100A8/9. When CD69 binds to its ligands, the JAK/STAT5 pathway is activated to promote Treg differentiation and prevent pro-inflammatory Th1/Th7 cell generation.
- CD69+/CD39+ Tregs in intestinal tissues may play an important role in immune system balance and the prevention of inflammation.
- Following treatment with ‘1805, macrophages harvested from RA subjects experienced a selective reduction in pro-inflammatory gene transcripts in comparison to healthy controls which showed very little alteration in transcripts.
- In macrophages from RA subjects, ‘1805 upregulated ~1900 genes involved in cell contact and downregulated ~1550 genes involved largely in hypermetabolic changes. Macrophages from healthy donors showed little change in gene transcripts after treatment with ‘1805.
‘1805 is a modified analogue of the endogenous immune-regulatory binding immunoglobulin protein (BiP), a key player in immune function that resets the immune system for long-term disease remission. Its mechanism of action creates vast optionality across multiple indications and routes of administration.
Revolo Biotherapeutics is developing therapies that reset the immune system to achieve superior long-term remission for patients with autoimmune and allergic diseases, without the immune system suppression seen with current therapies. Its two drug candidates, ‘1805 and ‘1104, a protein and a peptide respectively, reset the immune system to prevent the chronic pro-inflammatory immune response that results in autoimmune or allergic disease. ‘1104 is a peptide derived from a natural immune-regulatory protein and has recently completed two Phase 2a clinical trials for patients with eosinophilic esophagitis (EoE) and allergic disease. The disease-agnostic mechanism of action of Revolo Biotherapeutic’s assets provides a potential platform for the development of treatments for multiple autoimmune and allergic diseases.
For further information, please visit www.revolobio.com.
Marylyn Rigby, SVP Investor Relations & Marketing
Monica Rouco Molina, Ph.D.