QEL-005 is an autologous, B cell activated, FOXP3 Phenotype-Locked™ engineered nTreg therapy. QEL-005 is currently under investigation in the CHILL study in patients with difficult-to-treat rheumatoid arthritis and systemic sclerosis. Beyond that, there is opportunity to treat patients with many other diseases, including Lupus, Sjogren’s disease, ANCA associated Vasculitis, and renal diseases.

Phase 1/2 trial in Difficult to Treat Rheumatoid Arthritis and Systemic Sclerosis is ongoing across study sites/hospitals in the UK and Europe with plans to expand in USA.

Rheumatologic autoimmune diseases affect 5-10% of the population and are responsible for substantial reductions in duration and quality of life.

Difficult-to-treat rheumatoid arthritis (D2TRA), which affects >100,000 people in the US, is characterized by disease which is uncontrolled even with the most advanced approved therapies. People cycle through existing treatment options with inadequate response and experience poor quality of life from organ damage, disability and co-morbidities.

Clinical trials with B cell depleting approaches have seen transformational for some patients, but these treatment are often accompanied by toxicity. Quell is developing nTreg therapies designed to be both transformational and SAFE.

QEL-003 is a Th17-activated engineered nTreg therapy designed as a pipeline-in-a-product for multiple autoimmune diseases, starting with refractory inflammatory bowel disease (Crohn’s disease and ulcerative colitis).

IND/CTA filings are planned for H1 2027.

A substantial proportion of people with inflammatory bowel disease (IBD) remain refractory to multiple treatment lines. Persistent, severe symptoms can lead to complications, repeated hospitalizations and an increased likelihood of surgery – highlighting the need for more effective, disease-modifying therapies that can interrupt the cycle of relapse and prevent cumulative tissue damage.

QEL-002 is an islet-targeted engineered nTreg therapy for recent onset type 1 diabetes. It is designed to halt the inflammatory response against the pancreas, preventing further beta cell loss, resulting in durable control of dysglycemia with the potential to eliminate the need for exogenous insulin.​

Poor glycaemic control following shortly after type 1 diabetes onset is associated with a significant risk of developing severe complications such as cardiovascular disease, kidney damage, retinopathy and neuropathy. Inadequate management not only diminishes quality of life but also elevates the risk of early mortality, underscoring the critical need for effective and timely diabetes control.