Quell Therapeutics initiates CHILL phase 1/2 trial of novel QEL-005 CAR Treg therapy in Refractory Rheumatoid Arthritis and Systemic Sclerosis following UK CTA approval

Quell Therapeutics Ltd (“Quell”), announced last week that it has initiated a Phase 1/2 basket clinical study evaluating its autologous CAR-Treg therapy, QEL-005, in patients with Rheumatoid Arthritis and Systemic Sclerosis – the CHILL study following the recent approval by UK MHRA (Medicines and Healthcare products Regulatory Agency) of the company’s Clinical Trial Application (CTA).

CHILL is a multinational clinical study that will recruit participants in the UK, Germany and Spain, with patient enrolment underway at leading clinical centres across the UK. Early clinical findings are expected during Q1 2027.

QEL‑005 is a novel product candidate built on Quell’s proprietary Phenotype Locked™ CAR‑Treg platform. It is designed to be selectively activated and exert immune suppression within inflamed tissues and the surrounding lymphoid structures, providing broad control of disease activity. By leveraging a Treg-optimized CD19‑directed CAR, QEL‑005 CAR-Tregs are activated in the presence of B cells and mediate immune regulation through bystander suppression, modulating pro‑inflammatory T cells, B cells, macrophages and stroma – a unique approach.

Results from pre-clinical studies, presented at American College of Rheumatology annual meeting (ACR Convergence 2025) in October 2025, demonstrated the immunomodulatory activity of QEL-005 across multiple immune cell lineages involved in complex autoimmune inflammation, including B cells, T cells and inflammatory macrophages. QEL-005’s broad mechanism of action clearly differentiates it from CAR‑T and other B‑cell–depletion therapies, offering a safer, better‑tolerated option with potential broader efficacy in more complex autoimmune diseases.

In addition, findings from Quell’s LIBERATE Phase 1/2 trial in liver transplantation (see separate announcement) demonstrate the clinical safety, persistence, and functional stability of Quell’s Phenotype Locked™ CAR‑Treg cells for over one year, with evidence of trafficking and engraftment within target tissues in proximity to infiltrating immune cells and molecular drivers of inflammation.

Iain McGill, Chief Executive Officer of Quell, commented:

Initiating the CHILL study with QEL-005 following CTA approval marks an exciting milestone for Quell and our pre-clinical package adds to the growing evidence that Tregs can modulate multiple drivers of autoimmune inflammation, including T and B cells, macrophages and pro‑inflammatory fibroblasts. With QEL‑005, our goal is to ‘CHILL, not KILL’ – taking a differentiated therapeutic approach that restores immune balance rather than relying solely on B cell depletion. This milestone reflects the outstanding dedication of our team and collaborators as we work to deliver durable, transformative therapies for people living with autoimmune diseases.

Professor Christopher Buckley from the Kennedy Institute of Rheumatology and Chief Investigator for the CHILL study commented

People with Rheumatoid Arthritis and Systemic Sclerosis dream of a cure for their disease. Until now treatments for Immune Mediated Inflammatory Diseases have relied on suppressing inflammation. Excitingly, CAR-T cells which kill pathogenic cells have now emerged as therapies that appear to help reset damaged tissues. However CAR T cells kill, they don’t regulate. We believe that using CAR-Tregs, that are natural tissue regulators, we will be able to achieve deep and durable disease control and achieve a cure. As Chief Investigator in this study I am delighted to be working with Quell and an amazing team of European Clinician Scientists in the CHILL study that aims for durable cures for our patients.

Professor Georg Schett, Principal Investigator for the University Hospital Erlangen CHILL site, commented

Providing a stable regulatory immune cell environment at sites of inflammation is a mesmerizing therapeutic concept for chronic inflammatory diseases. The idea of activating T regulatory cells in a site-directed way, in B-cell rich lymphatic tissues and sites of inflammation, may provide peripheral immune tolerance and intercept autoimmune disease.