Quell Therapeutics Presents Promising Preclinical Data for QEL-005 CAR-Treg Therapy at ACR Convergence 2025
核心洞察
Quell Therapeutics (搜索) unveiled preclinical data for QEL-005 (搜索), a novel CAR-Treg (搜索) cell therapy targeting complex autoimmune diseases (搜索) like rheumatoid arthritis (搜索) and systemic sclerosis (搜索) at ACR Convergence 2025.
The therapy demonstrates broad immunomodulatory activity across multiple immune cell lineages including B cells, T cells, and inflammatory macrophages through a non-cytolytic "chill not kill" mechanism.
QEL-005 (搜索) utilizes a CD19 (搜索) CAR design with Quell's proprietary Foxp3 Phenotype Lock™ technology, offering potential safety advantages over conventional CAR-T and B-cell depletion approaches.
Quell Therapeutics (搜索) presented promising preclinical data for QEL-005 (搜索), a novel CAR-Treg (搜索) cell therapy designed to treat complex autoimmune inflammatory diseases, at the American College of Rheumatology annual meeting (ACR Convergence 2025) held in Chicago from October 24-29, 2025. The London-based company, a pioneer in engineered T-regulatory cell therapies, showcased data supporting the therapy's potential for treating rheumatoid arthritis (搜索) (RA) and systemic sclerosis (搜索) (SSc).
Novel CAR-Treg Design with Broad Mechanism of Action
QEL-005 (搜索) represents a novel approach to autoimmune disease treatment, utilizing Quell's multi-modular engineered Treg platform that incorporates the proprietary Foxp3 Phenotype Lock™ technology. The therapy employs a CD19 (搜索) CAR design that enables activation via B cells present in both inflamed tissue and lymph nodes, allowing for modulation of multiple pathogenic immune cells through a bystander mechanism of action.
The preclinical studies demonstrated QEL-005 (搜索)'s broad immunomodulatory activity across multiple immune cell lineages involved in complex autoimmune inflammation. The therapy showed suppression of T cell activity, modulation of B cell activity and antibody production, as well as modulation of other immune cells in the inflamed niche, including disease-associated inflammatory macrophages.
Differentiated "Chill Not Kill" Approach
QEL-005 (搜索)'s non-cytolytic mechanism of action, described by the company as "chill not kill," represents a significant differentiation from conventional CAR-T and other B-cell depletion approaches. This mechanism allows the therapy to control a breadth of immune cell types while potentially offering a safer and better tolerated therapeutic option compared to existing treatments.
Nathalie Belmonte PhD, SVP Research and Product Development at Quell, commented on the significance of the findings: "These exciting new data demonstrate the unique ability of QEL-005 (搜索) to control the pro-inflammatory effects of multiple immune cell types, with a single CAR-Treg (搜索) cell therapy. This includes modulation of pro-inflammatory macrophages into a pro-resolution phenotype."
Clinical Development Timeline
The preclinical data supports Quell's regulatory strategy, with the company planning to file Clinical Trial Applications (CTA) in Q4 2025. The Phase 1/2 CHILL clinical study is scheduled to initiate in the first half of 2026, focusing on patients with rheumatoid arthritis (搜索) and systemic sclerosis (搜索).
Belmonte emphasized the clinical development focus: "These mechanisms of QEL-005 (搜索) are highly differentiated from conventional CD19 (搜索)-focused CAR-T approaches that target only the B-cell compartment and will be crucial in developing the next generation of therapies for complex autoimmune diseases (搜索) such as RA and SSc, which are driven by multiple immune pathways."
Addressing Complex Autoimmune Diseases
Rheumatoid arthritis (搜索) and systemic sclerosis (搜索) represent significant medical challenges, characterized by complex interplay of tissue and activated immune cells that drive chronic inflammation loops resulting in substantial tissue damage. Current B cell depletion approaches, while highlighting the contribution of B cells in such diseases, are limited to targeting a single immune cell type and carry safety and tolerability risks in certain patient populations.
Regulatory T cells serve as key mediators of immune and tissue homeostasis with essential roles in restraining autoimmunity. Tregs employ a wide array of mechanisms to mediate this effect, enabling control over multiple immune pathways across a broad range of tissues and cell types.
The data presentation at ACR Convergence 2025 was delivered by Jenny McGovern, Director/Non-Clinical Group Leader at Quell Therapeutics (搜索), during the B Cell Biology & Targets in Autoimmune & Inflammatory Disease Poster session on Sunday, October 26, 2025.