Our Approach
Q32 Bio’s therapeutic approach is to target dysfunctional regulation of both the innate and adaptive immune systems so that homeostasis can be restored across a diversity of organ systems and disease indications.
Our Unique Approach to Complement
Innate immunity includes the complement system, which can be activated through three pathways, in which component proteins such as Complement Component 3 (C3) undergo cleavage into smaller protein fragments. These protein fragments have multiple functions, including clearance of cell debris, elimination of pathogenic intruders, and modulation of adaptive immunity. The complement system is tightly regulated by a broad tapestry of both positive and negative regulatory proteins. Disruption in the balance between complement activation and regulation can have pathological and potentially life-threatening consequences that derive from the complement system causing unrestricted and persistent tissue inflammation, cellular destruction, and ultimately impaired organ function. The number of diseases associated with hyperactivation or dysregulation of the complement system is extensive and encompasses all major organ systems including the kidney, skin, blood, lung, neuromuscular junction, and brain.
Q32 Bio is pioneering a new approach to treating complement-mediated diseases, by targeting our drugs directly to the affected tissue, while allowing for the other important functions of complement to remain largely unimpaired.
Complement ProgramTargeting IL-7
In partnership with Horizon Therapeutics, Q32 Bio is developing ADX-914, a high affinity anti-IL-7 receptor alpha (IL-7Rα) antibody that effectively blocks IL-7 and TSLP signaling, both of which contribute to inflammation and injury in a diversity of autoimmune disorders.
IL-7 is a cytokine that maintains the proliferation and survival of autoreactive T-effector cells and lowers their threshold for response in low antigen microenvironments. When these pathogenic T-effector cells expand and become activated they interfere with the immunosuppressive function of T-regulatory cells. As a result, IL-7 has the potent ability to promote and sustain inflammation and autoimmunity in multiple diseases.
TSLP is an epithelial-cell-derived cytokine that promotes inflammation in response to environmental stimuli. It is critically important for mediating Type 2 allergic immunity at barrier surfaces and has been implicated in several inflammatory and allergic conditions. Therefore, antagonism of the TSLP receptor has the potential to effectively treat a diverse group of diseases, including those in which both the IL-7 and TSLP pathways play a role in the disease pathogenesis together, in an overlapping manner (eg, rheumatoid arthritis), or sequentially (eg, atopic dermatitis).
IL-7/TSLP Program