Complex biological systems interact with the environment to achieve homeostasis – the physiological stability needed to sustain life. From basic functions that maintain normal body temperature regulation to calibrated immune signaling to fight disease, our bodies seek equilibrium to survive and thrive. Autoimmune and inflammatory diseases result from dysregulation of the healthy immune response, rooted in either the adaptive or innate immune systems. They include many debilitating and life-threatening conditions, affecting every organ system and causing dramatically decreased quality of life and significant morbidity and mortality for tens of millions of patients worldwide. For many autoimmune and inflammatory diseases, treatment options are inadequate or absent altogether. Systemic immunomodulators can help manage some inflammatory and autoimmune diseases, but they often deliver inadequate efficacy and are associated with treatment-limiting side effects that can be severe.
To meet the need for therapies that safely address underlying immune dysregulation, Q32 Bio has developed an integrated portfolio of therapies to modulate the innate and adaptive immune responses. Our team’s mission is to bring safer, more efficacious therapeutics to patients suffering from a wide range of devastating autoimmune and inflammatory diseases, starting with those rooted in the complement system and interleukin-7 (IL-7) signaling pathways. In pursuit of our bold vision, Q32 Bio has assembled leaders in the field of immunology uniquely positioned to develop novel biologics based on the body’s innate and adaptive immune systems. Our lead molecules include therapeutic fusion proteins that deliver negative regulators of complement activation directly to disease-affected tissues and a monoclonal antibody antagonist of the interleukin-7 receptor (IL-7R).
Proprietary tissue-targeted complement platform and best-in-class IL-7R antibody technology to treat patients with severe autoimmune and inflammatory disease; clinical trials begin in 2020 Read More >