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IMSA101, a novel small molecule analogue of cGAMP, is our lead product candidate and one of the most advanced STING agonist programs in development today. Designed with a unique defense-sensing mechanism that increases anti-tumor immunity to ultimately stimulate cytokines to turn “cold” tumors to “hot”, IMSA101 holds first-in-class potential for treating solid tumors.
In preclinical studies, IMSA101 showed promise in both monotherapy and immunotherapy combination settings, demonstrating robust tumor growth inhibition as a single agent and with an anti-PD-L1 in multiple mouse models. In these early studies, IMSA101 stimulated production of IFNs and cytokines and generated long-term memory immunity to tumors.
We are currently conducting Phase 2 studies evaluating IMSA101 in combination with radiation and checkpoint inhibitors in patients with oligoprogressive (OPD) and oligometastatic (OMD) solid tumor malignancies.
Drug Conjugate Platform
We are developing second-generation STING agonist drug candidates that are designed for targeted delivery of a STING agonist using a drug conjugate approach. We have developed a drug conjugate technology platform that conjugates, in a site specific manner, highly potent STING agonists to antibodies or other molecules directed at proven cancer targets. The resulting immune stimulating drug candidate enables the delivery of STING agonists to the targeted area.
IMSA201 is our lead candidate from our drug conjugate technology platform. In preclinical models, IMSA201 exhibited strong efficacy, activated myeloid cells and promoted intrinsic anti-tumor immunity.
Autoimmune disease arises when the body’s natural defense system cannot distinguish between its own cells and foreign cells, resulting in the body mistakenly attacking normal cells. Preventing aberrant activation of the cGAS-STING pathway is crucial for maintaining immune homeostasis. If the cGAS-STING pathway is unreasonably activated by lack of regulation, it causes activation of the immune system, resulting in autoimmune diseases.
Several enzymes (RNase H2, TREX1, and DNase II) regulate cGAS activation by controlling the basal level of cytosolic DNA. Mice deficient in these functional enzymes have been shown to develop autoimmune disease with inflammation and lethality in a cGAS- and STING-dependent manner, suggesting a critical role for the cGAS-STING pathway in the pathogenesis of autoimmune diseases.
We are evaluating novel small molecule cGAS antagonists for potential applications in the treatment of autoimmune diseases and other diseases characterized by excessive accumulation of cytosolic DNA. Our drug discovery team is currently evaluating several promising cGAS inhibitors as potential drug candidates.