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Evommune is a clinical-stage biotechnology company developing innovative therapies that target key drivers of chronic inflammatory diseases, with initial clinical development programs focusing on chronic spontaneous urticaria (“CSU”), atopic dermatitis (“AD”) and ulcerative colitis (“UC”). Chronic inflammation is a significant healthcare problem in the world, substantially impacting patients’ quality of life and leading to life-threatening conditions. These conditions, if not prevented, ultimately lead to fatal diseases, such as cardiovascular diseases, diabetes and cancer, which contribute to three out of every five deaths worldwide and result in an estimated $90 billion of annual cost to the healthcare system in the United States. Our mission is to improve patients’ daily lives and prevent the long-term effects of uncontrolled inflammation that are a consequence of the limitations of existing therapies. To achieve this, we are advancing a portfolio of differentiated product candidates that target key drivers of chronic inflammation. Our management team’s proven drug development expertise and experience in the field of immunology and inflammation, combined with advanced scientific tools, enable us to identify and advance potent, highly selective molecules with distinctive mechanisms of action. By identifying treatment gaps of chronic inflammatory diseases, we strive to transform the treatment landscape, developing therapies that have the potential to offer rapid symptom relief and provide safe, durable resolution of the underlying disease. Among our portfolio of programs, we currently have two product candidates, EVO756 and EVO301, in Phase 2 trials. We are initially developing EVO756 for the treatment of CSU and AD, and EVO301 for the treatment of AD and UC. We see broad expansion potential for both programs across additional chronic inflammatory diseases. We also intend to advance additional preclinical programs into clinical development. Our most advanced clinical-stage product candidate, EVO756, is a potent and highly selective oral small molecule antagonist of MRGPRX2, a receptor predominantly found on mast cells and peripheral sensory neurons. We conducted a Phase 1 proof-of-concept trial in 132 healthy volunteers designed to assess the safety, tolerability, pharmacokinetic (“PK”) properties and pharmacodynamic (“PD”) properties of orally administered EVO756. EVO756 was observed to be well-tolerated at all doses tested, with no serious adverse events (“SAEs”), and PK results supporting daily dosing. As part of the trial, we conducted a skin challenge test in which EVO756 was observed to robustly decrease the healthy volunteers’ wheals induced by a MRGPRX2 ligand (“icatibant”), evidencing meaningful target engagement at all doses tested. We are currently conducting a Phase 2b trial of EVO756 in CSU and have completed a Phase 2 trial of EVO756 in chronic inducible urticaria (“CIndU”, and together with CSU, chronic urticarias or “CU”). Our CIndU Phase 2 trial was completed in May 2025 and generated data that demonstrated clinical activity (including improvement in FricTest score and pruritus numerical rating score (“pruritus-NRS”), as described below) in a patient population with symptomatic dermographism. Given significant overlap between the diseases and patient populations along with the contribution of neurogenic inflammation, we believe this supports the continued advancement of our CSU program. In addition, we believe EVO756’s clinical activity in symptomatic dermographism patients strongly supports the role of MRGPRX2 in neurogenic inflammation and supports the initiation of our AD program, as neurogenic inflammation plays a crucial role in both symptomatic dermographism and AD. In our Phase 2 CIndU trial, 70% (n=19) of the 27 observed patients demonstrated improvement at just four weeks, with 30% (n=8) of the observed patients achieving a complete response (achieving a FricTest score of zero (a clinician rated measure of symptomatic dermographism severity ranging from 0 to 4, with higher scores indicating greater severity)), of which 50% were immunoglobulin E (“IgE”) high (as defined by a serum IgE level of ≥100 IU/mL). An additional 11% (n=3) achieved a partial response as defined by a ≥2-point decrease in FricTest score and a further 30% (n=8) demonstrated a one-point decrease in FricTest score. Observed patients in the 300 mg once daily (“QD”) cohort saw an average reduction of 1.4 points in FricTest score after four weeks and observed patients in the 50 mg twice daily (“BID”) cohort saw an average reduction of 1.5 points. By comparison, in separate, independent trials conducted by third parties, patients treated with 300 mg omalizumab (n=19) saw a reduction of 1.4 points and patients treated with 300 mg barzolvolimab (n=33) saw a reduction of 1.6 points in FricTest score after four weeks. In addition, in our Phase 2 CIndU trial, both the 300 mg QD and the 50 mg BID doses of EVO756 were observed to result in rapid itch relief to patients, with observed patients in the 300 mg QD cohort experiencing an average reduction in pruritus-NRS of 2.4 points and observed patients in the 50 mg BID cohort seeing an average reduction of 2.1 points. Importantly, 93% (n=25) of observed patients demonstrated improvement at just four weeks in either FricTest or pruritus-NRS. Further, 75% (n=6) of those who did not achieve a decrease in FricTest score demonstrated a decrease in pruritus-NRS, evidencing the impact of EVO756 on itch at this early time-point, even in the absence of FricTest response. We initiated a Phase 2b dose-ranging trial in CSU in April 2025 and expect to report initial results in the first half of 2026. We also initiated a Phase 2b dose-ranging trial in moderate-to-severe AD patients in August 2025 and expect to report initial results in the second half of 2026. We plan to evaluate EVO756 in additional indications in which mast cell degranulation and neuroinflammation are key drivers of disease. Our second clinical-stage product candidate, EVO301, is a long-acting fusion protein consisting of an IL-18 binding protein (“BP”) and an anti-serum albumin Fab-associated (“SAFA”) domain. IL-18 is a pro-inflammatory cytokine of the IL-1 family that regulates various immune processes that drive inflammation and is a potent modulator of ongoing inflammation. We believe EVO301’s optimized approach to IL-18 binding and neutralization could enable significant advantages and differentiated clinical outcomes for patients, including with respect to efficacy, tissue distribution, dosing profile and reduced immunogenicity risk. In addition, EVO301’s distinct mechanism and modality complement those of EVO756, providing us with multiple potential avenues to bring innovative therapeutics to the large, underserved and rapidly expanding patient population suffering from chronic inflammatory diseases. We initiated a Phase 2 trial of EVO301 in adult patients with moderate-to-severe AD in March 2025 and expect to report initial results in the first half of 2026. Beyond AD, we plan to initiate a Phase 2 trial in moderate-to-severe UC patients in 2026. After completion of this UC trial, we may also evaluate EVO301 in Crohn’s disease and additional indications for which regulating the IL-18 pathway may reduce pro-inflammatory mediators driving tissue damage and chronic inflammation. Our principal executive offices are located in Palo Alto, CA.
