Overview

Seaside founders understand the toll that brain development disorders, including intellectual disabilities and autism, take on families and share the sense of frustration that effective therapeutics are still not available despite recent scientific advances.

Seaside Therapeutics was founded to develop potential treatments for these underserved populations by translating breakthrough discoveries in neurobiology into therapeutics that improve the lives of patients and their families. Our lead drug development programs are currently focused on creating new treatments to correct or improve the course of Fragile X Syndrome and autism. We also continue to evaluate discoveries and explore opportunities to develop novel therapeutics for patients with other disorders of brain development.

Our Science

Historically, drug discovery in disorders of brain development has been unproductive largely due to the lack of a mechanistic understanding of these disorders as well as the absence of predictive animal models. Seaside Therapeutics is changing this paradigm through scientific exploration that focuses on identifying the fundamental pathophysiology of brain development disorders and application of this knowledge to develop targeted therapeutics. Recent discoveries by the Company's scientific founder, Dr. Mark Bear, have revealed a molecular pathway, the mGluR signaling cascade, that is disrupted in a specific disorder of brain development — Fragile X Syndrome. Specifically, the scientific evidence suggests that most, if not all, of the neurological and psychiatric consequences of Fragile X can be accounted for by exaggerated signaling through this mGluR pathway. The most important observation, however, is that treatment with medications designed to normalize this exaggerated mGluR signaling effectively normalizes numerous measures of brain function in the Fragile X animal models.

Our scientific discoveries suggest, for the first time, a sound rationale for the treatment of Fragile X Syndrome. We believe that medications designed to normalize function in this mGluR pathway will provide significant therapeutic benefit to humans with Fragile X Syndrome. Of note, a number of other human developmental disorders share similar characteristics with Fragile X such as developmental delay and cognitive impairment, anxiety, reduced motor coordination, altered gastrointestinal function, an increased incidence of childhood epilepsy and/or autism. We predict that some of these other disorders with similar symptoms will ultimately be traced to defects elsewhere in the same molecular pathways. If this prediction is correct, the mGluR theory may have broad applicability beyond Fragile X Syndrome and Seaside’s therapeutic candidates may provide benefit to patients with these other disorders.