Aditxt Says Mayo Clinic Pre-Clinical Studies Further Validates Findings Of ADI-100, Adimune's Lead Therapeutic Candidate for Autoimmune Diseases

Author: Benzinga Newsdesk | April 14, 2025 08:19am

Findings Further Support the Safety Profile and Immunomodulatory Effects of ADI-100, Adimune's Lead Therapeutic Candidate for Autoimmune Diseases

Aditxt, Inc. (NASDAQ:ADTX) ("Aditxt" or the "Company"), a social innovation platform accelerating promising health innovations, today announced that a recently completed study conducted by the Mayo Clinic further validates the preclinical findings of ADI-100, the lead therapeutic candidate developed by Aditxt's wholly owned subsidiary, Adimune™, Inc. ("Adimune").

The independent study, led by Dr. Sean Pittock and Dr. Charles Howe of the Mayo Clinic's neuroimmunology team, confirmed that ADI-100 induces immune tolerance to glutamic acid decarboxylase (GAD)—a key autoantigen implicated in multiple autoimmune conditions, including type 1 diabetes, stiff person syndrome, cerebellar ataxia, and autoimmune epilepsy.

"These results mark an important milestone not only for Adimune's platform but also for Aditxt's broader vision of transforming the way we approach autoimmune diseases," said Amro Albanna, co-founder and CEO of Aditxt. "We believe that autoimmunity represents one of the most underserved and challenging areas of medicine. ADI-100's potential ability to restore immune tolerance without broad immunosuppression is a meaningful step toward safer, more targeted treatments."

Key Findings from the Mayo Clinic Study Include:

• Encouraging Safety Profile: ADI-100 did not increase T cell reactivity to GAD, reinforcing the product candidate's preclinical safety profile.
• Immune Modulation at the Cellular Level: Dendritic cells treated with ADI-100 apoptotic bodies displayed increased tolerogenic markers.
• Antigen-Specific Suppression: ADI-100-induced tolerogenic dendritic cells reduced activation of T cells from GAD-sensitive patients, even in the presence of proinflammatory stimuli.

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