Azitra has screened the first subject in its Phase Ib clinical trial of ATR-12 for treating Netherton syndrome, a chronic genetic skin disease.
The patient is expected to commence treatment by the end of the month.
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This multi-centre, randomised, double-blind, vehicle-controlled study will involve approximately 12 adults with Netherton syndrome.
Participants will receive topical ATR-12 or vehicle control on opposite sides of the body twice daily for 14 days, with a dosage of 10⁹CFU/g.
Azitra founder and COO Travis Whitfill said: “Enrolling the first patient in our Phase Ib trial of ATR-12 will mark a significant milestone for Azitra and, more importantly, for patients suffering from Netherton syndrome, who currently have limited treatment options.
“Our recent preclinical data demonstrate ATR-12’s potential to effectively deliver an active LEKTI subunit into the skin and address the underlying mechanisms of Netherton syndrome.”
Evaluating the safety and tolerability of the asset are the trial’s primary endpoints while secondary and exploratory objectives include assessing efficacy signals, biomarkers, pharmacodynamics, anti-LEKTI response, and cytokine responses.
The company plans to report interim safety data from the trial earlier next year, with full trial results expected in the second half of the year.
ATR-12 is a lead candidate of Azitra and is a strain of Staphylococcus epidermidis engineered to produce therapeutic levels of an active LEKTI protein subunit for treating Netherton syndrome.
Azitra acting CMO Mary Spellman said: “We are thrilled to begin this clinical trial of ATR-12 in Netherton syndrome patients.
“These patients suffer from poor quality of life and often debilitating disease and this trial will inform future studies for the treatment of Netherton syndrome in paediatric patients and longer treatment durations.”
The design of the trial is based on strong preclinical data, which includes the topical use of ATR-12 offering a 93% reduction in IL-36γ levels versus skin extracts that were induced to overexpress IL-36γ in preclinical models.
The asset also reduced protease activity in skin samples relative to a Netherton Syndrome model skin.
