- The proof-of-concept open-label study evaluated the safety and tolerability, function of regulatory T cells (Tregs), biomarkers, and preliminary efficacy (as measured by the ALSFRS-R scale) of COYA 302 over 48 weeks and was conducted in four ALS patients at the Houston Methodist Hospital by Dr. Stanley Appel and Dr. Jason Thonhoff.
- Study data showed no decline or minimal decline at 24 and 48 weeks, respectively, after initiation of treatment in a group of patients experiencing a mean decline of -1.1 points/month in their ALSFRS-R score prior to initiation of treatment with COYA 302. The mean (±SD) ALSFRS-R scores at week 24 (33.75 ±3.3) and week 48 (32 ±7.8) after initiation of treatment were not statistically different compared to the ALSFRS-R score at baseline (33.5 ±5.9), indicating significant amelioration in the progression of the disease.
- COYA 302 is an investigational combination biologic for subcutaneous administration, comprised of COYA 301 (low dose IL-2) and CTLA4-Ig fusion protein. COYA 302 has a dual mechanism of action and is intended to enhance Treg function in vivo, and downregulate the function of T effector cells, proinflammatory cells, and lipid peroxides.
- Over the course of treatment, COYA 302 significantly enhanced Treg suppressive function at 24 weeks and 48 weeks and lowered serum biomarkers of inflammation and oxidative stress.
- COYA 302 appeared to be well tolerated in all study patients.
HOUSTON--(BUSINESS WIRE)-- Coya Therapeutics, Inc. (NASDAQ: COYA) (“Coya” or the “Company”), a clinical-stage biotechnology company developing multiple therapeutic platforms intended to enhance Treg function, including biologics and cell therapies, today reported 48-week clinical data for its proof-of-concept open-label study in 4 ALS patients indicating that treatment with COYA 302 appeared to ameliorate disease progression.
Four ALS patients with a mean decline of -1.1 points/month in the Revised ALS Functional Rating Scale (ALSFRS-R) score prior to study initiation, were treated for 48 consecutive weeks with COYA 302 and were evaluated for safety and tolerability, Treg suppressive function, serum biomarkers of oxidative stress and inflammation, and clinical functioning as measured by the ALSFRS-R scale. Following the administration of COYA 302 for 48 weeks, patients were evaluated over an 8-week washout period.
During the 48-week treatment period, COYA 302 appeared to be well tolerated. The most common adverse event was mild injection-site reactions. No patient discontinued the study, and no deaths or other serious adverse events were reported.
Preliminary efficacy of COYA 302 was measured by the ALSFRS-R scale, a validated rating tool for monitoring the progression of disability in patients with ALS. The mean (±SD) ALSFRS-R scores at week 24 (33.75 ±3.3) and week 48 (32 ±7.8) after initiation of treatment with COYA 302 were not statistically different compared to the ALSFRS-R score at baseline (33.5 ±5.9), indicating significant amelioration in the progression of the disease over the 48-week treatment period.
Treg suppressive function, expressed as percentage of inhibition of proinflammatory T cell proliferation, showed a statistically significant increase over the course of the treatment period and was significantly reduced at the end of the 8-week washout post-treatment period. Treg suppressive function at 24 weeks (79.9±9.6) and 48 weeks (89.5±4.1) were significantly higher compared to baseline (62.1±8.1) (p