MediciNova Announces Results of Studies under BARDA Contract to Develop MN 166 (ibudilast) as a Medical Countermeasure Against Chlorine Gas-induced Lung Injury - Seite 2

In the multi-dose study, based on the PK profile in test subjects, each treatment was given every 12 hours with a total of 4 doses after the Cl₂ gas challenge. Treatment with MN-166 (ibudilast) high dose resulted in greater improvement (p=0.0001) in the mean PaO₂/FiO₂ ratio than MN-166 (ibudilast) low dose, rolipram, and negative control. The mean PaO₂/FiO₂ ratio decreased (worsened) by 57% from 518.7 mmHg at baseline (the end of the chlorine gas exposure) to 224.8 mmHg at hour 48 in the negative control group. The mean PaO₂/FiO₂ ratio decreased (worsened) by 36% from 516.0 mmHg at baseline to 327.8 mmHg at hour 48 in the MN-166 (ibudilast) high dose group. At hour 48, the last time point measured in the study, the mean PaO₂/FiO₂ ratio was 46% higher (better) in the MN-166 (ibudilast) high dose group than in the negative control group (327.8 vs. 224.8 mmHg).   Since ARDS is defined as a PaO₂/FiO₂ ratio less than 300 mmHg, the mean PaO₂/FiO₂ ratio values indicate that the negative control group was still categorized as having mild ARDS at the end of the 48-hour evaluation period but the MN-166 (ibudilast) high dose group had recovered enough to no longer be defined as having ARDS. MN-166 (ibudilast) was well tolerated and no safety concerns were observed in the multi-dose study.

A preliminary proof-of-concept (POC) study was conducted to determine the feasibility of the second nonclinical model as a tool to evaluate MN-166 (ibudilast) as a MCM for chlorine gas exposure. After multiple attempts by MediciNova’s subcontractor to establish the feasibility of the second Cl₂-gas induced lung injury model, it was not deemed to be a feasible model to evaluate a drug candidate and there are no evaluable efficacy results from the second nonclinical model POC study.

Kazuko Matsuda, MD, PhD, MPH, Chief Medical Officer of MediciNova, Inc., commented, "We are very pleased to report the positive results from the multi-dose nonclinical model study in which MN-166 demonstrated a large and significant improvement in pulmonary function and a higher survival rate. We previously reported that MN-166 attenuated histological changes observed in an LPS-induced ARDS nonclinical model, including pulmonary edema in lung tissue, and protected against pulmonary injury by reducing cellular apoptosis in lung tissue. We also previously reported positive and significant outcomes from a clinical trial of MN-166 in hospitalized severe COVID-19 patients at risk of developing ARDS. Combining the positive nonclinical chlorine gas-induced ALI model study results with the positive results from the human clinical trial in severe COVID-19 patients at risk of developing ARDS, we believe MN-166 has potential to treat acute lung disease from various causes. We plan to meet with the FDA to discuss the next steps in this development program. Development of medical countermeasures does not require human clinical trials to establish efficacy when these trials would not be ethical or feasible. There is a great unmet medical need for treatments for chlorine gas exposure as there is no drug approved specifically for this indication. We thank BARDA for their support of this program.”