Chinese data propel InflaRx anti-complement mAb into clinic for severe COVID-19 pneumonia
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Backed by preclinical and clinical data that support blocking complement to mitigate coronavirus-mediated respiratory distress, InflaRx has begun a clinical study of its own complement inhibitor to treat COVID-19 patients with severe pneumonia.
InflaRx N.V. (NASDAQ:IFRX) announced after market close Tuesday that it has dosed the first patient in a randomized clinical trial of IFX-1, a mAb against C5a, to treat severe pneumonia due to SARS-CoV-2 infection.
Jordan Zwick, global head of business development and corporate strategy for the German company, told BioCentury the study is evaluating the safety and efficacy of IFX-1; he did not disclose the phase beyond saying it was not a Phase I trial. The company has yet to provide a timeline for a data readout.
Shares of InflaRx gained $1.91 (50%) to $5.73, adding $49.6 million in the company’s market cap to finish Wednesday’s session with a valuation of $149.6 million.
The company began the study based on early data from the first two severe COVID-19 patients who had received BDB-001 -- an anti-C5a mAb from Beijing Defengrei Biotechnology Co. Ltd. produced by the IFX-1 cell line but distinct from IFX-1 -- in an open-label Chinese trial. Defengrei gained rights in 2015 from InflaRx to use the IFX-1 cell line to develop and commercialize BDB-001 in China.
Data were reported in a preprint posted Monday to medRxiv by scientists at Beijing Institute of Biotechnology and the COVID-19 Investigation Team that it had dispatched to Wuhan; Army Medical University; and the COVID-19 Medical Team dispatched to Wuhan Huoshenshan Hospital by the People’s Liberation Army.
In both patients, one of whom had developed moderate acute respiratory distress syndrome (ARDS), BDB-001 began to reduce fever and CRP levels and improve lung and liver function within days.
ARDS is an inflammatory complication of lung damage, including that caused by SARS-CoV-2, SARS and Middle East respiratory syndrome coronavirus (MERS-CoV).
In the COVID-19 patient with ARDS, pneumonia severity assessed by CT scan was lower on day 20 vs. day 11 of BDB-001 administration. In the other patient, pneumonia was less severe 12 days after BDB-001 treatment onset.
The preprint further described a mechanism by which SARS-CoV-2 can cause ARDS. The researchers showed that the nucleocapsid (N) proteins of SARS-CoV-2, SARS and MERS-CoV all bound the complement activator MASP2 in vitro and in mice. The viruses’ N proteins also potentiated lipopolysaccharide (LPS)-induced pneumonia in mice.
C5a - Complement 5a
MASP2 - Mannan binding lectin serine peptidase 2 (MASP2)