InflaRx N.V. (NASDAQ:IFRX), a biopharmaceutical company pioneering anti-inflammatory therapeutics by targeting the complement system, today announced new in vitro findings demonstrating that izicopan does not exhibit time-dependent inhibition of CYP3A4, an important indicator for the risk for drug-drug interactions (DDIs) and liver toxicity. These results further support izicopan's potential as a differentiated, best-in-class oral C5a receptor (C5aR) inhibitor.

To build upon previous CYP interaction data for izicopan, which showed only marginal inhibition of CYP3A4 (IC₅₀ = 62 µM) in a time-dependent inhibition (TDI) IC₅₀ shift assay, InflaRx conducted a mechanistically informative Ki-based TDI (Ki/Kinact) study. While TDI shift assays serve as rapid screening tools to identify potential time-dependent inhibition, Ki/Kinact studies provide a more definitive and quantitative assessment, enabling a reliable determination of the presence or absence of time-dependent inhibition.

The Ki-based TDI study confirms that izicopan does not inhibit CYP3A4 (IC₅₀ > 100 µM) and exhibits no time-dependent inhibition up to the highest tested concentration (100 µM), supporting a low risk of clinically relevant DDIs. Using two probe substrates, midazolam (MDZ) and testosterone (TES), no evidence of CYP3A4 time-dependent inhibition was observed, providing mechanistic confirmation of izicopan's favorable pharmacological profile. This feature is particularly important, as time-dependent CYP3A4 inhibition can result in DDIs, hepatotoxicity, or reduced metabolism of concomitant medications such as corticosteroids.