Asthma is a heterogeneous disease, which may be classified into phenotypes and endotypes based on clinical characteristics and molecular mechanisms. The best described endotype of severe
asthma is type 2 (T2)-high
asthma, characterized by release of inflammatory
cytokines by T helper 2 (TH2) cells and type 2 innate lymphoid cells cells.
Prostaglandin D2 contributes to T2
inflammation through binding of the
G-protein-coupled receptor chemoattractant receptor-homologous molecule expressed on TH2 cells (CRTH2).
Fevipiprant is an oral competitive antagonist of CRTH2. Early-phase trials have demonstrated safety and potential efficacy in patients with
asthma, specifically, improvement in FEV1 and eosinophilic airway
inflammation. However, no clear
biomarker identified patients who responded favorably to
fevipiprant, although patients with moderate-to-severe
asthma and evidence of T2
inflammation may be more likely to respond to treatment. Additional studies are needed to determine the efficacy and target population for use of this drug in patients with
asthma.