Investigation into the anti-airway inflammatory role of the PI3Kγ inhibitor JN-PK1: An in vitro and in vivo study

•JN-PK1 concentration and time dependently inhibited the PI3Kγ-dependent cellular C5a-induced AKT Ser473 phosphorylation in RAW264.7 macrophages.•JN-PK1 suppressed the LPS-induced pro-inflammatory cytokines expression and nitric oxide production in RAW264.7 macrophages.•Oral administration of JN-PK1 attenuated OVA-induced asthma in association with the inhibition of the PI3K signaling pathway.•JN-PK1 inhibited increases in inflammatory cell counts and reduced T-helper type 2 cytokine production in an OVA-induced asthma model.