Gefapixant, a P2X3 receptor antagonist, for the treatment of refractory or unexplained chronic cough: a randomised, double-blind, controlled, parallel-group, phase 2b trial
PI: Professor Alyn Morice
Gefapixant is a P2X3 receptor antagonist that has shown promise for the treatment of refractory and unexplained chronic cough. The aim of this study was to evaluate the efficacy of gefapixant compared with placebo after 12 weeks of treatment for refractory chronic cough or unexplained chronic cough.
Outputs
Gefapixant, a P2X3 receptor antagonist, for the treatment of refractory or unexplained chronic cough: a randomised, double-blind, controlled, parallel-group, phase 2b trial. The Lancet Respiratory Medicine, 1 Aug 2020, 775-785
Sentinel: Hull Asthma Project
Funder: AstraZeneca UK Ltd (£238,410.55)
PI: Professor Michael Crooks
Collaborators: Dr Chao Huang, Professor Judith Cohen, Professor Alyn Morice, John Turgoose
Timeframe: November 2020 to February 2023
The SENITEL project is quality improvement project that is being undertaken to transform asthma care in Hull. Implementation of the 2018 Hull University Teaching Hospitals NHS Trust Guidelines for the Treatment of Adult Asthma into routine care is being promoted. This is being undertaken across the city's five Primary Care Networks (PCNs)/practices.
A longitudinal study of blood monocyte activation in sarcoidosis
PI: Professor Simon Hart
In sarcoidosis, organized collections of activated immune cells (granulomas) form in the lungs and other organs. How and why the immune cells become activated could identify targets for new treatment approaches. Our research demonstrated that the inhibitory molecule CD200R is reduced on circulating blood monocytes in people with sarcoidosis compared with healthy subjects (Fraser SD et al, Sci Rep. 2016 Dec 8;6:38689). Lack of CD200R leads to hyper-activation of monocytes, which in turn produce more inflammatory cytokines (proteins that drive inflammation in granulomas). CD200R normally serves to dampen down the immune response, so deficiency may contribute to the excessive inflammation in sarcoidosis.