Idorsia Pharmaceuticals Ltd. has described cystic fibrosis transmembrane conductance regulator (CFTR) modulators reported to be useful for the treatment of cystic fibrosis.
Researchers from National Institute of Health Sciences (Japan) have published data from a study that aimed to identify novel biomarkers for the diagnosis of diffuse alveolar damage (DAD), a drug-induced interstitial lung disease (DILD) associated with a poor prognosis.
Researchers from Almirall SA and affiliated organizations reported the discovery and preclinical characterization of LAS-200813, a novel peptide inhibitor of the Keap1-Nrf2 protein-protein interaction.
Researchers from Jagiellonian University presented the discovery of novel multifunctional inhibitors of phosphodiesterases (PDEs) and transient receptor potential ankyrin 1 (TRPA1) antagonists as potential therapeutic candidates for the treatment for chronic airway disorders.
Research Triangle Institute (RTI International) has described new heteroaryl derivatives acting as apelin receptor (angiotensin-receptor like 1; APJ) agonists reported to be useful for the treatment of lung fibrosis.
Researchers from GSK plc presented the discovery and preclinical characterization of novel potent and selective inhaled phosphatidylinositol 4-kinase β (PI4Kβ) inhibitor being developed for the treatment of human rhinovirus (HRV)-induced chronic obstructive pulmonary disease (COPD) exacerbations.
After a midstage trial showed no benefit from adding ELX-02 (exaluren) to Kalydeco (ivacaftor, Vertex Pharmaceuticals Inc.) for certain cystic fibrosis (CF) patients, Eloxx Pharmaceuticals Inc. said it will discuss next steps for the program, its lead candidate, with the trial's sponsor, the CF Foundation. A proof-of-concept trial for EXL-02 in the rare kidney disease Alport syndrome will start later this year, the company said.
Previous research has demonstrated that the expression of the calcium-activated potassium channel (Kca 3.1) is higher in patients with idiopathic pulmonary fibrosis (IPF), and that genetic and pharmacological inhibition of Kca3.1 was able to prevent or attenuate fibrosis.
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