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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.
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.
Bridge Biotherapeutics Inc. recently reported data for BBT-209, an endogenous G protein-coupled receptor 19 (GPCR19) agonist under development for the treatment of idiopathic pulmonary fibrosis (IPF).
It is known that dendritic cells and innate lymphoid cells type 2 (ILC2) play key roles in allergen sensitization, and humoral factors such as complement C3a and complement C5a are highly involved in the development and severity of asthma through the binding to their receptors C3AR1 and complement C5a receptor 1 (C5AR1), respectively.
The Massachusetts Institute of Technology (MIT) has developed collagen mimetic peptides for PET imaging to detect idiopathic pulmonary fibrosis (IPF), with [68Ga]DOTA-CMP showing selective identification of fibrotic collagen in vivo.
A metabolite derived from the airway microbiome, indole-3-acetic acid (IAA), could become a potential therapeutic candidate for chronic obstructive pulmonary disease (COPD). Researchers at South China Normal University (SCNU) have shown how IAA prevents lung function decline by reducing inflammation, apoptosis and emphysema through IL-22 in the interaction between macrophages and alveolar epithelial cells.
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