Prof Charlton joined the University of Nottingham in 2014 where he is Professor of Molecular Pharmacology and Drug Discovery in the School of Life Sciences. Prior to that he spent 16 years in the pharmaceutical industry, both at SmithKline Beecham and Novartis. At Novartis he was Director of Molecular Pharmacology in Respiratory Diseases, leading an assay development and compound profiling team of over 30 scientists providing expert opinion and support for GPCR, ion channel and enzyme projects. He has broad drug discovery experience, ranging from target validation through to leading full lead optimisation programmes to successful clinical proof of concept. He also served on global development teams for several inhaled compounds in Ph2, Ph3 and post-launch, including Onbrez™, Seebri™ and UltiBro™. In 2007 Prof Charlton was awarded Novartis Leading Scientist in recognition of his contribution to the field of quantitative pharmacology and to the Novartis pipeline.
Prof Charlton has research interests in two key areas:
Prof Charlton is interested in all aspects of the quantitative assessment of ligand-receptor interactions, with particular expertise in the kinetics of ligand binding and signalling. His current research areas include:
- Developing novel higher throughput methodologies to quantify kinetic rate constants for binding of drugs to proteins. Main focus is GPCRs but also tackling protein-protein interactions and soluble enzymes
- Investigating biased signaling at GPCRs by investigating spatiotemporal signaling at a single cell and subcellular level using fluorescent and luminescent biosensors
- Measuring the concentration of drugs at a sub-cellular level to determine the influence of physchem properties and rebinding on observed pharmacology (e.g. kinetics and biased agonism)
The main drug discovery focus of the group is the identification of novel therapies to treat remodelling diseases, particularly in the airways (e.g. IPF, PAH, severe asthma and COPD). Prof Charlton's team has expertise in the culture of primary human structural cells from the lung (e.g. lung fibroblasts and smooth muscle cells from both the airway and pulmonary vasculature) and employs both phenotypic and pathway assays in a chemical-biology approach to identify targets capable of preventing or reversing key aspects of tissue remodelling.