Professor Tommy B Andersson

Senior Principal Scientist


Tommy B Andersson joined AstraZeneca 1993 where he has held several positions in Drug metabolism and Pharmacokinetic departments as well as in Clinical Pharmacology. He was also appointed Professor at Karolinska Institutet in Drug Metabolism 2003. He is now a Senior Principal Scientist at AstraZeneca R&D, Gothenburg, at Cardiovascular and Metabolic disease function and currently leading the development of microphysiological systems at the department. He has an excellent track-record of developing and executing strategic and operational plans across boundaries in complex global matrix organisations. Extensive experience in leading cross-functional problem solving groups delivering expert evaluations, plans and solutions.  Strong scientific expertise with over 160 publications (H-index 56, over 9000 citations) and recognized as a key opinion leader in drug metabolism, disposition and toxicology.

Novel Microphysiological Multi-Organ Systems for Studies of Human Metabolic Diseases in Drug Discovery

Abstract: Multi organ-on-a-chip technologies, emulating human physiology and mimicking human disease states, could aid preclinical efforts by providing relevant translational models to validate targets and test tool compounds early in drug discovery. Such models have the potential to improve translation to patients, decrease time spent in early clinical programs and reduce the need for animal models.
Rodent studies have shown that insulin resistance causes hepatocytes to produce secreted factors that influence the islets. Whether similar cross talk exist in man remains to be determined. We therefore decided to develop a human liver - pancreatic islets chip model 1. Pancreatic islets and liver spheroids were applied in a two-organ microfluidic chip supplied by TissUse™ that allows cross talk between both organs. We have demonstrated that the model responds in a physiological way to a glucose load by increasing insulin secretion, which stimulates glucose consumption by the liver spheroids. Both islet and liver spheroids show stable functionality as indicated by insulin secretion, albumin production and glucose consumption over the experimental period of two weeks. Initial results indicate that the liver spheroids can be made insulin resistant, and thus represent a relevant metabolic disease model.