Matthias von Herrath,
Vice President and Senior Medical Officer, Novo Nordisk,
Professor, La Jolla Institute
Dr. Matthias von Herrath is committed to clinical translation of immune-based interventions in autoimmune and metabolic diseases, the latter in particular being an exciting emerging field. His expertise and main strength is working at the interface of experimental research to interpret and refine early phase I/II clinical trials in order to optimize strategies for phase 3 trials and drug approval. This comprises translation from various animal models to human interventions, optimization of immunotherapies and their relative ranking, assessment of combination therapies, development of biomarkers as primary or secondary outcomes, induction of antigen specific tolerance in autoimmunity, regulatory cells and clinical T cell assays. In order to be better able to pursue his goal of clinical translation, Dr. von Herrath accepted the position of Vice President and Head of Novo Nordisk’s diabetes R&D Center in Seattle in autumn of 2011. At Novo Nordisk, he built the diabetes translational unit, which is based on less conventional and innovative design. In addition, he took on the task of finding new treatments to diabetic kidney disease in 2017. In 2018 he moved to the CMO office as many of the interventions are now at a later developmental stage and the position allows bridging between patient needs and trial design, biomarkers and basic mechanistic insight.
Understanding disease pathology remains very close to Dr. von Herrath’s heart and Novo Nordisk enabled him to keep an appointment at La Jolla Institute, where he pursues NIH-funded research on the pathology of type 1 and 2 diabetes as part of the national pancreatic organ donor network (nPOD). This is a multinational collaborative effort where data are shared in real time and no intellectual property yet lots of new knowledge on the pathology of type 1 and 2 diabetes is being generated. It is a unique new collaborative paradigm for academic and also industry settings.
Liraglutide Protects Human Beta-Cell Function From Cytokine- And Immune Cell-Induced Stress In Human In Vitro Models of T1D
Wednesday, 14 December 2022 at 11:00
Add to Calendar ▼2022-12-14 11:00:002022-12-14 12:00:00Europe/LondonLiraglutide Protects Human Beta-Cell Function From Cytokine- And Immune Cell-Induced Stress In Human In Vitro Models of T1DOrganoids and Microphysiological Systems 2022 in Long Beach, CaliforniaLong Beach, CaliforniaSELECTBIOenquiries@selectbiosciences.com
GLP-1 receptor agonists (GLP-1 RA) are hypothesized to preserve beta-cell function and enhance insulin secretion in type 1 diabetes (T1D). We evaluated the effects of the GLP-1 RA, liraglutide, on reaggregated, uniform primary human islets under T1D-relevant stress. We established three high-throughput-compatible islet-immune injury models: a cytokine-induced stress assay, an activated peripheral blood mononuclear cell-islet co-culture, and an islet-HLA-A2-restricted preproinsulin-specific cytotoxic T lymphocyte co-culture. In all models, the decline in beta-cell health manifested as increased basal and decreased glucose-stimulated insulin release and decreased total insulin content. Liraglutide prevented loss of stimulated insulin secretion under cytokine- and immune-mediated stress, most notably by preserving the first-phase insulin response and decreasing immune cell infiltration and cytokine secretion. Our results corroborate the therapeutic potential of liraglutide for the preservation of beta-cell function at the time of T1D onset, provide further evidence of a GLP1-related anti-inflammatory effect, and support the utility of biomimetic islet-immune assays.
Add to Calendar ▼2022-12-12 00:00:002022-12-14 00:00:00Europe/LondonOrganoids and Microphysiological Systems 2022Organoids and Microphysiological Systems 2022 in Long Beach, CaliforniaLong Beach, CaliforniaSELECTBIOenquiries@selectbiosciences.com