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Bengt Hamrén

Researcher at AstraZeneca

Publications -  36
Citations -  956

Bengt Hamrén is an academic researcher from AstraZeneca. The author has contributed to research in topics: Population & Tesaglitazar. The author has an hindex of 12, co-authored 33 publications receiving 752 citations. Previous affiliations of Bengt Hamrén include Uppsala University & Hoffmann-La Roche.

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Impact of a five-dimensional framework on R&D productivity at AstraZeneca

TL;DR: The evolution of the approach to target validation, hit and lead optimization, pharmacokinetic/pharmacodynamic modelling and drug safety testing, which have helped improve the quality of candidate drug nomination, as well as the development of the right culture.
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Good Practices in Model‐Informed Drug Discovery and Development: Practice, Application, and Documentation

TL;DR: This document was developed to enable greater consistency in the practice, application, and documentation of Model‐Informed Drug Discovery and Development (MID3) across the pharmaceutical industry.
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Models for Plasma Glucose, HbA1c, and Hemoglobin Interrelationships in Patients with Type 2 Diabetes Following Tesaglitazar Treatment

TL;DR: The model indicated that the tesaglitazar effect on Hb was caused by hemodilution of RBCs, and a mechanism‐based PD model for the FPG–HbA1c relationship was developed.
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Longitudinal model-based meta-analysis in rheumatoid arthritis: an application toward model-based drug development

TL;DR: The first longitudinal model‐based meta‐analysis of ACR20 is presented, which shows that, with the tested doses/regimens of canakinumab, there was only a low probability that this drug would be better than the most effective current treatments.
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A Model for Glucose, Insulin, and Beta-Cell Dynamics in Subjects With Insulin Resistance and Patients With Type 2 Diabetes

TL;DR: A semi‐mechanistic PKPD model incorporating fasting plasma glucose, fasting insulin, insulin sensitivity, and BCM in patients at various disease stages was developed and well described the heterogeneous populations, ranging from nondiabetic, insulin‐resistant subjects to long‐term treated T2DM patients.