Journal
EXPERT OPINION ON INVESTIGATIONAL DRUGS
Volume 25, Issue 4, Pages 405-422Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1517/13543784.2016.1152260
Keywords
Beta cell; glucokinase activator; GPR agonist; imeglimin; incretin; insulin secretion; type 2 diabetes
Categories
Funding
- AstraZeneca
- Bristol-Myers Squibb
- Boehringer Ingelheim
- Eli Lilly and Company
- GlaxoSmithKline
- Janssen Pharmaceuticals
- Merck Sharp Dohme
- Novartis
- NovoNordisk
- Sanofi
- Takeda
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Introduction: Insulin secretory defects are a key feature in the pathophysiology of type 2 diabetes (T2D). Classical insulin-secreting agents such as sulfonlyureas stimulate insulin secretion independent of glucose and cause hypoglycemia. Despite the advantages offered by incretin-based therapies, there is still a medical need for developing new insulin secretagogues for treating T2D.Area covered: This article discusses: the new advances in the field of incretin-based therapies, glucokinase (GK) activators, free fatty acid receptor (FFAR) or G protein-coupled receptor (GPR) agonists (GPR40, GPR119, GPR120), imeglimin and some other insulin secretagogues with diverse mechanisms of action still in preclinical development.Expert opinion: New insulin secretagogues should offer major advantages over sulfonylureas and gliptins. The challenge is to avoid uncontrolled insulin secretion and minimize the risk of hypoglycemia, to protect cells from progressive loss of mass and function for a better durability of glucose control, and to offer a good safety profile. Numerous approaches are in development. However, it is too early to decide whether one new pharmacological class will emerge as a clinically useful insulin secretagogue in the near feature.
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