Reference & Guidelines

Mechanism of Action of Endocrine Drugs

How every endocrine drug class works — receptor binding, downstream pathways, and pharmacokinetics — organised by disease target.

Diabetes & Cardiometabolic

Every insulin, incretin, and cardiorenal-active class.

Pituitary Disorders

Somatostatin analogues, GH antagonists, dopamine agonists, and vasopressin analogues.

Internal Medicine Crossover

Endocrine-adjacent medicine — steroid replacement, HRT, and thyroid hormone.

Internal medicine MoA 2 articles

Drug-class quick reference

A compact mental model of receptor → downstream effect for the classes covered on the site.

Insulin secretagogues (SU, glinides): β-cell KATP channel — closes to depolarise → Ca²⁺ influx → insulin release.
Metformin: AMPK activation + mitochondrial complex I inhibition → reduced hepatic gluconeogenesis.
DPP-4 inhibitors: Block DPP-4 degradation of endogenous GLP-1 & GIP → prolonged incretin effect.
GLP-1 receptor agonists: Direct GLP-1R agonism — glucose-dependent insulin release, delayed gastric emptying, satiety.
Dual GIP/GLP-1 agonists: Concurrent GIP + GLP-1 receptor agonism → additive weight and glycaemic benefit.
SGLT2 inhibitors: Block SGLT2 in proximal tubule → glucosuria, natriuresis, tubuloglomerular feedback.
Thiazolidinediones: PPAR-γ agonism → adipocyte remodelling, improved insulin sensitivity.
Bisphosphonates: Bind hydroxyapatite → osteoclast apoptosis / farnesyl pyrophosphate synthase inhibition.
Denosumab: Monoclonal Ab vs RANKL → inhibits osteoclast differentiation and survival.
PTH analogues (teriparatide, abaloparatide): Intermittent PTH1R agonism → osteoblast recruitment, anabolic bone effect.
Romosozumab: Anti-sclerostin mAb → disinhibits Wnt signalling → dual anabolic/anti-resorptive.
Thionamides (methimazole, PTU): Inhibit thyroid peroxidase — organification and coupling; PTU also blocks 5'-deiodinase.
Somatostatin analogues: SSTR2 / SSTR5 agonism → inhibit GH and other pituitary secretion.
GH receptor antagonist (pegvisomant): GHR conformational block — no downstream JAK2/STAT5 signalling.
Dopamine agonists (cabergoline, bromocriptine): D2 receptor agonism → suppress prolactin release.
Osilodrostat, metyrapone, ketoconazole: Steroidogenesis inhibitors — block 11β-hydroxylase / P450 enzymes.
Mineralocorticoid receptor antagonists (spironolactone, eplerenone, finerenone): MR blockade — natriuresis, K⁺ retention, cardiorenal protection.

Mechanism of Action Series : This series of articles in clinical endocrinology is designed for endocrinology fellows interested in gaining a better understanding of endocrine pathophysiology. These carefully selected concise articles are part of our “Understanding endocrine pathophysiology series”

Why this series in endocrine pathophysiology?

We have sought to present endocrine pathophysiology in a manner that emphasizes more practical concepts compared to traditional textbooks on the topic. This text facilitates an integrated approach to learning endocrine pathophysiology through an appreciation of the mechanism of action of medical therapies. Relevant endocrine physiology is presented before a detailed description of the mechanism of action of selected medical interventions. Several illustrations and well-annotated line diagrams are used to enhance an efficient review of basic and advanced endocrine pathophysiology concepts. Also, clinical pharmacology pearls (side effects and therapeutic monitoring guidelines) are emphasized where applicable.
Clinical practice guidelines change over time as our knowledge of disease states evolves. Endocrinology is a complex subdiscipline of internal medicine characterized by a rapid turnover of knowledge. As a result, we have avoided emphasizing guideline-defined treatment protocols in favor of the pathophysiologic basis of endocrine therapies. This series of articles is by no means exhaustive concerning endocrine pathophysiology. We, however, hope that a discussion of various endocrine therapies will facilitate a better appreciation of complex concepts in endocrine physiology in a more clinically relevant manner.
Also, endocrinology fellows and practising physicians should be familiar with landmark clinical trials in the field. We have made a concerted effort to highlight practice-changing clinical trials where relevant. We hope this will enrich the training of not only endocrinology fellows but also internal medicine residents, medical students, and other allied health professionals such as pharmacists, nurse practitioners, and physician assistants.
We welcome feedback from our web audience regarding the limitations of this series and look forward to incorporating valuable suggestions in future editions. The MyEndoConsult team went through painstaking efforts to create this series of articles and welcome suggestions for improving it.

Mechanism of Action of Endocrine Drugs

Diabetes & Cardiometabolic

Pituitary Disorders

Internal Medicine Crossover

Drug-class quick reference

Why this series in endocrine pathophysiology?

Repaglinide Mechanism of Action

Metformin Mechanism of Action

Mechanism of action of inclisiran (leqvio)

Mechanism of Action of Insulin

Ezetimibe Mechanism of Action

Cinacalcet Mechanism of Action