How to read this map
Each column is a hormone receptor. Each row is a drug. A filled circle means the drug is a meaningful agonist (activator) at that receptor. We do not show partial antagonists, allosteric modulators, or receptor binding that is not pharmacologically active at clinical doses.
Why it matters
The history of obesity drugs over the last fifteen years can be told as a story of receptors stacked in a single molecule:
- 1 receptor (GLP-1 only): exenatide (2005), liraglutide (2010), semaglutide (2017). Approximate weight loss: 5–15%.
- 2 receptors (GLP-1 + GIP): tirzepatide (2022). Approximate weight loss: ~21%.
- 2 receptors (GLP-1 + glucagon): survodutide, mazdutide. ~14–19%.
- 2 mechanisms via combination (GLP-1 + amylin): cagrilintide + semaglutide. ~22%.
- 3 receptors (GLP-1 + GIP + glucagon): retatrutide. ~24% in Phase 2.
The pattern isn't guaranteed — adding receptors does not always add efficacy linearly, and side-effect burden tends to rise alongside. But it is the central design hypothesis driving the next wave of obesity drugs.
What the map doesn't show
- Receptor selectivity ratios. Two drugs that both hit GLP-1 and glucagon may have very different potency balances. Survodutide and mazdutide are not identical even though their map row looks the same.
- Pharmacokinetics. Daily-injected liraglutide and once-weekly semaglutide both target only GLP-1, but their dosing cadence and patient experience differ substantially.
- Earlier-stage candidates. Phase 1 and preclinical molecules are not on this map. New rows appear here when a drug enters Phase 2.
Update history
- April 2026 — Added orforglipron Phase 3 status. Refreshed CagriSema designation.
- February 2026 — Added mazdutide GLORY-1 Phase 3.
- October 2025 — Initial publication.