Who discovered GLP-1? No single person did. Joel Habener's group found a genetic clue. Svetlana Mojsov identified the active form.

Jens Juul Holst and Daniel Drucker helped show what it did. John Eng found a longer-lasting look-alike in Gila-monster venom. Lotte Bjerre Knudsen and her Novo Nordisk colleagues then helped turn the hormone idea into medicines designed to stay in the body longer.

That shared answer matters. GLP-1 wasn't one sudden eureka moment. It was a relay, and each handoff answered a different question.

Who discovered GLP-1? It started with a meal-time puzzle

Researchers already knew that swallowed glucose prompts more insulin than the same amount delivered into a vein. That suggested the intestine was sending an extra message to the pancreas after food arrived. They called that message an incretin, meaning a gut signal that helps the pancreas release insulin after a meal.

At Massachusetts General Hospital, endocrinologist Joel Habener, a doctor-scientist who studies hormones, was studying the gene for glucagon, a hormone that raises blood sugar. His team used anglerfish because the fish have a specialized organ rich in hormone-making cells. They weren't looking for an obesity medicine. They were trying to read glucagon's biological instructions.

Habener's group found a hidden genetic clue

In 1982, Patricia Lund, Richard Goodman, Philip Dee and Habener reported that the anglerfish gene encoded glucagon plus another related sequence (PMID 7043459). The larger starter protein is called proglucagon: the body cuts it into smaller hormones.

A 1983 human-gene paper by Graeme Bell and colleagues showed that this genetic package contained glucagon and two related peptides, GLP-1 and GLP-2 (PMID 6877358). That gave researchers a map. It did not yet reveal which piece the intestine actually made or whether it did anything useful.

Mojsov, Holst and Drucker showed which piece worked

Svetlana Mojsov, a peptide chemist at Massachusetts General, noticed that the predicted 37-amino-acid GLP-1 chain might be cut again. A peptide is a short chain of amino acids, the building blocks used in proteins. She proposed that the active piece began at position 7, made pure GLP-1(7-37), and developed antibodies, lab tools that latch onto particular molecules, to tell the longer and shorter forms apart.

In 1986, Mojsov, Habener and colleagues showed that the same proglucagon instructions were cut differently in pancreatic and intestinal tissue (PMID 3528148). In early 1987, Mojsov, Gordon Weir and Habener reported that GLP-1(7-37) stimulated insulin release from an isolated rat pancreas, while GLP-1(1-37) did not even at far higher concentrations (PMID 3543057).

In Copenhagen, Jens Juul Holst, Cathrine Ørskov, O. Vagn Nielsen and T.W. Schwartz independently isolated a closely related short form from pig intestine and showed that it stimulated insulin release in an isolated pig pancreas (PMID 3542566). Back in Boston, Daniel Drucker, Jacques Philippe, Mojsov, William Chick and Habener showed that the shorter GLP-1 form increased an internal cell signal, insulin-gene activity and insulin release in cultured rat cells (PMID 3033647).

Those papers are why the fairest answer names a group. Mojsov identified and made the active form; Habener's program uncovered the genetic path; Holst's team supplied independent intestinal evidence; and Drucker's experiments helped define the hormone's action. Semaglutide belongs to the later medicine branch built on this active GLP-1 sequence; the early papers are its biological foundation, not studies of the finished drug.

What the GLP-1 Lasker Award actually recognized

The Lasker Foundation's own 2024 citation names Joel Habener, Svetlana Mojsov and Lotte Bjerre Knudsen. It credits Habener and Mojsov with discerning the active hormone and Knudsen with turning the biology into longer-lasting medicines. Jens Juul Holst and Daniel Drucker did not share that particular award.

A different honor is often folded into the same memory. The 17th BBVA Foundation Frontiers of Knowledge Award, announced January 8, 2025, named Drucker, Habener, Holst and Mojsov for establishing GLP-1's biological foundations.

Mojsov's place in the story was not always reflected in high-profile summaries. In a 2023 Rockefeller University interview, she said omissions from later accounts prompted her to speak publicly. That year, Nature added two clarifications to a feature so it named Habener, Holst, Drucker and Mojsov among the scientists who discovered and characterized GLP-1 (Nature, 2023). The papers themselves remain the clearest record of who did what.

As of September 9, 2026, the day this article was written, the newest primary-source addition to this history is a JAMA dialogue published August 20, 2026, in which Holst and Knudsen trace the path from 1970s gut-hormone research to GLP-1 medicines. It changes no authorship in the original papers. It adds the researchers' own retrospective account of the handoff from hormone biology to drug design.

John Eng and the Gila-monster peptide

The Gila-monster chapter is real, but it is a side road into the drug class rather than the discovery of human GLP-1. In 1992, John Eng and colleagues at the Veterans Affairs Medical Center in the Bronx isolated exendin-4, a 39-amino-acid peptide, from Heloderma suspectum venom (PMID 1313797). Exendin-4 activates the GLP-1 receptor, the cell's receiving switch for the hormone, and lasts longer than natural GLP-1.

A synthetic version became exenatide. An FDA clinical review records Byetta's U.S. authorization on April 28, 2005. Exenatide is not the ingredient in Ozempic; the lizard story belongs to Byetta.

Tirzepatide came later through another design route. It activates the GLP-1 receptor and the receptor for glucose-dependent insulinotropic polypeptide (GIP), another meal-time gut signal, rather than copying exendin-4. Our guide to how tirzepatide works explains that two-receptor signal.

Who invented Ozempic? Knudsen's team built the bridge

The plain answer is that Ozempic was not invented by the person who discovered natural GLP-1. Lotte Bjerre Knudsen led work at Novo Nordisk on analogues, meaning designed molecules based on the natural hormone. The problem was time: natural GLP-1 disappears from the bloodstream within minutes.

Knudsen's team attached fatty acids so the molecules could bind to albumin, a common blood protein that acts like a carrier. Their 2000 paper on once-daily candidates describes the chemistry that led toward liraglutide. A separate 17-author Novo Nordisk paper, with Knudsen among the authors, documented the design of semaglutide for once-weekly exposure (PMID 26308095).

So “who invented Ozempic?” has a team answer too. Knudsen shaped the development strategy, and the semaglutide paper names the colleagues who designed and tested that molecule. Our plain-language guide explains how semaglutide works once it reaches its receptor.

What this discovery did not settle

These experiments established a hormone, its active forms and a path to medicines. They did not show that every GLP-1-based product is the same, predict one person's response, or decide whether treatment fits a particular medical history. Tirzepatide also adds GIP activity, so its story cannot be reduced to GLP-1 alone.

Promise's semaglutide and tirzepatide are dispensed as compounded medications, meaning a pharmacy prepares them for specific prescriptions. They are different from FDA-approved products: the formulations offered here are not FDA-approved. A licensed provider may still prescribe a compounded formulation; that decision is between the patient and doctor.

At Promise, a licensed provider reviews every request, and not everyone qualifies. That modern clinical decision sits at the end of a history built by many people, not one inventor.