Amycretin: Novo Nordisk's Amylin + GLP-1 Dual Agonist, in Oral and Subcutaneous Forms

May 10, 2026AI generatedglp-1weight-lossemerging

This article was AI-generated for informational purposes only. It is not medical advice. Always verify claims with the cited sources.

Amycretin is one of the more closely watched entries in the next wave of obesity and metabolic drug candidates. It is worth being precise about what it is and where it stands: as of mid-2026, amycretin is an investigational, early-stage molecule developed by Novo Nordisk. It is not approved by the FDA or any other regulator, and everything below comes from published early-phase trials and company disclosures — not from long-term outcome data.

What amycretin actually is

Amycretin is described by its developers as a novel, unimolecular GLP-1 and amylin receptor co-agonist. "Unimolecular" is the key word: rather than combining two separate drugs, amycretin is a single engineered peptide designed to activate two receptor systems at once — the GLP-1 receptor and the amylin receptor.

That design is notable because most incretin-based therapies to date have targeted one or two of the GLP-1 / GIP / glucagon receptors. Amylin is a different axis entirely. Amycretin is being developed in two formulations: a once-daily oral tablet and a once-weekly subcutaneous injection. Having both a pill and an injectable in the same program is unusual and is part of why the candidate has drawn attention.

Why add amylin to GLP-1?

GLP-1 receptor agonism — the mechanism behind semaglutide — drives appetite reduction, slowed gastric emptying, and improved glucose-dependent insulin response. Amylin is a separate pancreatic hormone, co-secreted with insulin, that contributes to satiety, slows gastric emptying, and helps regulate post-meal glucose. The working hypothesis behind dual agonism is that engaging the amylin pathway complements GLP-1 rather than duplicating it: the two mechanisms act on appetite and glucose control through partly distinct routes, and the hope is that combining them yields additive or synergistic weight and glycemic effects.

This is the same rationale behind cagrilintide, a long-acting amylin analog that Novo Nordisk has studied both on its own and paired with semaglutide (as CagriSema). Where CagriSema keeps the amylin and GLP-1 components as two separate molecules, amycretin folds both activities into one. Readers interested in the amylin mechanism itself will find more background on the cagrilintide reference page.

The early-phase data

Several datasets have now been published, and it is important to read them as early-phase signals, not confirmed efficacy.

Oral, first-in-human phase 1. In an early trial of the oral formulation, amycretin was associated with roughly 13.1% weight loss after 12 weeks. Tolerability was a clear theme: at the high dose, about 87.5% of participants reported gastrointestinal adverse events, driven largely by nausea (~75%) and vomiting (~56%).

Subcutaneous, phase 1b/2a. In a randomized controlled study of the once-weekly injectable, participants on the highest doses (up to 60 mg) saw body-weight reductions of up to ~24.3% after 36 weeks, versus about 1.1% with placebo. The safety and tolerability profile was described as consistent with what is seen across GLP-1 and amylin agonists — a high frequency of gastrointestinal events, but at rates broadly in line with early studies of similar molecules. Both the first-in-human and the phase 1b/2a subcutaneous results were published in The Lancet.

Phase 2 in type 2 diabetes. In November 2025, Novo Nordisk reported headline results from a phase 2 trial in people with type 2 diabetes inadequately controlled on metformin (with or without an SGLT2 inhibitor). The study enrolled 448 participants and tested both the once-weekly subcutaneous and once-daily oral forms against placebo. Reported at week 36: the subcutaneous formulation delivered roughly 11.9% placebo-adjusted weight loss and the oral form about 7.6%, with total weight loss reported up to ~14.5%. On glycemic control, placebo-adjusted HbA1c reductions were about 1.6% (subcutaneous) and 1.1% (oral). The company again described the profile as generally safe and well tolerated, with mostly mild-to-moderate gastrointestinal adverse events.

Where it stands

On the strength of these early-phase results, Novo Nordisk has said it is advancing amycretin to phase 3 development, with a phase 3 program in type 2 diabetes planned to begin in 2026, alongside obesity trials. That is a meaningful step, but phase 3 is where efficacy, durability, and — critically — real-world tolerability get tested at scale. The recurring gastrointestinal signal in early studies is the kind of thing large trials are designed to characterize properly.

A few points worth holding onto:

Cross-trial comparisons are unreliable. The eye-catching ~24% subcutaneous figure came from a small early-phase obesity-oriented study; the ~12% subcutaneous figure came from a phase 2 diabetes population. Different populations, doses, durations, and endpoints mean these numbers are not directly comparable to each other or to approved drugs.

Nothing here is approved. Amycretin has no marketing authorization. For the current regulatory standing of related and approved products, see our FDA status overview.

Tolerability may shape the story as much as efficacy. Gastrointestinal adverse events were common across formulations.

Amycretin is a genuinely interesting attempt to put amylin and GLP-1 agonism into a single molecule, in both a pill and an injection. Whether that translates into a durable, well-tolerated therapy is a question only larger, longer trials can answer.

PepStash is a research log and reference tool. This article is educational and is not medical advice — it does not diagnose, treat, or recommend any protocol. Regulatory status and trial data change; always verify against primary sources and consult a licensed physician before making any decisions about your health.

Not medical advice. For research purposes only. Consult a licensed physician before beginning any protocol.