Amycretin

Amycretin is investigational. The characterization report describes it as a molecule being investigated in weight management and type 2 diabetes, and development has reached phase 3. The ClinicalTrials.gov record NCT07339423, sponsored by Novo Nordisk A/S under protocol NN9490-8021 and known as AMAZE 1, registers a randomised, quadruple-masked phase 3 trial of once-weekly subcutaneous NNC0487-0111 against matching placebo in participants with obesity, with an estimated enrollment of 1,150. The record was first posted on January 14, 2026, gives an actual start date of February 24, 2026, was last updated on July 9, 2026, and shows the trial as recruiting with no results posted. No United States marketing approval was identified for amycretin or for its International Nonproprietary Name zenagamtide; that check is an editorial search of the FDA approved-application dataset, recorded on the registry source record, and not a finding of either document cited here.^[5][1]

Jurisdiction

United States

Product

Amycretin (NNC0487-0111), International Nonproprietary Name zenagamtide, investigational

Indication

No United States marketing approval identified under either name; a phase 3 obesity trial (AMAZE 1, NCT07339423) is registered and recruiting

Record date

2026-09-08

• A registered trial is not an approval, and a phase 3 programme is not evidence that a treatment works or is safe. No results are posted for this trial.
• The registry record for this trial names the intervention only as NNC0487-0111. Identifying that code as amycretin rests on the peer-reviewed characterization report cited alongside it, not on this registry record.
• No approved United States product was found when the FDA approved-application dataset was searched on September 9, 2026 under amycretin and under zenagamtide. That dataset covers approved applications only, FDA does not publish pending applications, and the search is an editorial currency check recorded on the registry source record rather than a passage of either cited document.
• This is one registered trial. A registry search on the development code returns further registered studies, including other phase 3 trials, so nothing here describes the whole development programme.
• This describes the United States registry and application record. It says nothing about the status of amycretin in any other jurisdiction.
• The recorded date is the date through which the status was confirmed still current, capped at the evidence cutoff. It is not the date of either cited document.

Amycretin is a single molecule that acts at both the GLP-1 receptor and the amylin receptor, rather than a mixture of two drugs. Its developers describe it as a 68-amino-acid peptide of molecular formula C343H550N94O116 and average molecular weight 7,847 daltons, made of a GLP-1 receptor agonist part and an amylin receptor agonist part joined by a linker of four glycine residues and one glutamic acid residue. It carries a C18 diacid side chain that binds reversibly to albumin, is amidated at one end, and contains the unnatural amino acid 2-aminoisobutyric acid in the GLP-1 sequence to resist breakdown by dipeptidyl peptidase-4. In laboratory assays it activated human, mouse and rat GLP-1, amylin and calcitonin receptors. The same report states that amycretin is the molecule developed under the code NNC0487-0111.^[1]

• This is a structural and receptor-level description published by the molecule's developers. It establishes what the molecule is, not what it does in people.
• Receptor activation in cell-based assays does not establish potency, selectivity or effect in a human body.
• The description identifies the investigational molecule. It says nothing about the identity or contents of any material sold under this name outside a clinical trial.

Zenagamtide is the World Health Organization International Nonproprietary Name that corresponds to amycretin. The name appears as a proposed name in List 133 of 2025 and as a recommended name in List 95 of 2026. Both entries describe a variant of human glucagon-like peptide 1 residues 7 to 37, fused through a four-glycine peptide linker to an artificial 33-residue amylin receptor agonist, amidated at residue 68 and substituted at a lysine with a dicarboxy side chain, and both give the molecular formula C343H550N94O116. The proposed-name entry adds two things the recommended list does not print: the Chemical Abstracts Service registry number 3038191-80-6 and the classification glucagon-like peptide 1 and amylin receptors agonist. That description matches the structure the developers published for amycretin, which carries the same molecular formula, is 68 residues long, has a glycine linker, a terminal amide, a diacid side chain on a lysine, and 2-methylalanine, also written as 2-aminoisobutyric acid, near the start of the glucagon-like peptide 1 sequence. The acylated lysine is the same residue in both accounts: the naming entry places it at residue 31 of its own numbering, which is position 37 in the glucagon-like peptide 1 numbering the developers use.^[2][1]

• The World Health Organization list does not use the name amycretin, and the developers' report does not use the name zenagamtide. The correspondence recorded here is a comparison made by this reference between two inspected descriptions, not a statement that either document makes on its own.
• The comparison rests on more than a family resemblance. Both documents give the identical molecular formula C343H550N94O116, the same total of 68 residues, an amide at residue 68, a diacid side chain on the same single lysine, and the same unnatural 2-aminoisobutyric acid substitution near the start of the glucagon-like peptide 1 sequence.
• The two descriptions differ in one detail. The naming entry describes a linker of four glycines occupying residues 32 to 35, which together with 31 residues of glucagon-like peptide 1 and a 33-residue amylin part accounts for all 68 residues, and it places a glutamic acid inside the glucagon-like peptide 1 part; the developers describe a linker of four glycine residues and one glutamic acid residue. Because both documents give the same molecular formula and the same residue total, this reads as a difference in how one molecule is divided into parts rather than as a difference between two molecules. This reference records the difference rather than resolving it.
• An International Nonproprietary Name is a naming decision. The list states that inclusion implies no recommendation of use, and it is not evidence of approval anywhere.

The first-in-human study of amycretin was a phase 1 trial of the oral formulation. It enrolled 144 adults aged 18 to 55 years with overweight or obesity at a single research unit between May 2022 and January 2024, across a single-dose part, a multiple-dose part and a twelve-week dose-escalation part. Its primary end point was the number of treatment-emergent adverse events. Across all parts there were 364 such events in 89 of the 144 participants (62%); all were mild or moderate in severity and became more frequent at higher doses. Gastrointestinal events made up 180 of the 364 events (49%) and occurred in 72 of the 89 participants who reported any event (81%). No deaths were reported, and plasma concentrations were consistent with dose proportionality. The investigators concluded that the results supported further investigation.^[3]

• A phase 1 study. It is designed to look at safety, tolerability and drug levels in a small group over a short period, and cannot show whether a treatment works.
• Abstract-only inspection: the tables and appendix were not read.
• Single-centre, in adults aged 18 to 55 years, with intervention periods of one day, ten days or twelve weeks. Nothing here describes longer use, older adults or people with other conditions.
• Bodyweight and fasting glucose were exploratory endpoints in one part of the study and are not reported here as outcomes.
• Sponsor-run and sponsor-authored, with the principal investigator employed by a contract research organisation the sponsor paid.

An early-phase 1b/2a study tested amycretin given by subcutaneous injection. Between September 2023 and April 2024, 125 adults aged 18 to 55 years with overweight or obesity were allocated at a single centre, 101 to amycretin and 24 to placebo, across five parts with different maintenance doses and treatment durations. The primary end point was the number of treatment-emergent adverse events; the most common were gastrointestinal, and the report describes the majority as mild to moderate and resolved by the end of the study. Estimated mean bodyweight change from baseline was greater with amycretin than placebo in each of the four multiple-dose parts: -24.3% against -1.1% at week 36, -22.0% against 1.9% at week 36, -16.2% against 2.3% at week 28, and -9.7% against 2.0% at week 20. The report itself states that a large number of participants withdrew, with a high proportion of discontinuations for reasons unrelated to adverse events.^[4]

• This is an early-phase study whose primary end point was adverse events, not weight. The bodyweight figures are secondary and come from small parts with different durations, so they are not one randomized efficacy comparison and must not be read as phase 3 results.
• The report states that a large number of participants withdrew. The abstract gives no withdrawal numbers, so how much that attrition affects the bodyweight estimates cannot be judged from this record.
• Each part is small, single-centre, and limited to adults aged 18 to 55 years with overweight or obesity.
• Abstract-only inspection: the tables and appendix were not read.
• Sponsor-run and largely sponsor-authored.
• Doses and durations appear here only because they identify the study parts whose results are reported.

In animal experiments reported by the developers, amycretin given to diet-induced obese rats for 21 days reduced total energy intake by 47% and lowered body weight by 18% relative to pre-treatment, compared with vehicle-treated animals, while energy expenditure was maintained. In a separate, longer experiment in diet-induced obese rats, insulin sensitivity improved, shown by higher glucose infusion rates during a hyperinsulinaemic euglycemic clamp. The compound reached areas of the mouse brain that regulate food intake, and in a mouse model of metabolic dysfunction-associated steatotic liver disease it improved histological features, mainly by reducing steatosis.^[1]

• These are results in mice and rats. Animal effect sizes do not transfer to people, and a benefit in a rodent model is not evidence of benefit in a person.
• Diet-induced obesity and diet-induced liver disease in rodents are laboratory models, not the human conditions they are named after.
• The experiments were designed, funded, conducted and written up by the sponsor, whose employees are the authors.
• The exposures used in animals are experimental conditions. They are not comparable to any human exposure and are not stated here.