Peptide knowledge, connected to its evidence.

At a glance

What is it—and why does it matter?

Amycretin is described as a novel, single-molecule co-agonist targeting the GLP-1 receptor and the amylin receptor. The stated objectives included assessing safety/tolerability, pharmacokinetics, and pharmacodynamic effects across single-ascending-dose and multiple-ascending-dose parts in adults with overweight or obesity. A frequentist random-effects network meta-analysis found that, versus placebo, high-dose subcutaneous amycretin was associated with a -23.95% mean difference in percent body weight change and had a P score of 1.00 (a ranking metric within the network). Reported pharmacokinetics indicated approximately dose-proportional plasma exposure across the studied dose groups.

Sources for this introduction: [1] [2] [3] [4]

This published profile is a reference in progress. Findings retain their source context; missing topics are marked below.

What is it?

A molecule, not a product name.

Identity

Amycretin is described as a single (unimolecular) agent designed to co-activate GLP-1 and amylin receptors.

Sources[5]

Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“Amycretin, a novel unimolecular co-agonist targeting glucagon-like peptide-1 (GLP-1) and amylin receptors,”
Amycretin in obesity: Mechanisms, clinical efficacy, and future perspectives. · Abstract
pubmed:41850421:807918bec797:807918bec797

Identity

The peptide name “amycretin” is an earlier name for zenagamtide.

Sources[8]

Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“Zenagamtide (formerly amycretin)”
Efficacy and safety of once-weekly subcutaneous zenagamtide, a novel unimolecular GLP-1 and amylin receptor agonist, in type 2 diabetes: a multicentre, randomised, parallel, double-blind, placebo-controlled, dose-finding, phase 2 trial. · BACKGROUND
pubmed:42532080:3e759eba8051:3e759eba8051

Identity

Amycretin is categorized among amylin-based agents (therapies based on amylin-related actions).

Sources[3]

Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“Amylin-based agents, including CagriSema (cagrilintide + semaglutide) and amycretin, enhance satiety and glycemic outcomes through complementary actions.”
Novel GLP-1-based Medications for Type 2 Diabetes and Obesity. · Abstract
pubmed:41054801:93c84d0dbf77:93c84d0dbf77

Identity

Amycretin is identified in the abstract as an investigational peptide-based amylin receptor agonist (AMYRA) considered in the review.

Sources[4]

Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“The article is a review of the emerging preclinical and clinical data regarding the application of peptide-based amylin receptor agonists (AMYRAs), including pramlintide and cagrilintide, KBP-series DACRAs, and investigational drugs, including ZP8396 and amycretin.”
Amylin receptors as therapeutic targets in obesity: Emerging peptide-based strategies. · Abstract
pubmed:41344603:563b292ecd37:563b292ecd37

Identity

The peptide now called zenagamtide previously had the name amycretin.

Sources[7]

Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“Zenagamtide (formerly amycretin)”
Efficacy and safety of once-daily oral zenagamtide, a novel unimolecular GLP-1 and amylin receptor agonist, in adults with type 2 diabetes: a multicentre, randomised, parallel, double-blind, placebo-controlled, dose-finding, phase 2 trial. · BACKGROUND
pubmed:42532079:a3dbbf3bd34b:a3dbbf3bd34b

Identity

Amycretin is described as a novel unimolecular dual agonist at the GLP-1 receptor and the amylin receptor.

Sources[2]

Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“Amycretin is a novel, unimolecular GLP-1 and amylin receptor agonist.”
Amycretin, a novel, unimolecular GLP-1 and amylin receptor agonist administered subcutaneously: results from a phase 1b/2a randomised controlled study. · BACKGROUND
pubmed:40550231:bfe3adfbbf8f:bfe3adfbbf8f

Identity

Amycretin is categorized with emerging multiagonists (multi-receptor agonist agents) in the review’s synthesis.

Sources[9]

Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“Numerically greater placebo-subtracted reductions were seen with emerging multiagonists, including -23.9% (CI, -29.3% to -18.5%) with amycretin and -22.1% (CI, -24.9% to -19.3%) with retatrutide.”
Efficacy and Safety of Glucagon-like Peptide-1 Receptor Agonists and Co-agonists for Weight Loss Among Adults Without Diabetes : An Updated Systematic Review. · DATA SYNTHESIS
pubmed:42673585:751e21bb0d54:751e21bb0d54

Identity

Amycretin is described as a novel, single-molecule co-agonist targeting the GLP-1 receptor and the amylin receptor.

Sources[1]

Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“Amycretin is a novel, single-molecule GLP-1 receptor and amylin receptor agonist.”
Safety, tolerability, pharmacokinetics, and pharmacodynamics of the first-in-class GLP-1 and amylin receptor agonist, amycretin: a first-in-human, phase 1, double-blind, randomised, placebo-controlled trial. · BACKGROUND
pubmed:40550229:529a7a802565:529a7a802565

How does it work?

Target, response, and disposition.

Mechanism

The stated objectives included assessing safety/tolerability, pharmacokinetics, and pharmacodynamic effects across single-ascending-dose and multiple-ascending-dose parts in adults with overweight or obesity.

Sources[1]

Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“We aimed to investigate the safety, tolerability, pharmacokinetic properties, and pharmacodynamic effects of single ascending doses (part A) and multiple ascending doses (parts B and C/D) of amycretin in adult participants with overweight or obesity.”
Safety, tolerability, pharmacokinetics, and pharmacodynamics of the first-in-class GLP-1 and amylin receptor agonist, amycretin: a first-in-human, phase 1, double-blind, randomised, placebo-controlled trial. · BACKGROUND
pubmed:40550229:529a7a802565:529a7a802565

Pharmacokinetics

Reported pharmacokinetics indicated approximately dose-proportional plasma exposure across the studied dose groups.

Sources[1]

Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“Amycretin plasma concentrations were consistent with dose proportionality across all treatment groups.”
Safety, tolerability, pharmacokinetics, and pharmacodynamics of the first-in-class GLP-1 and amylin receptor agonist, amycretin: a first-in-human, phase 1, double-blind, randomised, placebo-controlled trial. · FINDINGS
pubmed:40550229:529a7a802565:529a7a802565

Pharmacokinetics

The study listed pharmacokinetic secondary endpoints: AUC of the plasma concentration–time curve and maximum plasma concentration (Cmax).

Sources[2]

Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“Secondary endpoints were area under the plasma concentration-time curve, maximum plasma concentration, and relative change in bodyweight from baseline.”
Amycretin, a novel, unimolecular GLP-1 and amylin receptor agonist administered subcutaneously: results from a phase 1b/2a randomised controlled study. · METHODS
pubmed:40550231:bfe3adfbbf8f:bfe3adfbbf8f

What has been studied?

What the evidence says.

Comparative evidence

Within the network meta-analysis, the placebo-referenced percent body-weight reduction for high-dose subcutaneous amycretin was greater than the reported placebo-referenced reductions for semaglutide 2.4 mg and liraglutide 3.0 mg.

Sources[6]

Reported result: -23.95% (amycretin) vs -11.45% (semaglutide 2.4 mg) vs -6.4% (liraglutide 3.0 mg)
Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“Compared with placebo, high dose (HiD) subcutaneous amycretin produced the largest reduction in percent body weight (mean difference -23.95%; P score 1.00), followed by HiD eloralintide (-18.01%; P score 0.89) and HiD CagriSema (-17.18%; P score 0.85), all exceeding semaglutide 2.4 mg (-11.45%) and liraglutide 3.0 mg (-6.4%).”
Novel Amylin-Based Therapies for Weight Management in Adults With Overweight or Obesity Without Diabetes: A Network Meta-Analysis. · RESULTS
pubmed:42175595:f54879c42490:f54879c42490

Comparative evidence

The trial used randomization to amycretin versus placebo and employed masking of participants and investigators to allocation.

Sources[2]

Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“Participants were randomly allocated to receive amycretin or placebo, with participants and investigators masked to trial product allocation.”
Amycretin, a novel, unimolecular GLP-1 and amylin receptor agonist administered subcutaneously: results from a phase 1b/2a randomised controlled study. · METHODS
pubmed:40550231:bfe3adfbbf8f:bfe3adfbbf8f

Study findings

In this phase 2 trial, zenagamtide 25 mg reduced HbA1c from baseline by -1·3% at week 36, with an ETD versus placebo of -0·99% (95% CI -1·49 to -0·49; p=0·0001).

Sources[7]

Reported result: ETD vs placebo -0·99% (95% CI -1·49 to -0·49); p=0·0001
Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“-1·3% with zenagamtide 25 mg (-0·99% [-1·49 to -0·49]; p=0·0001)”
Efficacy and safety of once-daily oral zenagamtide, a novel unimolecular GLP-1 and amylin receptor agonist, in adults with type 2 diabetes: a multicentre, randomised, parallel, double-blind, placebo-controlled, dose-finding, phase 2 trial. · FINDINGS
pubmed:42532079:a3dbbf3bd34b:a3dbbf3bd34b

Study findings

In the authors’ interpretation, high-dose amycretin (grouped with other novel amylin-based therapies) is presented as potentially producing meaningful short- to medium-term weight loss while increasing GI adverse events, but the conclusion is explicitly qualified by sparse, low-certainty evidence and a need for larger confirmatory trials.

Sources[6]

Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“Novel ABTs, such as HiD amycretin, CagriSema and eloralintide, may induce substantial short- to medium-term weight loss but may also increase GI AEs; given sparse, low-certainty data, these findings are preliminary and require confirmation in larger trials.”
Novel Amylin-Based Therapies for Weight Management in Adults With Overweight or Obesity Without Diabetes: A Network Meta-Analysis. · CONCLUSIONS
pubmed:42175595:f54879c42490:f54879c42490

Study findings

In this phase 2 trial, zenagamtide 6 mg reduced HbA1c from baseline by -0·9% at week 36, with an ETD versus placebo of -0·5% (95% CI -1·04 to -0·04; p=0·033).

Sources[7]

Reported result: ETD vs placebo -0·5% (95% CI -1·04 to -0·04); p=0·033
Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“At week 36, from baseline (mean range 7·9-8·1%), estimated mean change in HbA1cwas -0·9% with zenagamtide 6 mg (estimated treatment difference [ETD] vs placebo -0·5% [95% CI -1·04 to -0·04]; p=0·033)”
Efficacy and safety of once-daily oral zenagamtide, a novel unimolecular GLP-1 and amylin receptor agonist, in adults with type 2 diabetes: a multicentre, randomised, parallel, double-blind, placebo-controlled, dose-finding, phase 2 trial. · FINDINGS
pubmed:42532079:a3dbbf3bd34b:a3dbbf3bd34b

Study findings

In this phase 2 trial, the 0·4 mg once-weekly subcutaneous dose showed a greater reduction in HbA1c than placebo at week 36, quantified by an estimated treatment difference with 95% CI and p value.

Sources[8]

Reported result: Estimated treatment difference vs placebo: -0·77% (95% CI -1·26 to -0·28); p=0·0021
Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“At week 36, estimated change in HbA1c(mean across all groups at baseline 7·8% [SD 0·8]) ranged from -0·9% with zenagamtide 0·4 mg (estimated treatment difference vs placebo: -0·77% [95% CI -1·26 to -0·28]; p=0·0021)”
Efficacy and safety of once-weekly subcutaneous zenagamtide, a novel unimolecular GLP-1 and amylin receptor agonist, in type 2 diabetes: a multicentre, randomised, parallel, double-blind, placebo-controlled, dose-finding, phase 2 trial. · FINDINGS
pubmed:42532080:3e759eba8051:3e759eba8051

Study findings

A frequentist random-effects network meta-analysis found that, versus placebo, high-dose subcutaneous amycretin was associated with a -23.95% mean difference in percent body weight change and had a P score of 1.00 (a ranking metric within the network).

Sources[6]

Reported result: mean difference -23.95%; P score 1.00
Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“Compared with placebo, high dose (HiD) subcutaneous amycretin produced the largest reduction in percent body weight (mean difference -23.95%; P score 1.00)”
Novel Amylin-Based Therapies for Weight Management in Adults With Overweight or Obesity Without Diabetes: A Network Meta-Analysis. · RESULTS
pubmed:42175595:f54879c42490:f54879c42490

Study findings

In this phase 2 trial, the 40 mg once-weekly subcutaneous dose showed a greater reduction in HbA1c than placebo at week 36, quantified by an estimated treatment difference with 95% CI and p value.

Sources[8]

Reported result: Estimated treatment difference vs placebo: -1·56% (95% CI -2·05 to -1·07); p<0·0001
Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“to -1·7% with zenagamtide 40 mg (-1·56% [-2·05 to -1·07]; p<0·0001).”
Efficacy and safety of once-weekly subcutaneous zenagamtide, a novel unimolecular GLP-1 and amylin receptor agonist, in type 2 diabetes: a multicentre, randomised, parallel, double-blind, placebo-controlled, dose-finding, phase 2 trial. · FINDINGS
pubmed:42532080:3e759eba8051:3e759eba8051

Study findings

In the synthesized trial evidence summarized by the review, amycretin is associated with a placebo-subtracted reduction in body weight of -23.9% with a confidence interval of -29.3% to -18.5%.

Sources[9]

Reported result: -23.9% (CI, -29.3% to -18.5%)
Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“Numerically greater placebo-subtracted reductions were seen with emerging multiagonists, including -23.9% (CI, -29.3% to -18.5%) with amycretin and -22.1% (CI, -24.9% to -19.3%) with retatrutide.”
Efficacy and Safety of Glucagon-like Peptide-1 Receptor Agonists and Co-agonists for Weight Loss Among Adults Without Diabetes : An Updated Systematic Review. · DATA SYNTHESIS
pubmed:42673585:751e21bb0d54:751e21bb0d54

Study findings

In this phase 2 trial, zenagamtide 50 mg reduced HbA1c from baseline by -1·4% at week 36, with an ETD versus placebo of -1·09% (95% CI -1·59 to -0·59; p<0·0001).

Sources[7]

Reported result: ETD vs placebo -1·09% (95% CI -1·59 to -0·59); p<0·0001
Source records: 1
Independent studies: 1

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance

supports · Source-backed record
“-1·4% with zenagamtide 50 mg (-1·09% [-1·59 to -0·59]; p<0·0001)”
Efficacy and safety of once-daily oral zenagamtide, a novel unimolecular GLP-1 and amylin receptor agonist, in adults with type 2 diabetes: a multicentre, randomised, parallel, double-blind, placebo-controlled, dose-finding, phase 2 trial. · FINDINGS
pubmed:42532079:a3dbbf3bd34b:a3dbbf3bd34b

Risks and interactions

Risks, organized for scanning.

This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.

Products and regulatory status

Same ingredient. Different records.

This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.

Administration context

The practical clinical context.

This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.

Research status + gaps

What still needs better answers?

No publishable claim yet for: administration, contraindication, interaction, regulatory, safety
124 compiled claim(s) withheld by automated assurance: assurance_score_below_0.58 (44), assurance_score_below_0.72 (54), current_regulatory_source_required (31), extraction_ambiguity (103), high_risk_requires_regulatory_or_two_independent_sources (77), no_direct_support (98), proposal_not_staged (7)

These are the limits of this profile, not an exhaustive list of scientific uncertainties.

References + discovery

Open the records yourself.

Search references

Safety, tolerability, pharmacokinetics, and pharmacodynamics of the first-in-class GLP-1 and amylin receptor agonist, amycretin: a first-in-human, phase 1, double-blind, randomised, placebo-controlled trial. ↗
pubmed · published 2025-07-12 · retrieved 2026-09-04T19:09:39Z
Amycretin, a novel, unimolecular GLP-1 and amylin receptor agonist administered subcutaneously: results from a phase 1b/2a randomised controlled study. ↗
pubmed · published 2025-07-12 · retrieved 2026-09-09T18:01:39Z
Novel GLP-1-based Medications for Type 2 Diabetes and Obesity. ↗
pubmed · published 2026-03-11 · retrieved 2026-08-25T22:43:25Z
Amylin receptors as therapeutic targets in obesity: Emerging peptide-based strategies. ↗
pubmed · published 2026-03-01 · retrieved 2026-09-02T08:48:30Z
Amycretin in obesity: Mechanisms, clinical efficacy, and future perspectives. ↗
pubmed · published 2026-06-01 · retrieved 2026-08-25T22:43:25Z
Novel Amylin-Based Therapies for Weight Management in Adults With Overweight or Obesity Without Diabetes: A Network Meta-Analysis. ↗
pubmed · published 2026-05-01 · retrieved 2026-08-25T22:43:25Z
Efficacy and safety of once-daily oral zenagamtide, a novel unimolecular GLP-1 and amylin receptor agonist, in adults with type 2 diabetes: a multicentre, randomised, parallel, double-blind, placebo-controlled, dose-finding, phase 2 trial. ↗
pubmed · published 2026-08-15 · retrieved 2026-08-25T22:43:25Z
Efficacy and safety of once-weekly subcutaneous zenagamtide, a novel unimolecular GLP-1 and amylin receptor agonist, in type 2 diabetes: a multicentre, randomised, parallel, double-blind, placebo-controlled, dose-finding, phase 2 trial. ↗
pubmed · published 2026-08-15 · retrieved 2026-08-25T22:43:25Z
Efficacy and Safety of Glucagon-like Peptide-1 Receptor Agonists and Co-agonists for Weight Loss Among Adults Without Diabetes : An Updated Systematic Review. ↗
pubmed · published 2026-09-01 · retrieved 2026-09-01T08:37:10Z

Publication history and provenance

Version 1 · Automated assessment · 2026-09-09T18:01:39Z

4d6ff1f8a0093d6aff5ff7c456fd843c6b67f92b77608546ab204293cc43dfc9

Anatomy evidence is still being assembled.

Amycretin is described as a single (unimolecular) agent designed to co-activate GLP-1 and amylin receptors.

The peptide name “amycretin” is an earlier name for zenagamtide.

Amycretin is categorized among amylin-based agents (therapies based on amylin-related actions).

Amycretin is identified in the abstract as an investigational peptide-based amylin receptor agonist (AMYRA) considered in the review.

The peptide now called zenagamtide previously had the name amycretin.

Amycretin is described as a novel unimolecular dual agonist at the GLP-1 receptor and the amylin receptor.

Amycretin is categorized with emerging multiagonists (multi-receptor agonist agents) in the review’s synthesis.

Amycretin is described as a novel, single-molecule co-agonist targeting the GLP-1 receptor and the amylin receptor.

The stated objectives included assessing safety/tolerability, pharmacokinetics, and pharmacodynamic effects across single-ascending-dose and multiple-ascending-dose parts in adults with overweight or obesity.

Reported pharmacokinetics indicated approximately dose-proportional plasma exposure across the studied dose groups.

The study listed pharmacokinetic secondary endpoints: AUC of the plasma concentration–time curve and maximum plasma concentration (Cmax).

Within the network meta-analysis, the placebo-referenced percent body-weight reduction for high-dose subcutaneous amycretin was greater than the reported placebo-referenced reductions for semaglutide 2.4 mg and liraglutide 3.0 mg.

The trial used randomization to amycretin versus placebo and employed masking of participants and investigators to allocation.

In this phase 2 trial, zenagamtide 25 mg reduced HbA1c from baseline by -1·3% at week 36, with an ETD versus placebo of -0·99% (95% CI -1·49 to -0·49; p=0·0001).

In this phase 2 trial, zenagamtide 6 mg reduced HbA1c from baseline by -0·9% at week 36, with an ETD versus placebo of -0·5% (95% CI -1·04 to -0·04; p=0·033).

In this phase 2 trial, the 0·4 mg once-weekly subcutaneous dose showed a greater reduction in HbA1c than placebo at week 36, quantified by an estimated treatment difference with 95% CI and p value.

A frequentist random-effects network meta-analysis found that, versus placebo, high-dose subcutaneous amycretin was associated with a -23.95% mean difference in percent body weight change and had a P score of 1.00 (a ranking metric within the network).

In this phase 2 trial, the 40 mg once-weekly subcutaneous dose showed a greater reduction in HbA1c than placebo at week 36, quantified by an estimated treatment difference with 95% CI and p value.

In the synthesized trial evidence summarized by the review, amycretin is associated with a placebo-subtracted reduction in body weight of -23.9% with a confidence interval of -29.3% to -18.5%.

In this phase 2 trial, zenagamtide 50 mg reduced HbA1c from baseline by -1·4% at week 36, with an ETD versus placebo of -1·09% (95% CI -1·59 to -0·59; p<0·0001).