Amycretin

TL;DR

Amycretin — also called zenagamtide, NN9487, and formerly NNC0487-0111 — is an investigational unimolecular dual GLP-1 and amylin receptor co-agonist from Novo Nordisk. It is a single polypeptide engineered to engage both receptors simultaneously, distinct from CagriSema (two separate molecules co-formulated) and from tirzepatide (GIP/GLP-1 dual). Not approved by any regulatory authority.

In a Phase 1b/2a randomized obesity trial (PMID 40550231), once-weekly subcutaneous Amycretin produced dose-dependent weight loss up to −24.3% at 36 weeks at the highest dose tier (60 mg), versus −1.1% to +2.3% placebo. An oral formulation showed approximately −13.1% at 12 weeks at the highest dose in a separate Phase 1 trial (PMID 40550229). Phase 2 in type 2 diabetes reported up to −14.5% weight loss and −1.8% HbA1c at 36 weeks — but this is from a company press release only, not peer-reviewed. Phase 3 (AMAZE program) is actively recruiting.

The amylin co-agonism component is mechanistically distinct but its independent contribution to weight loss in humans has not been quantified. Amylin agonism introduces an additional hypoglycemia risk when combined with insulin or insulin secretagogues.


Why it matters for Vitals

Amycretin is a likely future competitor in the GLP-1/incretin obesity landscape and forces a clean distinction between unimolecular GLP-1+amylin co-agonism versus co-formulated or co-administered dual therapy.

Vitals relevance — explicit:

DomainRelevanceConfidence
Body compositionRapid weight loss (~20%+) would trigger the same muscle-preservation safeguards as other GLP-1-class agents: protein intake optimization, resistance training, DXA/BIA monitoring. No Amycretin DXA or lean-mass data exist.Class extrapolation
GLP-1 receptor activityCore mechanism — same incretin pathway as semaglutide, tirzepatide, retatrutide. Will share resting HR elevation, GI side-effect burden, and class-level CV benefit extrapolation.High
Amylin-mediated satietyHindbrain area postrema pathway distinct from hypothalamic GLP-1. May produce more durable satiety signaling and gastric-emptying delay. Contribution not independently quantified in humans.Mechanistic inference
HRV / autonomic confoundWeight-loss–mediated HRV changes expected (positive autonomic shift from fat loss). GLP-1–mediated resting HR elevation is a confound during titration. No Amycretin-specific HRV data.Low–Moderate
SleepGI symptoms during titration may fragment sleep. No Amycretin-specific sleep architecture data.Low
Glucose (T2D)CGM improvement expected in T2D subgroup — glucose-dependent insulin secretion + weight loss. Phase 2 excluded insulin users; hypoglycemia risk with insulin/secretagogues is a safety concern extrapolated from pramlintide.Moderate (T2D only)
Cardiorenal biomarkersNo cardiorenal data published. GLP-1 class has established cardiorenal protection (semaglutide, tirzepatide); Amycretin’s specific cardiorenal profile is unknown.Gap

Mechanism summary

Amycretin activates two receptor systems via one engineered polypeptide:

GLP-1 receptor (GLP-1R): Full agonism — glucose-dependent insulin secretion, glucagon suppression, delayed gastric emptying, central hypothalamic satiety. Same incretin pathway as semaglutide, liraglutide, tirzepatide. Half-life supports once-weekly SC dosing but the exact value is proprietary.

Amylin receptor (AMYR/CTR complex): Amylin receptors are calcitonin receptor heterodimers (CTR + RAMP1/2/3 = AMY1/2/3). Expressed in the area postrema and nucleus of the solitary tract — hindbrain regions outside the blood-brain barrier. Amylin agonism slows gastric emptying, induces meal-terminating satiation, reduces postprandial glucagon, and has preclinical signals for increased energy expenditure. The independent contribution of amylin agonism to Amycretin’s weight loss in humans has not been quantified — synergy with GLP-1 is plausible but unproven for this specific molecule.

Unimolecular vs combination distinction:

  • Tirzepatide: single molecule, GLP-1R + GIPR — not amylin
  • CagriSema: semaglutide + cagrilintide — two separate molecules, different PK profiles
  • Amycretin: single molecule, GLP-1R + AMYR — shared pharmacokinetics

Preclinical synergy (Mack et al. 2019, DOI 10.1038/s41598-019-44591-8) supports GLP-1 + amylin combination weight-loss effect in animal models. This has not been independently confirmed for Amycretin in humans.

Full incretin receptor biology: see GLP-1 GIP Glucagon. Amylin receptor biology: see Amylin Receptor Biology (aspirational — not yet a standalone vault note; link exists as ghost until a second compound requires it).


What the current evidence suggests

Phase 1b/2a — Subcutaneous obesity trial

PMID 40550231 | NCT06064006 | Lancet 2025 | Supported

Randomized, double-blind, placebo-controlled, dose-escalation. Adults 18–55, BMI 27–39.9 kg/m², no T2D. N=101 active : 24 placebo. Primary endpoint was safety, not weight loss.

CohortMaintenance doseDurationMean weight changePlacebo
Part A–D1.25 mg SC weekly20 weeks−9.7%+2.0%
Part B–E5 mg SC weekly28 weeks−16.2%+2.3%
Part C20 mg SC weekly36 weeks−22.0%+1.9%
Part D (highest)60 mg escalation36 weeks−24.3%−1.1%

All active arms statistically significant vs placebo (p<0.0001 for parts A–D; p=0.0003 for part E).

Caveats: Large number of participant withdrawals; discontinuation-adjusted efficacy uncertain. 60 mg result is from an escalation cohort, not a defined maintenance dose. No DXA body composition data publicly available. Phase 1b/2a design — not a single pivotal registration trial.

Phase 1 — Oral Amycretin obesity trial

PMID 40550229 | NCT05369390 | Lancet 2025 | Supported (exploratory endpoint)

First-in-human, randomized, double-blind, placebo-controlled. 144 participants. Adults 18–55, BMI 25–39.9 kg/m². Fixed-titration cohort up to 100 mg/day for 12 weeks.

Exploratory efficacy: Approximately −13.1% bodyweight vs −1.2% placebo at highest oral dose. This is an exploratory endpoint — the trial was powered for safety, not efficacy. No food restriction or permeation enhancer required (unlike oral semaglutide/Rybelsus).

Phase 2 — Type 2 Diabetes

NCT06542874 | Reported only — press release Novo Nordisk, November 2025

Randomized, quadruple-masked, placebo-controlled dose-finding. 448 participants with T2D on metformin ± SGLT2 inhibitor. Excluded insulin users and patients with hypoglycemia unawareness.

OutcomeReported resultEvidence grade
Bodyweight changeup to −14.5% at 36 weeksReported (press release only)
HbA1c reductionup to −1.8% (SC); −1.5% (oral)Reported
HbA1c target achievers (≤6.5% or similar)89.1%Reported
SafetyGI events mostly mild-moderate; no new safety signals statedReported / incomplete

No peer-reviewed publication or ClinicalTrials.gov posted results found. Do not present these as confirmed findings.

Phase 3 — AMAZE program

TrialNCTPopulationPrimary endpointStatus
AMAZE-1NCT07339423Obesity (no T2D)Weight change, week 84Recruiting
AMAZE-2NCT07533175T2DWeight change, week 84Not yet recruiting
AMAZE-8NCT07400107T2D vs semaglutide 2.4 mgWeight change, week 84Not yet recruiting
AMAZE-12NCT07503210Weight maintenanceWeight change, weeks 40–92Not yet recruiting
AMAZE-5NCT07481630Knee OA + obesityWeight + WOMAC pain, week 80+Not yet recruiting
AMAZE-6NCT07509307Knee OA + obesityWeight + WOMAC pain, week 80+Not yet recruiting

AMAZE-8 is the key comparative trial — direct head-to-head vs semaglutide 2.4 mg. No Phase 3 results are available.


Safety

Amycretin-specific data

Oral Phase 1 (NCT05369390, 144 participants, up to 12 weeks):

  • 364 treatment-emergent AEs in 89/144 participants (62%)
  • All AEs were mild or moderate in severity
  • Gastrointestinal: 180/364 (49%) — nausea, vomiting, diarrhea, decreased appetite
  • 81% of participants reporting AEs had GI events
  • No deaths reported

Subcutaneous Phase 1b/2a (NCT06064006, 125 participants, up to 36 weeks):

  • Most common AEs: gastrointestinal, mild-to-moderate, majority resolved
  • Large number of participant withdrawals; many discontinuations were unrelated to AEs
  • Numeric SAE counts, injection-site reaction rates, and pancreatitis rates not publicly reported

Evidence gaps (Amycretin-specific):

Safety parameterStatus
Serious adverse event rates (Phase 1/2)Not publicly reported
Pancreatitis eventsNot reported in amycretin publications
Gallbladder disease eventsNot reported
Injection-site reaction ratesNot reported
Thyroid / calcitonin changesTrial excluded calcitonin ≥50 ng/L at screening; no follow-up data
Hypoglycemia in T2DPhase 2 excluded insulin users; no event rates posted
Anti-drug antibodies / immunogenicityNot reported
Long-term safety (>36 weeks)No data

Class safety context

GLP-1 class (semaglutide label):

  • Boxed warning: thyroid C-cell tumors in rodents — contraindicated in personal/family history of MTC or MEN2
  • Acute pancreatitis — requires discontinuation if suspected
  • Gallbladder disease (cholelithiasis, cholecystitis)
  • GI events (nausea, vomiting, diarrhea) — leading cause of discontinuation

Amylin class (pramlintide/Symlin label — applies by mechanism extrapolation):

  • Boxed warning: severe hypoglycemia when combined with insulin — especially in Type 1 DM, typically within 3 hours of injection; requires 50% mealtime insulin reduction
  • Contraindications: hypoglycemia unawareness, gastroparesis, known hypersensitivity
  • Gastic-emptying delay: can delay absorption of concomitant oral medications — separate critical oral drugs by ≥1 hour before or ≥2 hours after pramlintide
  • Pancreatitis: listed in postmarketing adverse reactions

Amycretin-specific relevance: Amylin agonism adds a hypoglycemia risk when combined with insulin or insulin secretagogues — this is the primary clinical safety distinction from pure GLP-1 agents. Amycretin Phase 3 in T2D will need to manage this risk carefully. Coaches should flag this to prescribing clinicians.

Drug-drug interactions

  • NCT06461039 (completed): amycretin’s effect on ethinylestradiol/levonorgestrel and acetaminophen PK — results not yet posted
  • CYP3A4/P-gp interaction profile: not characterized
  • Gastric-emptying delay from amylin agonism may affect oral drug absorption (class-level concern from pramlintide)

Wearable / Vitals relevance

Coaching status: Investigational — no Amycretin-specific wearable protocol is validated.

Wearable-accessible endpoints relevant to Amycretin if/when approved:

EndpointWearable sourceConfidenceNotes
Body weight trendScaleHighPrimary endpoint; weight trajectory monitorable
Resting heart rateWrist HR / chest strapModerateGLP-1 class effect: resting HR elevation of +3–5 bpm typical
HRV / autonomic balanceWrist HRVLow–ModerateWeight-loss–mediated HRV improvement expected; GLP-1 titration confound real
Sleep fragmentationWrist accelerometerLow–ModerateGI symptoms during titration may disrupt sleep
Glucose (T2D population)CGMModerateT2D subgroup; glucose-dependent insulin secretion + weight loss
Food noise / appetiteSelf-report onlyNot wearableAmylin may reduce food noise via hindbrain pathway — not instrumentally trackable

Practical coaching notes:

  • No validated wearable signature for Amycretin response or non-response exists
  • GI tolerability management protocol for semaglutide/tirzepatide would be applicable by class extrapolation
  • Human sign-off required before any operationalization
  • Autonomic metrics during titration (weeks 1–8) should be interpreted with caution due to acute GI stress

Risks and uncertainty

Risk / uncertaintyWhy it mattersCurrent status
Phase 3 efficacyCurrent evidence is early-phase with design limitationsAMAZE-1 readout ~2029
Cardiovascular outcomesNo CVOT announced or registered — significant evidence gapWatch for CVOT announcement
Hypoglycemia in T2DAmylin + insulin/secretagogues = severe hypoglycemia riskPhase 3 hypoglycemia endpoints; human sign-off required
Oral formulation efficacyMay change access paradigm if sufficient efficacy at viable dosePhase 2 oral dose-response
Long-term safety (>36 weeks)Unknown autoimmune, pancreatic, thyroid signalsPhase 3 safety monitoring
Head-to-head vs tirzepatideCompetitive differentiation unknownAMAZE-8 vs semaglutide only
Discontinuation-adjusted efficacyHigh dropout in Phase 1b/2a; true efficacy uncertainPhase 3 full analysis set
ImmunogenicityNovel dual-receptor molecule; anti-drug antibody riskPhase 3 ADA data
Lean mass / DXANo body composition data publishedUnknown — critical for Vitals coaching
Amylin synergy quantificationIndependent contribution of amylin agonism unknownMechanistic inference only

Best stack context

If Amycretin is approved in the future, the following vault notes represent the likely coaching and stack context:

Body composition:

Safety monitoring:

Mechanism / comparison:

  • GLP-1 GIP Glucagon — incretin and glucagon receptor comparison frame
  • CagriSema — semaglutide + cagrilintide; not the same as Amycretin
  • Cagrilintide — amylin pathway anchor
  • Pramlintide — approved amylin analog; relevant for hypoglycemia risk context

Tier 2 / aspirational links (ghost links — note does not yet exist):

  • Amylin Receptor Biology — amylin receptor CTR/RAMP heterodimers, area postrema; aspirational note for when a second compound needs it

What stays inside this hub

The following are kept inline in this hub rather than split into standalone notes:

  • Proprietary PK parameters — half-life, bioavailability, Cmax, AUC are not publicly disclosed; no standalone PK note warranted
  • Formulation details — salt form, storage requirements, injection device not publicly described; no separate note
  • Obscure metabolite names — active metabolites uncharacterized; no note
  • Company development trivia — pipeline positioning, competitive strategy; inline only
  • NCT06049329 (Japanese males Phase 1) — single-population study, not decision-relevant for Vitals; inline only
  • NCT06461039 drug-interaction study — registered but results not posted; watchpoint, not standalone note

Evidence summary table

ClaimEvidence gradeSourceBoundary
Amycretin = NN9487 = zenagamtide = NNC0487-0111SupportedBatch 180 synthesis + canonical KBAvoid NN9931 (semaglutide/MASH) and NN9838 (cagrilintide/CagriSema) misidentification
Unimolecular GLP-1R + amylin receptor co-agonistSupportedPMID 40550231, 40550229Mechanism does not prove clinical superiority to other incretin agents
−24.3% bodyweight at 36 weeks (60 mg SC)SupportedPMID 40550231Highest dose escalation cohort; Phase 1b/2a; primary endpoint was safety
−22.0% at 36 weeks (20 mg SC)SupportedPMID 40550231Phase 1b/2a; likely more realistic maintenance signal
−16.2% at 28 weeks (5 mg SC)SupportedPMID 40550231Phase 1b/2a
−9.7% at 20 weeks (1.25 mg SC)SupportedPMID 40550231Phase 1b/2a
Oral Amycretin −13.1% at 12 weeks (100 mg/day)Supported (exploratory)PMID 40550229Exploratory endpoint; trial powered for safety
Phase 2 T2D: −14.5% weight, −1.8% HbA1cReportedNovo Nordisk press release Nov 2025Not peer-reviewed; not confirmed
Phase 2 T2D: 89.1% HbA1c target achieversReportedNovo Nordisk press release Nov 2025Not peer-reviewed
Six AMAZE Phase 3 trials registeredSupportedClinicalTrials.govNo outcomes yet
AMAZE-8 is head-to-head vs semaglutide 2.4 mgSupportedNCT07400107Results pending
GLP-1 + amylin synergy in animalsSupported (preclinical)Mack et al. 2019Not isolated in Amycretin human studies
Amylin component adds hypoglycemia risk with insulinSupported (class)Pramlintide/Symlin labelAmycretin-specific risk not quantified
Wearable signature validatedGapNo Amycretin-specific wearable studiesClass extrapolation only
Long-term safety / CVOTGapNo >36-week safety; no CVOTCannot claim cardiovascular protection
No regulatory approval anywhereConfirmedAll sourcesInvestigational only