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Peptide Encyclopedia · Metabolic research

Eloralintide

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LY3841136: an investigational, long-acting amylin analogue being studied for obesity. It belongs in the metabolic peptide encyclopedia, but it is not the same kind of receptor agonist as retatrutide.

Evidence: Controlled trialsInvestigational · Phase 3Weight & metabolism

Sources checked November 11, 2026 · AI-assisted research and editorial preparation · No independent expert review recorded

Profile reference

Follow the evidence

Modified amylin analogue, not an incretin/glucagon triple agonist.

In this articleBrowse the A–Z encyclopedia →

Overview

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In plain language

Eloralintide is a laboratory-designed version of amylin, a hormone involved in metabolic regulation, being developed as a potential obesity medicine (discovery paper).

It has human trial evidence and an ongoing Phase 3 program, but remains investigational rather than an approved treatment (ENLIGHTEN-1; current sponsor development update).

How it works

Mechanism under study

Selected source-backed mechanisms. A biological effect does not by itself prove a clinical benefit.

Unfamiliar term? Use the scientific glossary.

Main target or biological role

Eloralintide (LY3841136) preferentially activates human AMY1R in vitro. Research article on PMC

What happens downstream

The company describes its potential calorie-intake effect as likely mediated by satiety, or the feeling of fullness. Lilly company statement

Evidence and boundaries

The source says calcitonin receptor's role in human weight loss remains unclear. Research article on PMC

Nutrients & supplements

Requirement not established in reviewed sources

A specific supplement requirement has not been established from the sources used for this section. This does not rule out nutrient effects or interactions.

Biological involvement, a change in a laboratory result and a proven need for supplementation are different claims. Product-label conditions are not personal treatment recommendations.

Source check: November 11, 2026. Educational mechanisms only; no dosing, treatment protocols or supplement-pairing instructions.

Life of this compound

Origin, release and breakdown are different questions. Engineered compounds do not automatically share the life cycle of a related natural peptide.

Origin and production

Eloralintide is a synthetic human-amylin analogue, not the naturally secreted peptide. The supplied article reports that Lilly synthesized it using solid-phase peptide synthesis. Read supporting source ↗

Release or activation

In human cell assays, eloralintide activated the amylin 1 receptor more potently than the amylin 3 receptor or calcitonin receptor. This is an in-vitro finding, not proof of receptor selectivity in people. Read supporting source ↗

Engineering and identity

The reported molecule is a 37-amino-acid amylin analogue with a stabilizing bridge and a fatty-acid side chain linked at lysine 26. The article describes these structural features as supporting chemical stability and albumin binding. Read supporting source ↗

Breakdown and handling

The article reports albumin binding as part of the design for extending the molecule’s time in the body. It does not establish a specific clearance pathway or describe how the molecule is broken down. Read supporting source ↗

Research in context

Source types answer different questions. Original experiments report particular results; reviews synthesize studies; labels describe a regulated product; registry and company records describe their own scope.

Human trial

Original study record

Eloralintide, a selective amylin receptor agonist for the treatment of obesity: a 48-week phase 2, multicentre, double-blind, randomised, placebo-controlled trial

Research question
Did once-weekly eloralintide at different doses and dose-escalation schemes reduce body weight over 48 weeks in adults with obesity or overweight and a weight-related comorbidity? Read supporting source ↗
Reported finding
The trial abstract reports reductions in mean body weight across the eloralintide groups compared with placebo; nausea and fatigue were among the most common adverse events. Read supporting source ↗
How to read it
Participants with type 2 diabetes were excluded, so the findings described in this trial do not directly address that population. Read supporting source ↗

What these references contribute

Original study

Eloralintide (LY3841136), a novel amylin receptor agonist for the treatment of obesity: From discovery to clinical proof of concept

Reports receptor assays, animal experiments, and a phase 1 single-dose trial, including molecular design, human-cell receptor activity, and preliminary clinical findings. Read supporting source ↗

Original study

Eloralintide, a selective amylin receptor agonist for the treatment of obesity: a 48-week phase 2, multicentre, double-blind, randomised, placebo-controlled trial

The trial record gives the phase 2 study design and abstract findings on weight change and adverse events in adults with overweight or obesity. Read supporting source ↗

See also, explained

Amylin and its analogues

Peptide and analogue family

Eloralintide is described as a synthetic analogue of human amylin and as an amylin-receptor agonist. Read supporting source ↗

Read alongside: Amylin, Cagrilintide, Pramlintide. Membership is a reading connection, not evidence of equivalent effects.

Amylin 1 receptor

Eloralintide activated the human receptor in cell assays and was more potent there than at the human calcitonin receptor or amylin 3 receptor. Read supporting source ↗

Amylin 3 receptor

Eloralintide activated this human receptor in cell assays, with lower potency than at the human amylin 1 receptor. Read supporting source ↗

Calcitonin receptor

Eloralintide activated this human receptor in cell assays, with lower potency than at the human amylin 1 receptor. Read supporting source ↗

Atlas: Pancreas. The article describes naturally occurring amylin as being co-secreted with insulin by pancreatic beta cells. This is background physiology of native amylin, not evidence that eloralintide is produced by the pancreas. Read supporting source ↗

Article update history

The earlier review date above applies to the existing profile. The entries here record this encyclopedia extension, not independent scientific review.

  • : Added encyclopedia navigation, source-linked life-cycle and research context where supported, explained connections and a dated editorial history.

Suggest a correction · Editorial standards

Molecular identity

  • Class: modified human amylin analogue; 37 main-chain residues (Original record).
  • Modifications: three non-coded residues at positions 11, 15 and 22; Cys2–Cys7 methylene thioacetal bridge; C-terminal amidation; Lys26-linked side chain containing gamma-glutamyl linkers and a C20 fatty diacid (Original record).
  • Formula: C201H319N49O65S2; average molecular weight 4,526.11 Da, as listed by KEGG (D12886).

No standard-residue sequence animation or calculated structure is shown. A modified peptide cannot be represented accurately by silently substituting ordinary amino acids for its non-coded residues and conjugate.

Origin and development

Lilly's discovery program describes engineering an amylin analogue for receptor pharmacology, chemical stability and prolonged exposure, followed by preclinical and early-human testing (Briere et al., 2025).

Human evidence

A randomized, double-blind, placebo-controlled Phase 2 trial enrolled 263 adults with obesity, or overweight plus a comorbidity, without type 2 diabetes and evaluated body-weight change over 48 weeks (Billings et al., The Lancet).

In the fixed 9 mg study arm, efficacy-estimand mean body-weight change was approximately −20% (95% CI −22.7 to −17.5), versus −0.4% (−2.2 to 1.4) with placebo; these are trial-arm estimates, not individual predictions or dosing instructions (primary endpoint report).

ENLIGHTEN-1 / NCT07321886 is listed as a Phase III study with an enrollment goal of 1,980; the trial listing is a research-status record, not a completed efficacy result (sponsor trial listing, checked November 11, 2026).

Keep combination studies separate

EloraTZP combines eloralintide with tirzepatide, and Lilly's September 30, 2026 announcement reports a Phase 2b study in adults with type 2 diabetes using separate injections; those findings must not be attributed to eloralintide monotherapy (sponsor announcement).

Safety and regulatory status

Eloralintide remains investigational in the cited development records, with no FDA approval identified in those records as of this source check (Phase 3 program; 2026 development update).

Nausea and fatigue were common adverse events in the Phase 2 monotherapy study, with rates differing by group; 48-week findings do not establish all long-term or rare risks (primary trial report).

Not an approved treatment, prescribing guide or recommendation to purchase research products. This profile does not provide administration, sourcing or self-treatment instructions.

How is it different from RETA?

Eloralintide targets amylin-receptor biology, while retatrutide is an investigational GIP/GLP-1/glucagon triple receptor agonist; sharing an obesity research area does not make them interchangeable (eloralintide pharmacology; retatrutide pharmacology).

The cited eloralintide monotherapy trial did not include retatrutide as a comparator, so it cannot establish which compound is more effective or safer (trial design).

Original sources

  1. Briere et al. Discovery, receptor pharmacology and Phase 1 (2025).
  2. Billings et al. Randomized Phase 2 monotherapy trial, The Lancet (2025).
  3. ClinicalTrials.gov: NCT06230523, Phase 2 registry.
  4. Lilly Trials: ENLIGHTEN-1 / NCT07321886, Phase 3 listing.
  5. KEGG Drug D12886: molecular identity.
  6. Lilly: EloraTZP combination announcement, September 30, 2026.
  7. Lilly: retatrutide mechanism and investigational status.

Research connections

Selected Eloralintide trials · Regulatory tracker · Published News · Questions for evaluating a claim

Loading related published reports. These links add context without changing this profile’s evidence grade.