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Eloralintide 5 mg
Peptide Library · Profile
Eloralintide 5 mg
The two things eloralintide is most often taken for are the two things it is not. It is not a GLP-1, and it is not cagrilintide — the nearest compound in this catalogue, and the one it was deliberately engineered to differ from. Its developer is Eli Lilly, its target is the amylin receptor, and the most useful finding in its published record is not the weight number at the top of the dose range. It is the shape of the side effects: in the 263-person phase 2 trial, the lowest arm recorded less nausea than placebo, and the highest nausea rate in the whole trial was not in the highest arm.
Randomised human trialsThreetwo phase 1 · one phase 2
Largest trial263participants · 48 weeks · Lancet
Human half-life12.9–15.3days · 310–366 h · measured, phase 1
Published sequenceNone foundthree non-coded residues · no weight computed
The short version
Plain English first. Everything below this section is the same material with the sources, the numbers and the caveats attached.
What it is
A synthetic analogue of human amylin — the hormone your pancreas releases alongside insulin every time you eat. Amylin tells the brain the meal is over. Eloralintide is a redesigned version built to last in the bloodstream and, unlike the amylin drugs before it, to hit one receptor subtype preferentially rather than the whole family. It is an Eli Lilly molecule, development code LY3841136. It is not a GLP-1 drug and shares no mechanism with one.
What has actually been measured
Three randomised, placebo-controlled human trials, all injected, all published. Two phase 1 studies — one single-dose in 48 healthy participants, one 12-week repeat-dose in 100 participants with obesity or overweight — and one 48-week phase 2 in 263 participants published in The Lancet. That last one is a genuine, properly reported, moderately sized trial with a placebo arm, which puts eloralintide ahead of almost everything else in this library on evidence. Weight change at 48 weeks ran from −9% in the lowest arm to −20% in the highest, against −0.4% on placebo.
What has not been measured
No phase 3. No published amino-acid sequence, which is why this page carries no molecular weight and no counterion arithmetic — we do not estimate those. No head-to-head trial against cagrilintide or against any GLP-1 in humans; the only direct comparison with cagrilintide is in rats, and the only human comparison is indirect. Trials combining it with tirzepatide are under way and unreported. No cardiovascular outcomes trial. No independent analysis of research-grade vials, and no stability study for this molecule.
What most people get wrong
Three things, in order of how often we hear them. That it is a GLP-1 — it is not, and it does not work through that pathway at all. That it is cagrilintide, or close enough — cagrilintide hits the amylin and calcitonin receptors about equally; eloralintide was built to avoid the calcitonin receptor, and in rats that difference showed up as measurably less food aversion and less lean-mass loss. And that more is better: the phase 2 nausea figures do not rise smoothly with dose, and the arm with the worst nausea in the entire trial was not the arm on the largest amount.
What eloralintide is
A 37-residue amylin analogue with three chemical modifications, each doing a specific job. The published description of the molecule is detailed about the modifications and silent about the sequence, and that silence has a consequence for this page.
| Class | Selective amylin receptor agonist — preferential for the amylin 1 receptor (AMY1R) |
| Development code | LY3841136 |
| Originator | Eli Lilly and Company. Every published study to date is Lilly-funded and Lilly-authored |
| Main chain | 37 amino acids, including three non-coded residues at positions 11, 15 and 22 |
| Ring closure | The disulfide bridge of native amylin is replaced by a methylene thioacetal bridge, which the developers state improves chemical stability |
| Half-life extension | A C20 fatty diacid conjugated through a linker to the lysine at position 26, giving albumin binding |
| Published sequence | None found. Searched and not found — see below |
Why there is no molecular weight on this page
Every other profile in this library computes its own molecular weight, net charge, counterion sites and worst-case trifluoroacetate cost from the published sequence. We cannot do that here, and we are not going to guess.
Two reasons, and the second is the stronger one. First, no primary source we found prints the sequence: the discovery paper describes the modifications in prose and gives no residue list, and the vendor pages we checked carry no sequence either. Second, even a residue list would not be enough. Three of the 37 positions are non-coded amino acids — residues outside the standard twenty, whose masses are not in any standard table. Add a methylene thioacetal bridge in place of a disulfide and a C20 fatty diacid on a linker, and a calculation from standard average residue masses would be wrong by an unknown amount in an unknown direction.
So: no weight, no net charge, no counterion table, no TFA arithmetic. Searched and not found is the honest entry, and an estimate dressed up as a calculation would be worse than a blank.
The only molecular identifiers we located for this compound sit on commercial supplier pages, and one of them carried a registry number only in the page’s hidden keyword metadata, not in the body of the page as a labelled field. We are not reproducing it. An identifier we cannot see asserted in a primary source is not an identifier we will print.
Three names, one molecule — and two neighbours it is not
| Name | What it refers to |
|---|---|
| Eloralintide | The international non-proprietary name. This is what is in the vial |
| LY3841136 | Lilly’s development code. Most of the preclinical literature uses this |
| Amylin / IAPP | The natural hormone, not this molecule. Papers on amylin physiology are background, not evidence about eloralintide |
| Cagrilintide | A different drug, from a different company. Also an amylin analogue, but non-selective — it engages the calcitonin receptor about as readily as the amylin receptors. We stock it; it is not this |
| Pramlintide | The first approved amylin analogue. Short-acting, needed several injections a day, and is a different molecule again |
The fourth row is the one that causes trouble in practice, because cagrilintide is the closest thing we sell and the names rhyme. The -lintide stem simply means amylin analogue; it tells you the family and nothing about the receptor profile. On the evidence below, the receptor profile is the entire point of this compound.
The human evidence, trial by trial
Three randomised, placebo-controlled, injected trials in humans, all published in peer-reviewed journals, all funded and authored by the originator. That last point is a real limitation and we are stating it once here rather than repeating it: there is no independent human trial of this compound.
| Trial | Design | Result as reported |
|---|---|---|
| Phase 2 Billings et al. · Lancet 2025 · NCT06230523 | 263 participants, 46 US centres, 48 weeks, double-blind, seven arms: placebo, four fixed amounts, and two stepped-up schemes. Adults with obesity, or overweight plus one weight-related condition, without type 2 diabetes | Positive and dose-related. Mean weight change at 48 weeks: −9% in the lowest arm through −20% in the highest, against −0.4% on placebo. Confidence intervals on every arm exclude placebo |
| Phase 1, repeat dose Bhattachar et al. · Diabetes Obes Metab 2026 | 100 participants with obesity or overweight, three US centres, 12 weeks, five cohorts, weekly injection with no step-up. Mean BMI 32.6 | Positive. Weight reduction across cohorts of 2.6% to 11.3%. Exposure rose in proportion to amount given. One serious adverse event, judged unrelated. Most adverse events mild |
| Phase 1, single dose Briere et al. · Mol Metab 2025 · NCT05295940 | 48 healthy participants, mean BMI 27.5, six escalating single-dose cohorts, six on drug and two on placebo per cohort, followed 60 days | Tolerated; weight signal only at the top two amounts. The lower four cohorts showed no significant separation from placebo on weight. The top two reached −2.5% and −4.4% at day 29. All 48 completed; no serious adverse events |
What makes the phase 2 unusually readable
Most trials of this kind run one or two amounts and a placebo. This one ran four fixed amounts and two stepped-up schemes side by side in the same trial, which means the effect of how you get there can be read off against the effect of where you end up. Almost nothing in this library permits that comparison, and it is where the interesting result lives — see the next section.
The weight result itself is about what the dose–response predicts: more produced more, and the two highest-ending arms landed in the same place. There is no surprise in that half of the paper.
What none of the three trials did
- None ran to phase 3. We found no phase 3 trial of eloralintide published anywhere — searched and not found. The largest study on record is 263 people.
- None compared it head-to-head with another drug. Every arm in all three trials is against placebo. There is no human trial of eloralintide versus cagrilintide, versus semaglutide, or versus anything else.
- None ran longer than 48 weeks. There is no data beyond that, in either direction — no durability, and no long-term safety.
- None was independent. All three are Lilly-funded with Lilly authors, which is normal for a drug at this stage and is still a limitation worth naming.
- None tested a combination. The discovery paper states that trials of eloralintide with tirzepatide are under way; we found no published results from any of them.
One indirect comparison does exist and is worth having, with its limits attached. A 2026 network meta-analysis pooled six trials across this whole drug class, 4,642 participants in total, and ranked them against each other statistically rather than by direct experiment. Eloralintide’s high-exposure arms came out at −18.0% versus placebo, behind one competitor at −24.0%, slightly ahead of cagrilintide-with-semaglutide at −17.2%, and well ahead of semaglutide 2.4 mg at −11.5% and liraglutide 3.0 mg at −6.4%. Its authors describe the underlying data as sparse and of low certainty, and a statistical ranking is not a trial. Treat it as the best available answer to a question nobody has actually tested.
The tolerability shape, which is the real finding
This is the most useful thing in the published record, and it is the part that gets flattened into a single side-effect percentage everywhere else. The phase 2 trial did not find a flat rate of nausea. It found a threshold — and the threshold does not sit where a simple dose–response would put it.
Read the table below as a report of one trial, not as advice. The amounts named are the amounts that trial administered to its own arms, in its own units, and they are printed here only because the differences between arms are the finding. Sentient Biogenix supplies this compound for laboratory research use only and publishes no dose, no schedule and no duration for any compound in this library. Nothing on this page is a protocol.
| Trial arm | Nausea | Fatigue | Weight change at 48 weeks |
|---|---|---|---|
| Placebo | 14% | 12% | −0.4% |
| 1 mg fixed | 11% | 0% | −9% |
| 3 mg fixed | 13% | 13% | −12% |
| 6 mg fixed | 64% | 29% | −18% |
| 9 mg fixed | 33% | 43% | −20% |
| 6 stepped to 9 mg | 54% | 46% | −20% |
| 3 stepped to 9 mg | 25% | 21% | −16% |
Two things in that table are not what you would expect
One: at the bottom of the range there is no excess at all. Nausea in the 1 mg arm was 11% and in the 3 mg arm 13%, against 14% on placebo. Fatigue in the 1 mg arm was 0%, against 12% on placebo. Those arms are not reporting a milder version of a side effect; on these two measures they are reporting no signal above background — while still separating from placebo on weight by nine and twelve percentage points. That is an unusual combination and it is the honest reason the low end of this compound’s range is the interesting part.
Two: the curve is not monotonic, and we have to correct a common reading of it. The worst nausea in the entire trial — 64% — was in the 6 mg arm, not the 9 mg arm, which reported 33%. It is tempting to describe this as a cliff that rises with dose. It does not. It rises sharply somewhere between 3 and 6 mg and then, by arm, falls again.
The two stepped arms point at why. Both of them finished at 9 mg. The one that started at 6 reported 54% nausea; the one that started at 3 reported 25% — less than half as much, for a weight result of −16% against −20%. On this evidence how the exposure is approached appears to matter at least as much as where it ends up, and a single-number side-effect rate for this compound is close to meaningless.
Stated as the limitation it is: these are seven arms of between 24 and 54 participants each, in one trial, and adverse-event rates in groups that size carry wide uncertainty. The 64%-versus-33% inversion could be noise. What is harder to explain away is the consistency of the two low arms with the two phase 1 studies: the 12-week repeat-dose study reported nausea in 8% and vomiting in 4% of participants with gastrointestinal events described by its authors as infrequent, and the single-dose study produced gastrointestinal events in only 2 of 36 participants given drug. Three separate trials agree that the low end of this molecule’s range is quiet. They do not agree on what happens above it.
The other adverse events, which are not the GLP-1 list
Across the phase 1 repeat-dose study the most common events were decreased appetite in 19% of participants, headache in 12%, fatigue in 11% and COVID-19 in 11%, with diarrhoea at 10%, nausea at 8% and vomiting at 4%. Reviews of this drug class describe eloralintide’s profile as distinct from the incretin drugs for exactly this reason: the leading complaints are appetite loss, headache and fatigue rather than the gastrointestinal cluster that dominates GLP-1 reporting.
Fatigue is the one to weigh against that framing, because it is the adverse event that does track the dose range fairly cleanly in the phase 2 trial — 0%, 13%, 29%, 43% across the four fixed arms against 12% on placebo. Nausea has a threshold; fatigue looks more like a gradient. A page that quoted only the nausea improvement would be selecting.
How it works, and why selectivity is the whole pitch
Amylin signals through receptors built from a shared calcitonin receptor core plus one of three accessory proteins. Which combinations a drug hits is what separates the compounds in this class, and eloralintide exists because of a hypothesis about which combination you want to miss.
| Receptor family | The calcitonin receptor (CTR) pairs with accessory proteins to form AMY1R, AMY2R and AMY3R. Natural amylin prefers the amylin receptors; natural calcitonin prefers CTR alone |
| Eloralintide, human cells | Roughly 12-fold more potent at AMY1R than at CTR, and 11-fold more potent at AMY1R than at AMY3R, in cyclic-AMP activation assays. Binding assays give a similar picture at about 8-fold each way |
| Full or partial? | Full agonist at all three receptors it was tested against — the selectivity is in potency, not in ceiling |
| Eloralintide, rat cells | Different, and the paper says so. In rat assays it activates both AMY1R and AMY3R more potently than CTR — about 45-fold over CTR at AMY1R. So the rat data is about avoiding CTR; the human data is about AMY1R specifically |
| Cagrilintide, for contrast | Non-selective. Activates AMY1R, AMY3R and CTR with comparable relative potency in both human and rat assays |
The hypothesis, and the fact that it is still a hypothesis
The reasoning behind this molecule is that the calcitonin receptor is where the unpleasantness lives — that engaging it buys you nausea and malaise without buying you much extra weight loss, so a drug that skips it should be better tolerated at equivalent effect. The phase 2 tolerability numbers above are consistent with that.
Consistent with is not the same as demonstrated. The developers say so themselves, in two places worth quoting the substance of: the rat results may reflect CTR engagement rather than any distinction between the two amylin receptor subtypes, and there is no established minimum selectivity threshold defining what counts as biologically relevant selectivity in the first place. Twelve-fold is a number; nobody has established what number is enough. The role of the individual amylin receptor subtypes is described in the same paper as poorly understood.
Against cagrilintide, and against a GLP-1
Customers ask this in one of two forms: is it better than the cagrilintide you already sell, and is it better than the GLP-1 I have heard of. The accurate answers are nobody has run that trial, followed by what does exist.
What exists against cagrilintide: rats
The discovery paper ran a genuine head-to-head in diet-induced obese rats, which is the only direct comparison of these two molecules in existence. Three results came out of it:
| Weight and food intake | Comparable. At matched amounts the two produced similar reductions, with no significant difference in the measures the authors used |
| Conditioned taste avoidance | Eloralintide significantly less (p < 0.05). In rodents this is the standard proxy for the malaise that produces nausea in people. Both caused some; cagrilintide caused more at equivalent effect |
| Body composition | Eloralintide matched the fat loss with less lean loss (p = 0.0101). Fat accounted for 80–91% of weight lost on eloralintide against 63% on cagrilintide at the matched amount |
Two caveats the authors raise and we are repeating rather than burying. These were acute food-intake and saccharin-preference experiments, and the difference in potency between the two drugs could come from their different pharmacokinetics rather than from receptor selectivity — eloralintide simply lasts longer. Also, lean mass as measured here includes muscle, bone and water, so less lean-mass loss in a rat is not the same claim as muscle preservation in a person. And this is a rat. No human study has compared these two compounds on anything.
What exists against a GLP-1: the half-life, and an indirect ranking
| Eloralintide half-life, humans | 310–366 h — 12.9 to 15.3 days — measured across the 0.4–12 mg single-dose range. Time to peak 72–132 h |
| Cagrilintide half-life, for comparison | 159–195 h — 6.6 to 8.1 days — with time to peak of 24–72 h, as cited in the same paper |
| So | Eloralintide persists roughly twice as long. Its developers note that the consequences of that for both effect and side effects are not yet understood |
| Mechanism overlap with GLP-1 | None. Different hormone, different receptor family, different signal. It is not a GLP-1, a dual agonist or a triple agonist |
Against the incretin drugs the only quantitative comparison is the network meta-analysis described in the previous section, which put eloralintide’s high-exposure arms at −18.0% against semaglutide 2.4 mg at −11.5% — indirect, low-certainty, and not a trial. On tolerability, the discovery paper sets its own 2-of-36 gastrointestinal event count against a published 44% nausea rate for semaglutide 2.4 mg in a phase 3 obesity trial, and against 25–33% for the GIP/GLP-1 class. Those are different trials in different populations, so the comparison is suggestive at best.
One cardiometabolic observation is worth recording because it runs the opposite way to the GLP-1 drugs rather than merely further in the same direction. A 2026 review of the early eloralintide studies notes a reduction in pulse rate, where GLP-1 receptor agonists are associated with a modest increase in heart rate, alongside reported improvements in blood pressure, hs-CRP, lipids and the fat-to-lean ratio of weight lost. The same review is explicit that no amylin receptor agonist has been through a cardiovascular outcomes trial, that the evidence base is preclinical plus phase 1 and 2 with small samples and short durations, and that epidemiological benchmarks here should be read as contextual rather than predictive. It is a signal pointing in a good direction; it is not an outcome.
Reconstitution
Settled, and simple, because it lands on the same arithmetic as the cagrilintide vial most people here have already handled.
| Vial | Standard 3 mL glass, lyophilised, nominal 5 mg |
| House diluent volume | 1 mL of bacteriostatic water |
| Resulting concentration | 5 mg/mL |
| Per unit on an insulin syringe | 50 µg — because one unit is 0.01 mL |
| Same as | Cagrilintide 5 mg at 1 mL. The per-unit figure is identical, which is the one piece of handling knowledge that transfers between the two |
Our arithmetic, from the nominal vial contents and the stated volume. It is not a dosing calculation and must not be read as one. It tells you what a unit on a syringe contains after reconstituting at 1 mL, which is a statement about the liquid in the vial and nothing else. This catalogue publishes no dose, no schedule and no duration for any compound, and the concentration above does not imply any particular volume being appropriate for anything. See our handling guides for the general conventions.
One handling note specific to this molecule rather than inherited from the class. The published preclinical work formulated eloralintide in a pH 8 buffer, and formulated cagrilintide in a pH 4 buffer, in the same set of experiments. That is a formulation choice in an animal study and not a reconstitution instruction, and we found no study of this compound in bacteriostatic water at any pH. We are recording it because the contrast is published, because it points the opposite way from the acid-diluent handling some amylin material gets, and because the absence of any solvent-compatibility study for this molecule is itself the finding — searched and not found.
Storage
No stability study specific to eloralintide was found — not in solution, not lyophilised, at any temperature, by any party. Searched and not found. The guidance available is generic peptide handling: keep the lyophilised solid frozen, dry and dark, and avoid repeated freeze–thaw once it is in solution.
Our general conventions, including the 28-day figure for a reconstituted vial, are in the storage guide. As always, the sterility half of that 28 days transfers here unchanged — benzyl alcohol does not care what is dissolved in it — and the stability half has never been measured for this molecule. We would add one compound-specific caution as an inference, flagged as an inference: this is a lipidated 37-residue chain carrying a C20 fatty diacid on a linker, which is a materially different stability proposition from a short unmodified peptide, and the developers specifically describe the engineered bridge as present to improve chemical stability — which tells you the unmodified parent had a stability problem worth solving. None of that is a measurement.
Regulatory status
Eloralintide is absent from both of the lists this library checks every compound against. That is a genuine finding and it is also the most easily misread sentence on this page, so it comes with its reasoning attached.
| Body | Eloralintide named? | What that does and does not mean |
|---|---|---|
| Health Canada, 1 Aug 2025 | No — not named | Read in full this session. The affected-products table runs to 44 entries and eloralintide is not among them. Neither is cagrilintide. Retatrutide and tirzepatide are. Critically, the table’s lead-in reads “Unauthorized injectable peptide drugs, including:” — so the list is explicitly not exhaustive |
| FDA bulk substances, current 22 Apr 2026 | No — not named | Read in full this session. Eloralintide appears nowhere on that page, in the category 2 table or the nominated-but-withdrawn table. No amylin analogue appears at all — not cagrilintide, not pramlintide |
| Approved medicine anywhere | No | The furthest it has reached is a phase 2 trial. There is no marketing authorisation in any jurisdiction, and we found no phase 3 |
| WADA 2026 Prohibited List | Not named — S0 applies | S0 covers substances with no current approval by any governmental regulatory health authority for human therapeutic use. That is this compound exactly. Our application of S0, using the list’s own definition |
| Australia | Not checked. We make no claim | |
Being absent from both lists is not a clearance, and it is not a loophole. Two reasons, and they are different. The Health Canada advisory names the products seized from one specific seller and says in its own lead-in that the list is not complete — absence from it is absence from one enforcement action, nothing more. And the simplest explanation for the absence is chronological: eloralintide is a current investigational drug whose first phase 2 publication landed in November 2025, after that advisory was issued, and it was never nominated for compounding in the United States because it is an active clinical candidate rather than a legacy substance. An unapproved investigational drug is an unapproved drug whether or not a list has caught up with it. On the rule that actually governs here — no approval anywhere — eloralintide sits in exactly the same position as everything else in this library.
Sentient Biogenix supplies eloralintide for laboratory research use only. It is not for human or veterinary use.
Questions we actually get
What is it?
A redesigned copy of amylin, the hormone your pancreas releases with insulin when you eat, whose job is to signal that the meal is over. Eloralintide is engineered to last about two weeks in the bloodstream and to act preferentially on one amylin receptor subtype rather than the whole receptor family. It is an Eli Lilly molecule, code LY3841136, currently investigational.
Is it a GLP-1?
No. Not a GLP-1, not a dual agonist, not a triple agonist. Different hormone, different receptor family, different signalling. It has no mechanism in common with semaglutide, tirzepatide or retatrutide. The only thing it shares with them is the problem it is aimed at.
Is it the same as cagrilintide?
No, and this is the confusion worth clearing up, because cagrilintide is the nearest thing we stock and the names rhyme. Both are long-acting amylin analogues, so the family is the same. The difference is which receptors they touch: cagrilintide engages the amylin receptors and the calcitonin receptor at comparable potency, while eloralintide is roughly 12-fold selective for the amylin 1 receptor over the calcitonin receptor in human assays. In the one head-to-head that exists — in rats — that difference showed up as significantly less food aversion and significantly less lean-mass loss at matched fat loss. It has never been compared with cagrilintide in a person.
What is the half-life?
310 to 366 hours — roughly 13 to 15 days — measured in humans in the phase 1 single-dose study. Time to peak concentration was 72 to 132 hours. For context, the same paper cites cagrilintide at 159–195 hours, so eloralintide persists about twice as long. Its developers state plainly that what that longer exposure means for both effect and side effects is not yet understood.
How much weight did it take off?
In the 48-week phase 2 trial, between 9% and 20% depending on the arm, against 0.4% on placebo. The 12-week phase 1 repeat-dose study reported 2.6% to 11.3%. Both are trial results in trial populations under trial supervision, and the top of that range came with the side-effect rates in the table above.
Is it better tolerated than the GLP-1 drugs?
At the bottom of its tested range the published numbers are striking — nausea at or below placebo, fatigue at zero in the lowest arm — and three separate trials agree on that. Above a threshold somewhere between the 3 mg and 6 mg arms, it is not: one arm reported 64% nausea. So the honest answer is that depends entirely on where in the range you are, which is exactly the thing most summaries leave out. And no trial has ever compared it directly with a GLP-1 drug in humans.
Why is there no molecular weight on this page?
Because the amino-acid sequence has not been published anywhere we could find, and because even if it were, three of its 37 positions are non-coded amino acids whose masses are not in any standard table — on top of a modified bridge and an attached C20 fatty diacid. Every other profile in this library calculates its own weight, charge and counterion arithmetic from a published sequence. Here we cannot, so we have not. An estimate presented as a calculation would be worse than this blank.
Is it legal in Canada?
It is not an approved drug in Canada or anywhere else — there is no marketing authorisation in any jurisdiction, and the furthest it has reached is phase 2. It is not named on Health Canada’s August 2025 advisory, but that advisory lists products seized from one seller and states in its own lead-in that the list is not exhaustive, so read that absence as absence from one enforcement action rather than as clearance. We supply it for laboratory research use only.
Has it been combined with tirzepatide?
Trials doing exactly that are under way — the discovery paper says so directly — in adults with overweight and obesity, with and without type 2 diabetes. We found no published results from any of them, and nothing at all pairing it with retatrutide. Searched and not found, which will change; this page will be updated when it does.
What is the catch?
Three, stated plainly. There is no phase 3 — the largest study on record is 263 people over 48 weeks. Every human trial is run by the company that owns the molecule, which is normal at this stage and still means there is no independent confirmation of anything on this page. And the whole selectivity argument remains a hypothesis: the developers themselves write that there is no established threshold for what counts as meaningful receptor selectivity, and that the roles of the individual amylin receptor subtypes are poorly understood.
So why do you stock it?
Because on evidence it is near the top of this catalogue, not the bottom. A 263-person, 48-week, placebo-controlled trial in The Lancet is more and better human data than most of what is sold as a research peptide will ever have, and the tolerability finding inside it is genuinely interesting rather than marketing. What we will not do is sell the 20% figure without the 64% figure that came with it, or let the family resemblance to cagrilintide stand in for a comparison nobody has run in a human being.
References
- Billings LK, Hsia S, Bays H, et al. Eloralintide, a selective amylin receptor agonist for the treatment of obesity: a 48-week phase 2, multicentre, double-blind, randomised, placebo-controlled trial. Lancet 2025;406(10520):2631–2643. DOI 10.1016/S0140-6736(25)02155-5. PMID 41207310. Registered NCT06230523. — the single most important source on this page. 263 participants, 46 US centres, 48 weeks, seven arms. Origin of every weight figure and every nausea and fatigue percentage in the tolerability table, including the 64% nausea in the 6 mg arm against 33% in the 9 mg arm that makes the curve non-monotonic, and the 11% and 13% nausea in the two lowest arms against 14% on placebo. Also the source for the two stepped arms finishing at the same point with 54% versus 25% nausea.
- Briere DA, Qu H, Lansu K, et al. Eloralintide (LY3841136), a novel amylin receptor agonist for the treatment of obesity: from discovery to clinical proof of concept. Molecular Metabolism 2025;102:102271. DOI 10.1016/j.molmet.2025.102271. PMID 41109426. PMC12640043. Registered NCT05295940. — read in full this session. The discovery paper, and the source for everything structural and mechanistic here: the 37-residue chain with three non-coded residues at positions 11, 15 and 22, the methylene thioacetal bridge replacing the disulfide, the C20 fatty diacid at lysine 26, the 12-fold and 11-fold human selectivity ratios, the rat-versus-human selectivity difference, the 310–366 h human half-life and the 159–195 h cagrilintide figure it is compared against, the single-dose phase 1 in 48 healthy participants, the rat head-to-head against cagrilintide on taste avoidance and body composition, the pH 8 versus pH 4 formulation contrast, and the statement that combination trials with tirzepatide are under way. Also the source of the two honest limitations we quote: that the rat difference may reflect calcitonin receptor engagement rather than amylin subtype selectivity, and that no established minimum selectivity threshold exists. It describes the modifications and does not print the sequence — which is why this page has no molecular weight.
- Bhattachar S, Tham LS, Tidemann-Miller B, et al. Eloralintide, a selective, long-acting amylin receptor agonist for treatment of obesity: phase 1 proof of concept. Diabetes, Obesity and Metabolism 2026;28(4):2651–2660. DOI 10.1111/dom.70439. PMID 41559929. PMC12992164. — the 12-week repeat-dose phase 1, 100 participants, mean BMI 32.6, five cohorts, no dose escalation. Source of the 2.6% to 11.3% weight range and of the adverse-event list we use as the non-GLP-1 profile: decreased appetite 19%, headache 12%, fatigue 11%, diarrhoea 10%, nausea 8%, vomiting 4%, with its authors describing gastrointestinal events as infrequent. One serious adverse event, judged unrelated. Note the publication year: this appeared in 2026, after the phase 2 paper, despite being the earlier-stage study.
- Kamrul-Hasan ABM, Khalil I, Mahajan K, Dutta D, Banerjee M, Pappachan JM. Novel amylin-based therapies for weight management in adults with overweight or obesity without diabetes: a network meta-analysis. Endocrinology, Diabetes & Metabolism 2026;9(3):e70247. DOI 10.1002/edm2.70247. PMID 42175595. PROSPERO CRD420261340457. — the only quantitative comparison of this compound against a GLP-1 that exists, and it is indirect. Six trials, 4,642 participants, 12 to 68 weeks. Source of the −18.0% figure for high-exposure eloralintide, against −24.0% for high-dose amycretin, −17.2% for CagriSema, −11.5% for semaglutide 2.4 mg and −6.4% for liraglutide 3.0 mg. Its own authors call the data sparse and of low certainty and the findings preliminary, and we have printed that caveat wherever we use the number.
- Sigalov A, Frishman WH. Cardiometabolic risk reduction through selective amylin receptor agonism: emerging cardiovascular implications of eloralintide. Cardiology in Review, published online 16 September 2026. DOI 10.1097/CRD.0000000000001468. PMID 42745233. — source of the pulse-rate reduction observation and its contrast with the heart-rate increase seen with GLP-1 receptor agonists, plus the reported blood pressure, hs-CRP, lipid and preferential-fat-loss findings. Equally the source of our caveats: the evidence is preclinical plus phase 1 and 2 with small samples and short durations, no amylin receptor agonist has had a cardiovascular outcomes trial, and in the authors’ own framing epidemiological benchmarks here are contextual rather than predictive.
- Fischer SL, Borner T. Beyond GLP-1: amylin-based pharmacotherapy and the search for better-tolerated weight-loss drugs. Pharmacological Research 2026;232:108382. DOI 10.1016/j.phrs.2026.108382. PMID 42586227. — read for the class-level tolerability argument. Places eloralintide among the selective agonists against the dual amylin/calcitonin agonists, and sets out the open question this page keeps returning to: whether reduced food intake on these drugs reflects physiological satiation or aversive signalling, and how far calcitonin receptor engagement and exposure kinetics decide which.
- Bailey CJ, Flatt PR, Conlon JM. Long-acting amylin-related peptides as therapies for obesity and type 2 diabetes. Peptides 2026;196:171480. DOI 10.1016/j.peptides.2026.171480. PMID 41747885. — class review, read for the position of eloralintide among the agents showing strong monotherapy efficacy, and for the generic statement that gastrointestinal effects across this class are commonplace during initiation and up-titration but mostly resolve with continued use. That is a class-level statement and we have not applied it to eloralintide specifically, because the phase 2 arms are the compound-specific answer.
- Alhazmi A, le Roux CW. Amylin analogs: the next major class of weight loss therapy — a review of experimental data and early-phase clinical trials. Diabetes, Obesity and Metabolism 2026;28(Suppl 5):42–50. DOI 10.1111/dom.71074. PMID 42452898. PMC13588232. — read to confirm the competitive landscape as of 30 April 2026 and that no eloralintide combination results had been published by then.
- Panou T, Gouveri E, Popovic DS, Papanas N. New amylin-based agonists for the treatment of obesity and type 2 diabetes mellitus. Diabetes Therapy, published online 28 September 2026. DOI 10.1007/s13300-026-01921-0. PMID 42803913. — the most recent review located, searched to June 2026. Independently characterises eloralintide’s adverse-event profile as distinct from the GLP-1 class, naming fatigue, headache and appetite loss, which is the corroboration for that framing on this page. Note one discrepancy we are flagging rather than smoothing: it reports the phase 2 result as up to 20.1%, where the Lancet paper itself prints −20% with a confidence interval of −22.7 to −17.5. We have used the primary paper’s own figure throughout.
- Lempesis IG, Dalamaga M. Obesity pharmacotherapy reimagined: the era of multi-receptor agonists and next-generation metabolic modulators. Metabolism Open 2026;30:100463. DOI 10.1016/j.metop.2026.100463. PMID 41948476. PMC13051938. — read for context on where the amylin pathway sits against the incretin and multi-receptor agents, and for confirmation that eloralintide is discussed as an emerging monotherapy rather than an approved option.
- Health Canada. Unauthorized injectable peptide drugs seized and sold by Canada Peptide may pose serious health risks. Advisory, 1 August 2025. recalls-rappels.canada.ca — read in full this session. Eloralintide does not appear. The affected-products table runs to 44 entries; cagrilintide is also absent, while retatrutide and tirzepatide are present. The table’s lead-in is “Unauthorized injectable peptide drugs, including:”, so the list is on its own terms not exhaustive and absence from it is not a clearance.
- US Food and Drug Administration. Certain bulk drug substances for use in compounding that may present significant safety risks. Content current as of 22 April 2026. fda.gov — read in full this session. Eloralintide does not appear anywhere on the page, in the category 2 table or the nominated-but-withdrawn table. No amylin analogue appears at all — neither cagrilintide nor pramlintide. The straightforward reading is that an active clinical candidate was never nominated for compounding, not that it was considered and cleared.
- World Anti-Doping Agency. Prohibited List 2026, section S0. — eloralintide is not named. The application of S0 is ours, using the list’s own definition of a substance with no current approval by any governmental regulatory health authority for human therapeutic use.
Listed rather than hidden, what we could not find. Searches for this page were run against PubMed, which was reachable throughout; identifiers and abstracts above come from it, the Molecular Metabolism paper was read in full text, and the DOI links go to the publishers. The two regulatory pages were fetched and read directly. Searched and not found: any phase 3 trial of eloralintide; any published result from the eloralintide-plus-tirzepatide trials the discovery paper says are under way; anything at all pairing it with retatrutide; any head-to-head human trial against cagrilintide, against a GLP-1, or against any other drug — the only direct comparison with cagrilintide is in rats and the only human comparison is the indirect network meta-analysis above; any cardiovascular outcomes trial; any published amino-acid sequence, which is why no molecular weight, net charge, counterion count or trifluoroacetate cost is computed on this page, unlike every other profile in this library; any stability or solvent-compatibility study for this molecule; and any independent analysis of research-grade eloralintide vials by a regulator, academic group or third-party laboratory. We did not check Australian regulatory sources and make no claim about them. Every figure above is reported as what a published trial or assay measured, in that study’s own terms. This page carries no dose, no schedule and no duration, and the trial arms named in the tolerability table are a report of one trial rather than guidance of any kind.
For laboratory research use only. Not for human or veterinary use. Nothing on this page is dosing guidance, and no figure here should be read as a recommendation.