Eloralintide
LY3841136 (selective amylin agonist)
Eloralintide (LY3841136 (selective amylin agonist)) is a metabolic & fat loss research compound. Selective long-acting amylin receptor agonist (AMY1R-preferring) — appetite suppression via amylin pathways; C20 fatty-diacid acylation gives once-weekly dosing. More receptor-selective than cagrilintide.
Eloralintide quick facts
| Reported research dose | 1mg-9mg weekly |
| Route | Subq |
| Frequency | 1x Weekly |
| Half-life | ~Weekly dosing |
| Forms | Injectable |
| Evidence level | Phase 2 human |
Lilly's clean amylin play — selective for the amylin receptor, so potentially fewer off-target effects. New and promising.
How Eloralintide works
Selective long-acting amylin receptor agonist (AMY1R-preferring) — appetite suppression via amylin pathways; C20 fatty-diacid acylation gives once-weekly dosing. More receptor-selective than cagrilintide.
Proposed benefits
Researched for fat oxidation, appetite and energy regulation, insulin sensitivity and endurance capacity.
Where to get Eloralintide
Buy Eloralintide at Flawless Compounds →Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for Eloralintide
Graded by what exists behind each claim.
✅ Clinically validated
- In phase 2. Eli Lilly's selective amylin receptor agonist. Early data reported meaningful weight loss with notably low rates of nausea and vomiting compared with GLP-1 agonists — which, if it holds, is the commercially important finding rather than the weight number.
📊 Correlative data
- No marketed use and no real-world record. The tolerability claim comes from small early cohorts and needs phase 3 scale before it means anything.
🧪 Theoretical / extrapolated
- A selective amylin analog — no GLP-1 activity at all, which is the point. Pramlintide proved amylin agonism causes weight loss twenty years ago; the field left it there because of dosing inconvenience, not failure.
- Selectivity is the bet on tolerability. If most of the GI burden comes from GLP-1's effect on gastric emptying, then an amylin-only agent should deliver satiety with less nausea — and that is precisely what the early data suggests.
- It also predicts a smaller glycemic effect than a GLP-1, since amylin does not stimulate insulin secretion.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Eloralintide actually does
This is the only compound in this cohort whose receptor selectivity ratio is actually published, so start there, because for a receptor-selective drug the ratio is the drug.
In cell lines expressing human receptors, eloralintide preferentially activated the human amylin 1 receptor: 12-fold over the calcitonin receptor and 11-fold over the amylin 3 receptor Briere 2025. Hold those numbers next to what the receptors are. AMY1 is the calcitonin receptor with RAMP1 bolted on; AMY3 is the same core with RAMP3 Boyle 2022. So ‘12-fold selective’ here does not mean selective for one protein over another protein — it means selective for one dressing of the calcitonin receptor over the bare receptor underneath it, by a single order of magnitude. That is a real engineering achievement and it is also a narrower window than the word ‘selective’ implies to a buyer.
The species result is the one that matters for reading the animal data. The same paper reports that in rat receptors, both AMY1R and AMY3R were activated more potently than the calcitonin receptor Briere 2025. Read the two sentences together: the human profile is AMY1R-preferring, the rat profile is AMY1R and AMY3R over CTR. The rodent efficacy data was generated through a different receptor mixture than a human dose meets. Nobody states that, and it is in the drug’s own discovery paper.
The tolerability thesis, and the single experiment behind it. The commercial argument for a selective amylin agonist is that the nausea comes from the non-selective activity, so a cleaner molecule should give satiety without the gut. The evidence for that is one comparison: eloralintide induced significantly less conditioned taste avoidance in lean rats than cagrilintide, a non-selective amylin receptor agonist (p < 0.05) Briere 2025. Conditioned taste avoidance is the closest behavioral proxy a rodent has for nausea. It is a real head-to-head and it is the only head-to-head between a selective and a non-selective amylin agonist that exists — in any species.
Where it acts. Amylin’s physiological effects are mediated by direct brain activation with the caudal hindbrain the most prominent site Boyle 2022, which sits outside the blood-brain barrier. That is why a large acylated peptide can produce a central satiety effect without any blood-brain-barrier engineering at all, and it is the structural reason amylin agonism is a different appetite lever from GLP-1 rather than a weaker copy of one.
And what it deliberately does not do. No GLP-1 activity. Amylin does not stimulate insulin secretion Boyle 2022, so the glycemic effect of this drug should be whatever the weight loss buys and nothing more — a prediction the phase 2 could not test, because it excluded people with type 2 diabetes Billings 2025.
Cell, rodent, human — and where it stops
Step one, in cells. Human and rat AMY1R, AMY3R and CTR lines, with the selectivity numbers above Briere 2025.
Step two, in rats and monkeys. In diet-induced obese rats, eloralintide dose-dependently reduced food intake and lowered body weight primarily through fat mass loss, and the conditioned taste avoidance comparison against cagrilintide was run in lean rats Briere 2025. Pharmacokinetics were favorable in both rats and monkeys. Note what the fat-mass claim rests on: rodent body composition, not a human scan.
Step three, phase 1 single dose — and the number here is striking. 48 healthy participants, mean BMI 27.5 kg/m2, single ascending subcutaneous doses from 0.04 to 12 mg (NCT05295940). 9 participants reported 16 adverse events, 15 of the 16 mild; 2 participants reported 4 gastrointestinal events including one moderate vomiting event. At week 4 after a single injection, mean weight change from baseline was −2.5% at 4 mg (p < 0.01) and −4.4% at 12 mg (p < 0.001), against +0.6% on placebo Briere 2025. One injection, still measurable four weeks later.
Step four, phase 1 multiple dose. 100 participants with obesity or overweight, mean age 44, mean BMI 32.6 kg/m2, at 3 US centers, dosed once weekly for 12 weeks with no dose escalation Bhattachar 2026. Exposure was dose-proportional — dose-normalized geometric mean ratios of 1.1 for AUC at steady state and 1.0 for Cmax. The adverse events are the point: decreased appetite 19%, headache 12%, fatigue 11%, COVID-19 11%; diarrhea 10%, nausea 8%, vomiting 4%. Week-12 least-squares mean weight reduction ran from 2.6% to 11.3% across dose groups. Single-digit nausea without any titration is genuinely unusual in this space.
Step five, phase 2, and it met its primary endpoint. 263 participants at 46 US research centers, BMI ≥ 30 or ≥ 27 with a weight-related comorbidity, no type 2 diabetes, randomized to placebo or eloralintide at 1, 3, 6 or 9 mg or escalations of 6→9 or 3→9 mg, once weekly for 48 weeks (NCT06230523). Primary endpoint: percent change in bodyweight at 48 weeks. Result: −9% (1 mg), −12% (3 mg), −18% (6 mg), −20% (9 mg), −20% (6–9 mg) and −16% (3–9 mg), against −0.4% on placebo Billings 2025.
The obstacles, and the first one is inside the phase 2’s own adverse-event table. (1) The nausea numbers are not monotonic. Nausea was 64% at 6 mg and 33% at 9 mg; fatigue was 29% at 6 mg and 43% at 9 mg; the 6→9 mg escalation arm reported 54% nausea and 46% fatigue, higher than the flat 9 mg arm Billings 2025. A dose that produces twice the nausea of a higher dose is not a dose-response curve, it is small-group noise — and the arms it comes from are n=28 at 6 mg and n=24 at 6–9 mg against n=54 at 9 mg. The headline ‘well tolerated’ is true and it is resting on arms of 24 to 28 people. (2) Fatigue is the signal nobody quotes. 43% at 9 mg against 12% on placebo Billings 2025. If the selling point is satiety without nausea, the trade that shows up in the trial is satiety with fatigue. (3) No published body composition. Neither phase 1 nor phase 2 reports DXA, and the fat-mass-selectivity claim is still a rodent claim Briere 2025. (4) No phase 3, no head-to-head against a GLP-1, and no cardiovascular outcome data. (5) Nobody with type 2 diabetes has been in a randomized eloralintide trial Billings 2025, so its behavior alongside insulin or a sulfonylurea is unmeasured.
Eloralintide pharmacokinetics — how much of it actually gets in
The catalog says ‘~Weekly dosing’. That is a schedule, not a half-life, and the published data lets you go further.
What holds it in the body. A C20 fatty diacid is attached to the peptide, which is the same trick every once-weekly peptide in this catalog uses: the fatty chain binds serum albumin reversibly, the albumin-bound fraction is too large for glomerular filtration and is shielded from peptidases, and the free fraction is continuously topped up from that reservoir Muller 2022. The measured consequence is in the phase 1 data: over 12 weeks of once-weekly dosing without escalation, steady-state AUC and Cmax were dose-proportional, with dose-normalized geometric mean ratios of 1.1 and 1.0 Bhattachar 2026. Linear kinetics across a dose range is what a clean albumin-depot mechanism looks like.
The number that bounds the duration. A single 12 mg subcutaneous injection still produced a 4.4% weight reduction at week 4 Briere 2025. Weight is a slow integrator, so that is not proof of four weeks of drug exposure — but a single dose whose effect is measurable a month later is not a peptide clearing in hours. Against pramlintide’s roughly 48 minutes, the same receptor family is being addressed on schedules that differ by more than two orders of magnitude.
What degrades it. Once it comes off albumin, an acylated peptide is subject to proteolysis by plasma and tissue peptidases and to renal handling of the free fraction. It is not a cytochrome substrate, which is why peptides of this class do not carry the interaction lists small molecules do.
The oral barrier. Absolute for this molecule. Swallowed, an acylated peptide meets gastric acid and pancreatic proteases, has no transporter to carry it intact across the enterocyte, and would face hepatic first-pass extraction if it crossed. Oral amylin formulations are named as an open research goal for the whole class rather than an available product Volcansek 2025, and no oral eloralintide exists.
The route, and what the trials actually did. Every human dose was a subcutaneous injection, once weekly. The phase 1 multiple-dose study deliberately used no dose escalation for 12 weeks Bhattachar 2026 — which for a satiety drug is a tolerability claim in itself, since escalation exists to hide nausea.
What would have to be true, and how you would know it was not
Four predictions. The first argues against the compound and is the one that decides whether a 20% weight loss was worth having.
1. Lean mass will not be spared just because the mechanism is amylin. The fat-mass-selectivity claim comes from diet-induced obese rats Briere 2025; neither the phase 1 nor the phase 2 publication reports human body composition Bhattachar 2026 Billings 2025. The class base rate is that over 25% of total weight lost through pharmacotherapy comes from fat-free mass Stefanakis 2024. At the phase 2’s −20% at 9 mg, that is roughly 5% of starting body weight as fat-free mass. Measure grip strength at baseline, 12 and 24 weeks, and a DXA if you can get one. Falling grip strength alongside falling weight is the failure mode this drug’s marketing does not mention.
2. HbA1c should fall only as far as the weight drags it. Amylin does not stimulate insulin secretion Boyle 2022, and the phase 2 excluded type 2 diabetes entirely Billings 2025, so there is no glycemic efficacy dataset for this molecule at all. Prediction: HbA1c (Hemoglobin A1c) and Fasting Insulin fall roughly in proportion to weight, and no faster. If HbA1c falls faster than weight, something other than amylin agonism is acting — which on a research-market vial is the question worth asking. Baseline and 12 weeks.
3. Lipase and amylase should stay flat. The mechanism is hindbrain and gastric, not pancreatic Boyle 2022, and neither published trial reports a pancreatic-enzyme signal Bhattachar 2026 Billings 2025. Baseline and 12 weeks; a rising lipase or amylase here would not be explained by anything in the drug’s published pharmacology.
4. Fatigue will track dose, not weight loss, and it will show up by week 4. 43% at 9 mg against 12% on placebo Billings 2025. This is falsifiable in one person without a laboratory: score fatigue daily on a fixed 0–10 scale through a dose step and hold sleep, training and calories constant across the window. If fatigue rises within a fortnight of the step and before any meaningful weight has moved, it is the drug. If it tracks the weight curve instead, it is the deficit.
What nobody has tested yet
Four experiments. The third one is the one nobody in this market will think of and it has a 41% prior attached to it.
1. Nobody has published a body-composition arm. Not in the single-dose study, not in the 12-week multiple-dose study, not in the 48-week phase 2 Briere 2025 Bhattachar 2026 Billings 2025. The entire commercial thesis for amylin over incretin is tolerability and body composition; the tolerability half has data and the body composition half does not.
2. Nobody has measured calcitonin or bone turnover on a chronic amylin agonist. Twelve-fold selectivity over the calcitonin receptor Briere 2025 is one order of magnitude, and 9 mg weekly for 48 weeks Billings 2025 is a great deal of receptor-time. Calcitonin is an ordinary send-out assay and bone turnover markers are routine. Neither appears in any published eloralintide trial.
3. Nobody has stratified the headache signal by migraine history. Pramlintide, an amylin analog, provoked migraine-like attacks in 41% of patients with migraine without aura, and the pharmacology in that paper placed the effect at an amylin receptor rather than the CGRP receptor Ghanizada 2021. Eloralintide is a more selective amylin receptor agonist held at steady concentration for a year. Headache was reported as a treatment-emergent adverse event in 12% of the phase 1 multiple-dose cohort Bhattachar 2026, with no breakdown by migraine history in either that study or the phase 2. The experiment is trivial: recruit 20 people with migraine and 20 without, dose both, count attacks. It has never been done for any long-acting amylin agonist.
4. Nobody has run the selectivity thesis in a human. The entire case for a selective amylin agonist rests on one rat comparison against cagrilintide Briere 2025. A head-to-head in people, titrated to matched weight loss, with nausea incidence as the primary endpoint, is the trial that would either establish this molecule’s reason to exist or remove it — and it has not been registered.
Eloralintide — its own safety story, not its class's
The class block on this page describes GLP-1 receptor agonists. Eloralintide has no GLP-1 activity, and the differences run in both directions — some class risks do not apply, and two risks specific to the amylin axis are missing from the block entirely.
1. What the trials reported, which is the good news and is real. In 12 weeks of weekly dosing without escalation in 100 people: diarrhea 10%, nausea 8%, vomiting 4%, most treatment-emergent events mild, no deaths, and the single serious adverse event judged unrelated Bhattachar 2026. In the 48-week phase 2 the most common events were nausea and fatigue Billings 2025. For a drug producing up to 20% weight loss, single-digit vomiting without titration is not a small finding.
2. And the number that complicates it. Fatigue reached 43% at 9 mg and 46% in the 6→9 mg escalation arm, against 12% on placebo Billings 2025. Nausea was 64% at 6 mg. Both are far from the phase 1 numbers, and the difference is 48 weeks against 12 and 24–54 people per arm against a larger pooled cohort. The honest summary is that the tolerability advantage is real at 12 weeks and less clean at 48.
3. Hypoglycemia: the mechanism says no, and the trials cannot confirm it. Amylin does not stimulate insulin secretion Boyle 2022, so an amylin agonist alone should not drive glucose below normal — and unlike pramlintide, eloralintide carries no boxed warning and no mandated insulin reduction. But the phase 2 excluded people with type 2 diabetes Billings 2025 and the phase 1 studies were in healthy or otherwise-well participants Briere 2025 Bhattachar 2026. So the interaction with insulin or a sulfonylurea has never been studied in this molecule. The precedent to import is pramlintide’s: an amylin analog that slows the arrival of glucose will unmask a mealtime insulin dose that was already too high, and the collision happens in the first hours after the injection.
4. The migraine risk, which belongs to the amylin axis and to no other drug in this catalog. Amylin is a close structural relative of CGRP, and infused pramlintide induced headache in 88% and migraine-like attacks in 41% of patients with migraine without aura, through an amylin receptor Ghanizada 2021. No eloralintide trial has reported migraine history or migraine outcomes. If you get migraines, this is the specific question to raise before starting, and it is not in any product literature.
5. The calcitonin receptor underneath the amylin receptor. The 12-fold AMY1R selectivity Briere 2025 is over the calcitonin receptor itself Boyle 2022. Chronic partial calcitonin agonism has an obvious bone and calcium question and no published data in either direction.
6. What partly transfers from the class block, and why. The gallbladder signal is a GLP-1 finding — relative risk 1.37 across 76 randomized trials and 103,371 patients, rising to 2.29 in weight-loss trials and higher at greater doses and longer durations He 2022. Part of that risk is the GLP-1 receptor and part of it is rapid weight loss, and eloralintide produces the second without the first. Nobody has measured which half is which, and no eloralintide publication reports a biliary event category. The thyroid C-cell contraindication in the class block is a GLP-1 labeling matter and does not apply here — but note the irony that the receptor this drug is selective against is the calcitonin receptor, which is the C cell’s own receptor system.
Sources read for this page
- Briere DA, et al. Eloralintide (LY3841136), a novel amylin receptor agonist for the treatment of obesity: From discovery to clinical proof of concept. Molecular Metabolism 2025 · PMID 41109426
- Billings LK, 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 · PMID 41207310
- Bhattachar S, et al. Eloralintide, a selective, long-acting amylin receptor agonist for treatment of obesity: Phase 1 proof of concept. Diabetes, Obesity and Metabolism 2026 · PMID 41559929
- Boyle CN, Le Foll C, Lutz TA. Mediators of Amylin Action in Metabolic Control. Journal of Clinical Medicine 2022 · PMID 35456307
- Ghanizada H, et al. Amylin Analog Pramlintide Induces Migraine-like Attacks in Patients. Annals of Neurology 2021 · PMID 33772845
- Stefanakis K, et al. The impact of weight loss on fat-free mass, muscle, bone and hematopoiesis health: Implications for emerging pharmacotherapies aiming at fat reduction and lean mass preservation. Metabolism 2024 · PMID 39481534
- He L, et al. Association of Glucagon-Like Peptide-1 Receptor Agonist Use With Risk of Gallbladder and Biliary Diseases: A Systematic Review and Meta-analysis of Randomized Clinical Trials. JAMA Internal Medicine 2022 · PMID 35344001
- Volcansek S, et al. Amylin: From Mode of Action to Future Clinical Potential in Diabetes and Obesity. Diabetes Therapy 2025 · PMID 40332747
- Muller TD, et al. Anti-obesity drug discovery: advances and challenges. Nature Reviews Drug Discovery 2022 · PMID 34815532
Eloralintide — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- These slow gastric emptying and act on hypothalamic and brainstem appetite centers. Almost everything that goes wrong follows from the gastric emptying, not from anything exotic: nausea, early fullness, reflux, constipation, and — when someone titrates faster than their gut adapts — vomiting.
- The composition risk is the one nobody warns about. Appetite suppression does not discriminate. It suppresses the appetite for protein too, and in a deficit without adequate protein and a resistance stimulus a meaningful share of the loss is lean mass. That lowers the maintenance intake you eventually eat back into, which is the mechanism behind most of the rebound stories.
- Slowed emptying also delays absorption of anything else taken by mouth — a pharmacokinetic consequence rather than a drug interaction, but it matters for anything time-critical.
What has actually been reported
- GI effects are extremely common and mostly settle over weeks. Gallbladder problems are a recognized signal, and rapid weight loss of any cause raises gallstone risk — the drug is not doing something unusual, it is doing rapid weight loss well.
- Pancreatitis is reported and rare. The presentation to know is severe upper abdominal pain radiating to the back, usually with vomiting.
- A thyroid C-cell tumor signal exists in rodents and has not been demonstrated in humans; it is why the labeled contraindication for medullary thyroid carcinoma and MEN2 exists.
How to reduce the risk
Same mechanism as the prediction.
- Follow the titration schedule even if you feel fine. It exists for gut adaptation, not for legal cover. Almost everyone who quits in the first month escalated faster than their stomach could keep up.
- Hit your protein target first at every meal, before anything else on the plate. This is the single highest-leverage habit on the drug — 1.6–2.2 g/kg, and eat it while you still have the appetite to.
- Lift while you are on it. The compound handles intake; resistance training is the only thing handling what you keep.
- Aim for 0.5–1% of bodyweight per week, deliberately. The drug removes the hunger signal that would normally stop you going too hard, so the rate has to be a decision rather than a by-product.
- Fiber and electrolytes from day one, not from week four when constipation has already made up your mind about the drug.
- If nausea is winning, step back one dose rather than quitting the class. Almost nobody needs to be at the top of the range.
What it does to your bloodwork
A fact about the assay.
- HbA1c and fasting glucose should improve — that is the drug working, and it is the cleanest confirmation you have.
- Rapid loss moves lipids, liver enzymes and uric acid transiently. A wobble at 8 weeks into aggressive loss is usually the loss, not a new problem — but it is a reason to have the baseline.
- Worth a thyroid panel and a lipid panel before starting, simply so a later result has something to be compared against.
Don't run this if
- Personal or family history of medullary thyroid carcinoma, or MEN2.
- Previous pancreatitis.
- Active gastroparesis — you would be adding a drug whose main action is the thing already wrong.
The honest unknown
- What happens to body composition over repeated multi-year cycles of loss and regain on and off these drugs. Weight is well studied; the muscle-to-fat ratio of what comes back is not.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Eloralintide — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Eloralintide moves on your bloodwork
Expected direction, not a measured one.
- HbA1c (Hemoglobin A1c) — ↓ expected to fall
Falling HbA1c is the compound working. Expect it.
What to do: Baseline and 12 weeks. It moves slowly by design — a 4-week retest tells you very little. - Fasting Insulin — ↓ expected to fall
Insulin sensitivity improves as weight falls and the incretin effect restores first-phase insulin release.
What to do: Useful alongside HbA1c; the two together read the trend properly. - Lipid Panel (Cholesterol, HDL, LDL, Triglycerides) — ↓ expected to fall
Triglycerides in particular fall with weight loss and improved insulin sensitivity.
What to do: Re-check at 12 weeks rather than chasing early numbers. - Lipase — ↑ expected to rise
Lipase and amylase can rise without pancreatitis on this class. An isolated mild elevation in someone with no symptoms is common.
What to do: Severe, persistent abdominal pain radiating to the back is the thing that matters, not the number. Symptoms decide, not a mild enzyme rise. - Comprehensive Metabolic Panel (CMP) — ◆ worth watching
Rapid weight loss and reduced intake shift electrolytes and kidney markers; dehydration from nausea or vomiting shows up here first.
What to do: Worth a baseline. If you have been vomiting, this is the panel that catches the consequence. - Ferritin — ↓ expected to fall
Not the drug — the eating. Sharply reduced intake drops iron, B12 and protein intake with it, and this is the most commonly missed consequence of a good response.
What to do: Check ferritin and B12 at 12 weeks. Muscle loss and hair shedding on a GLP-1 is very often a nutrition problem wearing a drug's name.
The pattern with this class is that the frightening-looking numbers (lipase) are usually fine and the boring ones (ferritin, B12) are where the real damage happens.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Needle gauge and injection site
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Eloralintide in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Eloralintide
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| HbA1c (Hemoglobin A1c) | Where you started, so you can prove the change was real |
| Fasting Insulin | Moves years before HbA1c does — the earliest signal you get |
| Lipid Panel (Cholesterol, HDL, LDL, Triglycerides) | Rapid fat loss shifts triglycerides fast, in both directions |
| Comprehensive Metabolic Panel (CMP) | Liver, kidney and electrolytes while intake is restricted |
The Metabolic Health & Prediabetes panel covers these in one order — 8 markers, $81.45 with the discount applied.
Check results you already have → · All 103 markers A–Z
Eloralintide — frequently asked questions
What is Eloralintide?
Eloralintide (LY3841136 (selective amylin agonist)) is a metabolic & fat loss research compound. Selective long-acting amylin receptor agonist (AMY1R-preferring) — appetite suppression via amylin pathways; C20 fatty-diacid acylation gives once-weekly dosing. More receptor-selective than cagrilintide.
Is the full Eloralintide protocol on this page?
The reported research dose is on this page, along with how Eloralintide works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of Eloralintide?
Eloralintide has an approximate half-life of ~Weekly dosing, which is part of what determines how often it's dosed.
What's the evidence behind Eloralintide?
Current evidence level: Phase 2 human. Eloralintide is offered for research purposes only and is not an approved medicine.
Eloralintide inside a finished plan
One arm of 1 Protocol Blueprint, free to read in full.
What Eloralintide is used for
Eloralintide appears under 2 goals in the goal router.
Related Metabolic & Fat Loss compounds
Where this goes next
Eloralintide is the appetite arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.