Hexarelin

Examorelin

Hexarelin (Examorelin) is a gh & growth research compound. Potent GHRP/ghrelin agonist — strong GH pulse, but with more cortisol/prolactin and faster desensitization than Ipamorelin.

How Hexarelin works

Potent GHRP/ghrelin agonist — strong GH pulse, but with more cortisol/prolactin and faster desensitization than Ipamorelin.

Proposed benefits

Researched for lean-mass support, recovery, sleep depth, connective-tissue repair and improved body composition via the GH/IGF-1 axis.

Where to get Hexarelin

The evidence for Hexarelin

Graded by what exists behind each claim.

✅ Clinically validated

• Human studies exist, including work in cardiac patients where it showed effects on left ventricular function that appeared independent of growth hormone — one of the more interesting orphan findings in this category.
• No development program followed.

📊 Correlative data

• The most potent GH releaser of the GHRP family and the least used, because desensitization is fast and well documented — receptor downregulation within weeks of continuous use is the consistent report and matches the published pharmacology.
• Raises cortisol and prolactin like the other non-selective GHRPs.

🧪 Theoretical / extrapolated

• A ghrelin-receptor agonist with the strongest binding of the group. It also binds CD36, a scavenger receptor in cardiac tissue, which is the proposed mechanism for the GH-independent cardiac effects.
• The potency and the desensitization are the same property. Strong sustained receptor occupancy is what downregulates the receptor, which is why every practical protocol for it is short and pulsed.

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 Hexarelin actually does

Hexarelin is six residues: His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH₂. That sequence is not a claim — it is readable directly off the structure record, whose systematic name specifies a 2-methyl indole side chain in the R configuration at position 2, an R-configured phenylalanine at position 5, and a C-terminal hexanamide rather than a free acid; formula C47H58N12O6, molecular weight 887.0 National Center for Biotechnology Information 2026. Every one of those three modifications is a defense against a peptidase.

Why the modifications matter more here than on almost any other peptide in this vault. Aminopeptidases attack from the N-terminus and are stereospecific for L-residues, so a D-residue at position 2 stops the first cut. Carboxypeptidases attack a free C-terminal carboxyl, so the amide blocks the other end. The second D-residue at position 5 obstructs endopeptidase attack in the middle. The measured result is startling for an 887 Da peptide: subcutaneous bioavailability of 77.0 ± 10.5% Ghigo 1994, and in rats, hexarelin recovered from bile 90% unchanged and from urine 71% unchanged Roumi 2000. Most injected peptides are shredded. This one is largely excreted intact.

Target one: the growth hormone secretagogue receptor. Hexarelin is a GHRP-family agonist at GHS-R1a, the ghrelin receptor, on pituitary somatotrophs and in the hypothalamus. It works through a different receptor from GHRH and the two are additive — Massoud 1996 showed that GHRH 1.0 µg/kg combined with a tiny hexarelin dose of 0.125 µg/kg produced GH release of 115 ± 32.8 mU/L. On its own, hexarelin 1 µg/kg IV produced a GH area under the curve of 3175 ± 506 against GHRH's 1544 ± 161 at the same dose (p < 0.001) — roughly twice the GH release of the physiological releasing hormone Ghigo 1994. That potency is real and it is why the compound has the reputation it does.

Target two, and this is the part that is genuinely under-reported: CD36. Bodart 2002 identified an 84,000 Da hexarelin-binding protein in cardiac membranes as CD36, a scavenger receptor expressed on cardiomyocytes and microvascular endothelial cells; Demers 2004 then mapped the binding site by photoaffinity cross-linking. This is not GHS-R1a and it is not in the pituitary. It is a fatty-acid-translocase receptor in the heart, and hexarelin binds it directly.

And what CD36 activation does is not what you would guess from the marketing. In Bodart 2002's perfused hearts, hexarelin acting through CD36 increased coronary perfusion pressure in a dose-dependent manner — that is coronary vasoconstriction — and the response was absent in CD36-null mice and in CD36-deficient spontaneously hypertensive rats, with the size of the response tracking CD36 expression. The authors' own conclusion is that CD36 may mediate the coronary vasospasm seen in hypercholesterolemia and atherosclerosis. So hexarelin has a second, GH-independent cardiac action that is well evidenced, mechanistically specific, and points in a direction opposite to the cardioprotection story it is usually sold with. Both findings are real. Holding them together is the honest position.

Cell, rodent, human — and where it stops

Step one, isolated hearts and knockout animals. Bodart 2002 and Demers 2004 established CD36 as a cardiac hexarelin receptor by cross-linking and by loss of response in CD36-null mice.

Step two, rodent cardioprotection, in an animal with no pituitary. Locatelli 1999 used hypophysectomized rats — the clean design, because an animal with no pituitary cannot release GH — and gave hexarelin 80 µg/kg subcutaneously for 7 days. Ischemia-reperfusion damage was prevented: left ventricular end-diastolic pressure and coronary perfusion pressure fell, creatine kinase release fell, prostacyclin release was preserved and contractile recovery improved. GH itself at 400 µg/kg produced similar protection; the related peptide EP 51389 did not. Cardioprotection without a pituitary is about as direct a demonstration of GH-independence as exists.

Step three, humans, acutely — and the dissociation is visible in the same experiment. Broglio 2001 gave 2.0 µg/kg intravenously to 7 normal adults, 7 severely GH-deficient patients and 12 patients with dilated cardiomyopathy. Left ventricular ejection fraction rose significantly in the normal subjects and in the GH-deficient patients (p < 0.05) — people who could not mount a GH response, and in whom GH did not rise — while GH rose in the normal and cardiomyopathy groups. Blood pressure and heart rate did not change. The inotropic effect and the GH effect appeared in different people. But note the group where ejection fraction did not improve: the dilated cardiomyopathy patients, who are the population an inotrope would be for.

Step four, the dose-response study that should govern every protocol and governs none of them. Massoud 1996 gave intravenous hexarelin from 0 to 1.0 µg/kg in healthy adult men and fitted the curves. GH: ED50 0.48 ± 0.02 µg/kg, plateau 140 mU/L. Prolactin: ED50 0.39 ± 0.02 µg/kg, plateau a 180% rise from baseline. Cortisol: a step increase of about 40% at 0.5 µg/kg. Read the two ED50s against each other. Prolactin's is lower than GH's. There is no dose at which you release growth hormone and leave prolactin alone — prolactin is already moving before GH is half-maximal. The only maneuver in the literature that separates them is the combination: GHRH plus 0.125 µg/kg hexarelin gave GH of 115 mU/L with a prolactin rise of only 84.9% and no cortisol rise at all.

Step five, chronic dosing, where it falls apart — and where a second study says it does not. Rahim 1998 gave 1.5 µg/kg subcutaneously twice daily for 16 weeks. The GH area under the curve fell from 19.1 ± 2.4 to 10.5 ± 1.8 (p < 0.01) — a 45% loss of response — and recovered to 19.4 ± 3.7 four weeks after stopping. That is textbook tachyphylaxis: partial, and fully reversible in a month. Then the finding that matters more: IGF-1 did not change (p = 0.24), IGFBP-3 did not change (p = 0.74), and total body fat, lean mass and bone density were all unchanged. Sixteen weeks of a genuine GH pulse, twice a day, and the downstream axis never moved.

Ghigo 1996 is the counter-case and it changes the interpretation. Intranasal hexarelin 1.25 mg (about 18 µg/kg) three times daily for 8 days in seven elderly subjects, and oral 20 mg (about 300 µg/kg) three times daily for 15 days in seven elderly women, produced no desensitization of the GH response — and did raise the downstream markers, with IGFBP-3 rising from 1.6 to 2.4 mg/L (p < 0.02) on the intranasal route and IGF-1 from 141.6 to 156.0 (p < 0.03) on the oral one. So desensitization is a property of the dosing pattern, not of the molecule. Sustained twice-daily subcutaneous exposure desensitizes; short intermittent exposure by a low-bioavailability route does not.

The obstacle. The chronic human studies are seven to a handful of subjects each, in elderly or GH-deficient people, and the longest is 16 weeks Rahim 1998. Laron 1995 showed intranasal hexarelin accelerated growth in short children, which is a real clinical signal, and no development program followed any of it. Nothing has been published in healthy trained adults, at the 100–200 µg doses actually used, for any duration. And there is no published human pharmacokinetic study at all — the half-life below comes from rats.

Hexarelin pharmacokinetics — how much of it actually gets in

The routes were compared head to head in one study, and the numbers decide everything. Ghigo 1994 gave hexarelin to 12 healthy young volunteers by four routes and measured bioavailability against intravenous: subcutaneous 77.0 ± 10.5%, intranasal 4.8 ± 0.9%, oral 0.3 ± 0.1%. Oral is three parts in a thousand. That is why the oral arm of Ghigo 1996 needed 20 mg to do what 1.5 µg/kg does subcutaneously — a roughly 200-fold dose penalty, which is exactly what a 0.3% bioavailability predicts.

What clears it, measured in rats because nobody measured it in people. Roumi 2000 dosed male Sprague-Dawley rats: intravenous half-life 75.9 ± 9.3 minutes, systemic clearance 7.6 ± 0.7 mL/min/kg, steady-state volume of distribution 744 ± 81 mL/kg, subcutaneous bioavailability 64%, first-order kinetics up to 50 µg/kg. Elimination was principally biliary — 60% of the dose in bile, of which 90% was unchanged peptide — with 22% in urine (71% unchanged) and 10% in feces, and accumulation in kidney, liver and duodenum. The authors' conclusion was stability against proteolytic degradation, which is the sequence doing its job.

Read the site's own half-life figure against that. The commonly quoted 30–60 minutes is in the right region but has no human citation behind it; the only measured number in the literature is 75.9 minutes, intravenously, in a rat Roumi 2000. Peptide clearance generally scales with body size in the direction that would make a human value longer, not shorter, so treating 30–60 minutes as a floor rather than a fact is the defensible position.

The arithmetic that should reframe every protocol. The intravenous GH ED50 is 0.48 µg/kg and the prolactin ED50 is 0.39 µg/kg Massoud 1996. A 100 µg subcutaneous dose in an 80 kg person is 1.25 µg/kg, and at 77% subcutaneous bioavailability that is roughly 0.96 µg/kg delivered — about twice the GH ED50 and two and a half times the prolactin ED50. A 200 µg dose is roughly four to five times both. In other words the doses in common use sit at or above the plateau of the GH curve while sitting well past the top of the prolactin and cortisol curves. The extra microgram buys prolactin and cortisol, not growth hormone, and that arithmetic is available from a 1996 paper.

What would have to be true, and how you would know it was not

Four predictions with markers and windows. The first is the one that cuts against the compound, and it is the most important number on this page.

1. IGF-1 will probably not move, and if it does not, the compound is not doing the thing it is bought for. This is not skepticism, it is Rahim 1998's finding: 16 weeks of 1.5 µg/kg twice daily left IGF-1 statistically unchanged (p = 0.24) while the acute GH response fell 45%. Draw IGF-1 at baseline and at 6–8 weeks. IGF-1 is the stable integrator of GH exposure; a GH pulse that does not raise it has not produced a sustained anabolic signal, whatever the acute assay says. If IGF-1 is flat at eight weeks, the honest conclusion is that this protocol is not working, and the fix indicated by the literature is not more dose — it is a different pattern Ghigo 1996.

2. Prolactin and Cortisol (AM) should rise, and at common doses they should rise before growth hormone plateaus. Prolactin ED50 0.39 µg/kg, cortisol stepping up about 40% at 0.5 µg/kg Massoud 1996. Draw both at baseline and again 60–90 minutes after a dose at 4 weeks. This is the single most useful pair of numbers for deciding whether your dose is too high: if prolactin has climbed well out of range, you are paying for hormones you did not want. Halving the dose should reduce prolactin proportionally more than it reduces GH, because you are further up the prolactin curve than the GH one.

3. Fasting glucose handling should drift, and it is measurable before anything is noticeable. GH is a counter-regulatory hormone and antagonizes insulin at the liver and muscle. Fasting Insulin and HbA1c at baseline and 12 weeks. Prediction: fasting insulin up first, HbA1c later and less, and both reversible on stopping. In a person with strong GH response this is the earliest quantitative cost.

4. The tachyphylaxis prediction, with a designed test. Rahim 1998 lost 45% of the GH response over 16 weeks of continuous twice-daily dosing and recovered it fully in 4 weeks off; Ghigo 1996 lost nothing over 8–15 days of intermittent dosing. So the testable claim is that the pattern, not the molecule, causes the fade. Measure a stimulated Growth Hormone response — a single dose with GH sampled at 0, 15, 30, 45 and 60 minutes — at week 0, week 4 and week 8 of continuous use, then repeat after 4 weeks off. Prediction: response down at week 4 to 8, back to baseline after the break. If it does not recover after a month off, the desensitization is not the reversible kind these studies describe.

What nobody has tested yet

There is no published human pharmacokinetic study of hexarelin. Thirty years after the route-comparison study Ghigo 1994, the only measured half-life, clearance and volume of distribution belong to a rat Roumi 2000. A ten-person single-dose study with plasma hexarelin by LC-MS/MS at 0, 15, 30, 60, 120 and 240 minutes would produce the number every protocol on the internet currently guesses at, and it is an afternoon's work in a clinical pharmacology unit.

Nobody has run the pulse-versus-continuous experiment deliberately. Rahim 1998 and Ghigo 1996 disagree about desensitization and differ in route, dose, duration and population, so the pattern hypothesis is an inference from two non-comparable studies. A three-arm trial — daily subcutaneous, five-on two-off, and three weeks on one week off, at matched weekly dose, with stimulated GH and IGF-1 at weeks 0, 4, 8 and 12 — would establish whether the standard cycling advice is right for the right reason.

Nobody has tested the CD36 finding in the people it would matter to. Bodart 2002 showed hexarelin raising coronary perfusion pressure through CD36 and explicitly linked CD36 to coronary vasospasm in hypercholesterolemia and atherosclerosis, while Broglio 2001 showed an inotropic benefit in normal and GH-deficient people but not in dilated cardiomyopathy. The unrun study is the obvious one: hexarelin with coronary flow reserve or stress-echocardiographic imaging in people with established coronary disease. Until it exists, the cardiac story has a benefit arm measured in healthy hearts and a risk arm measured in isolated ones.

And nobody has revisited the children. Laron 1995 showed intranasal hexarelin accelerating growth in short children — a genuine clinical efficacy result, by a non-injected route, published in 1995 — and no program followed. Whether that reflects a safety finding, a commercial decision or the arrival of recombinant GH is not in the published record.

Hexarelin — its own safety story, not its class's

This compound's own risk story is not the generic GH-axis one, and it has three parts the class block cannot give you.

One: it is not selective, and the numbers say the selectivity problem is unavoidable. Ipamorelin's selling point is GH release without prolactin or cortisol. Hexarelin is the opposite molecule: prolactin's ED50 (0.39 µg/kg) is lower than GH's (0.48 µg/kg), and cortisol steps up about 40% at 0.5 µg/kg Massoud 1996. There is no dose window that gives you the GH without the rest. Rahim 1999 looked specifically at the pituitary-adrenal axis and prolactin under chronic administration. Practically: sustained prolactin elevation suppresses gonadal function, and sustained cortisol elevation opposes the exact body composition outcome the compound is taken for.

Two: the response fades, and knowing it is reversible is the useful half. Sixteen weeks of twice-daily dosing cost 45% of the GH response, and four weeks off restored it completely Rahim 1998. Escalating the dose to chase a fading response moves you further up the prolactin and cortisol curves while the GH curve is already flat — the worst possible trade. The literature's own answer is a break, not a bigger vial.

Three: the cardiac action is real, GH-independent, and double-edged. Hexarelin binds CD36 in cardiomyocytes and coronary microvascular endothelium Bodart 2002 Demers 2004. In hypophysectomized rats that produced genuine protection against ischemia-reperfusion injury Locatelli 1999, and in humans a single 2 µg/kg intravenous dose raised ejection fraction even in people who released no GH Broglio 2001. But in the isolated heart, CD36 activation by hexarelin raised coronary perfusion pressure dose-dependently — constriction — and the authors linked CD36 explicitly to the coronary vasospasm of hypercholesterolemia and atherosclerosis Bodart 2002. Nobody has given hexarelin to a person with coronary disease and measured coronary flow. Anyone with known atherosclerosis is, on the published pharmacology, taking a drug with a specific and unstudied mechanism for constricting their coronary arteries.

The dose most people use is above the plateau. At 77% subcutaneous bioavailability Ghigo 1994, a 100 µg dose in an 80 kg person delivers roughly 0.96 µg/kg — twice the GH ED50. 200 µg is four to five times it. If the goal is growth hormone, the published pharmacology says the cheapest improvement available is to halve the dose, or to use the combination that Massoud 1996 showed produced 115 mU/L of GH with an 85% prolactin rise and no cortisol response at all at a hexarelin dose of 0.125 µg/kg alongside GHRH.

And the standing GH-axis cautions still apply — insulin resistance, fluid retention, carpal tunnel symptoms, and the general rule that an IGF-1 raised out of range for a prolonged period has never been shown to be safe. The distinguishing point for hexarelin is that in the one 16-week study, IGF-1 never rose at all Rahim 1998, so the user is exposed to the prolactin and cortisol cost without necessarily obtaining the anabolic signal.

Sources read for this page

• Ghigo E, Arvat E, Gianotti L. Growth hormone-releasing activity of hexarelin, a new synthetic hexapeptide, after intravenous, subcutaneous, intranasal, and oral administration in man.. J Clin Endocrinol Metab 1994 · PMID 8126144
• Massoud AF, Hindmarsh PC, Brook CG. Hexarelin-induced growth hormone, cortisol, and prolactin release: a dose-response study.. J Clin Endocrinol Metab 1996 · PMID 8954038
• Ghigo E, Arvat E, Gianotti L. Short-term administration of intranasal or oral Hexarelin, a synthetic hexapeptide, does not desensitize the growth hormone responsiveness in human aging.. Eur J Endocrinol 1996 · PMID 8921821
• Rahim A, O'Neill PA, Shalet SM. Growth hormone status during long-term hexarelin therapy.. J Clin Endocrinol Metab 1998 · PMID 9589671
• Rahim A, O'Neill PA, Shalet SM. The effect of chronic hexarelin administration on the pituitary-adrenal axis and prolactin.. Clin Endocrinol (Oxf) 1999 · PMID 10341859
• Laron Z, Frenkel J, Deghenghi R. Intranasal administration of the GHRP hexarelin accelerates growth in short children.. Clin Endocrinol (Oxf) 1995 · PMID 8548949
• Roumi M, Marleau S, du Souich P. Kinetics and disposition of hexarelin, a peptidic growth hormone secretagogue, in rats.. Drug Metab Dispos 2000 · PMID 10611139
• Bodart V, Febbraio M, Demers A. CD36 mediates the cardiovascular action of growth hormone-releasing peptides in the heart.. Circ Res 2002 · PMID 11988484
• Demers A, McNicoll N, Febbraio M. Identification of the growth hormone-releasing peptide binding site in CD36: a photoaffinity cross-linking study.. Biochem J 2004 · PMID 15176951
• Locatelli V, Rossoni G, Schweiger F. Growth hormone-independent cardioprotective effects of hexarelin in the rat.. Endocrinology 1999 · PMID 10465272
• Broglio F, Benso A, Valetto MR. Growth hormone-independent cardiotropic activities of growth hormone-releasing peptides in normal subjects, in patients with growth hormone deficiency, and in patients with idiopathic or ischemic dilated cardiomyopathy.. Endocrine 2001 · PMID 11322491
• National Center for Biotechnology Information. PubChem Compound Summary for CID 6918297, Hexarelin.. PubChem, retrieved 2026

Hexarelin — safety, predicted from mechanism

Hexarelin — interference & stacking

Bloodwork to run alongside Hexarelin

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Hexarelin — frequently asked questions

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