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Hexarelin

The most potent of the classical GH-releasing hexapeptides, with genuinely interesting cardioprotective activity through CD36, but also the fastest to desensitise its own receptor.

Also known as Examorelin, Hexarelin acetate, EP-23905, MF-6003

Human trials — Studied in people, typically early phase or small — promising rather than proven.

There is real human pharmacology data from the 1990s showing potent, dose-dependent GH release and from small cardiac studies showing improved left ventricular function. Development was discontinued, no phase 3 programme exists, and the cardioprotective claims that get repeated online rest largely on rodent ischaemia models.

How it works

Hexarelin is a 2-methyl-tryptophan analogue of GHRP-6 with substantially higher GHS-R1a potency, producing the largest single GH pulse of the classical GHRPs. It also binds CD36 in cardiomyocytes and vascular tissue, a GHS-R1a-independent action that underlies its documented cardioprotective effects in ischaemia-reperfusion models and its ability to improve left ventricular function independently of GH. The catch is rapid tachyphylaxis: GH responsiveness falls measurably within about two weeks of continuous daily dosing, more quickly than with any other compound in this class. It also raises cortisol and prolactin at higher doses, though less than GHRP-2 per unit of GH released at low doses.

Targets: GHS-R1a (ghrelin receptor), CD36 scavenger receptor, Pituitary somatotrophs, Cardiac tissue

Dosing

ProtocolDoseFrequencyRoute
Standard short-cycle protocolFasted, one dose at bedtime.100 mcg – 200 mcgonce or twice dailysubcutaneous
Cardiac-interest low-dose protocolAny consistent time.50 mcg – 100 mcgonce dailysubcutaneous
  • · 100 mcg is near the saturation dose. Two to three weeks maximum, then a break, because of tachyphylaxis.
  • · Based on the CD36 pathway rather than GH release; entirely extrapolated from animal work and small human cardiac studies.

Titration

None. Start at 100 mcg; higher doses buy cortisol, not growth hormone.

Cycling

Run two to three weeks, then take at least two to four weeks off. This is the one GHRP where continuous dosing reliably stops working, and pushing through with higher doses just adds cortisol and prolactin.

Work out your exact syringe units →

Pharmacology

Half-life
Roughly 55 minutes.
Onset
GH peaks 20 to 30 minutes post-injection. Desensitisation typically begins within 14 days of continuous use.
Routes
subcutaneous, intramuscular, intranasal
Molecule
Synthetic hexapeptide GHRP (GHS-R1a agonist)
Sequence length
6 amino acids
Molecular weight
887 Da

Handling

Diluent
Bacteriostatic water
Typical mix
2 mL
Vial sizes
2, 5 mg
Lyophilised
Refrigerate; freeze for long-term.
Reconstituted
Refrigerated, use within about 30 days.
Light sensitive
Yes — keep it out of the light

Intranasal — usable, with a caveat

Intranasal hexarelin has human pharmacokinetic data and produces a GH response at several times the subcutaneous dose. The route is real; what makes it a poor default is hexarelin's rapid desensitisation, which is dose-driven - and a route you cannot dose precisely is a bad match for a compound where overshooting costs you the response itself.

Mixing

A 5 mg vial in 2 mL gives 2500 mcg/mL; 4 units on a U-100 syringe is 100 mcg.

Side effects

  • very commonLoss of GH response over time— Tachyphylaxis within roughly two weeks of daily use - expected, not an adverse event as such.
  • commonIncreased hunger— Less than GHRP-6 but clearly present.
  • commonElevated cortisol and prolactin— Dose-dependent; the main reason it lost ground to ipamorelin.
  • commonWater retention
  • commonHead rush, flushing or transient sweating
  • uncommonLethargy or fatigue— Often attributed to the cortisol effect.
  • rareGynaecomastia-type symptoms from prolactin elevation— Reported anecdotally at high sustained doses.

Do not use if

  • Active malignancy.
  • Existing hyperprolactinaemia or a prolactinoma.
  • Poorly controlled diabetes.
  • Pregnancy and breastfeeding.

Combining it

  • synergycjc-1295-no-dac — Produces the largest acute GH pulse of any common pairing, at the cost of cortisol.
  • redundantipamorelin — Same receptor; no reason to run both.
  • cautionDopamine agonists such as cabergoline — Sometimes used to offset prolactin elevation, which says something about how often that elevation occurs.

What to monitor

  • · Prolactin and morning cortisol if running beyond two weeks or above 200 mcg per day.
  • · IGF-1 before and after a cycle to confirm the axis actually responded.
  • · Fasting glucose.

Legal status

Never approved for human use; sold as a research chemical. Prohibited in sport under WADA S2.

References

  • Imbimbo et al. 1994, GH-releasing activity of hexarelin in healthy volunteers (trial)
  • Studies of hexarelin binding to CD36 and cardioprotection in ischaemia-reperfusion models (preclinical)

Mechanism in depth

Hexarelin is GHRP-6 with one methyl group added to the position-2 tryptophan, and that single change roughly doubles GH-releasing potency while conferring enough protease resistance to make intranasal and even oral administration produce a measurable GH response. Imbimbo's 1994 dose-response study in healthy volunteers is the primary human characterisation and it is a proper dose-ranging study, which is more than most compounds in this class have. Where hexarelin diverges from the rest of the GHRP family is at two points. The first is the HPA axis. Korbonits showed in 1999 that hexarelin stimulates the hypothalamo-pituitary-adrenal axis specifically via arginine vasopressin - not via CRH, which Arvat's earlier work had already ruled out. That is a mechanistically specific finding and it explains why the cortisol elevation is real, dose-dependent and not avoidable by clever timing. It also explains the fatigue people report. The second divergence is CD36, a scavenger receptor expressed on cardiomyocytes, macrophages and vascular tissue that hexarelin binds independently of GHS-R1a. CD36 engagement is the proposed basis for the cardioprotective effects seen in rodent ischaemia-reperfusion models, and the effect is GH-independent - it persists in hypophysectomised animals. This is the most interesting pharmacology in the entire class and it is also the least translated: the human cardiac studies are small, old and mostly acute haemodynamic measurements rather than outcome trials. Tachyphylaxis is the practical governor. GHS-R1a desensitises through beta-arrestin recruitment and receptor internalisation, and hexarelin's high efficacy drives that faster than any other compound here - GH responsiveness falls measurably within about two weeks of daily dosing. Maccario's study of two or three daily subcutaneous injections found exactly this pattern of falling GH with sustained prolactin, ACTH and cortisol responses, which is the worst possible combination: the thing you want fades and the thing you do not want does not.

What usually goes wrong

Hexarelin is the compound where pushing through a plateau is actively counterproductive. GH responsiveness falls within about two weeks; the cortisol and prolactin responses do not. So the person who feels the effect fading at day fourteen and doubles the dose ends up with the full endocrine cost and none of the benefit, and if they keep going for a month they get lethargy, water retention, possibly nipple sensitivity, and a flat IGF-1. The second mistake is bedtime dosing. Everyone doses GH secretagogues at night by habit, but the polysomnography data shows hexarelin reduces slow-wave sleep while raising nocturnal cortisol - it is arguably the one compound in this class you should not take before bed. Third, the cardioprotective marketing is doing a lot of work that the evidence does not support. The CD36 mechanism is real and interesting; the human cardiac data is small, old and largely acute haemodynamic; and nobody has shown that a low-dose hexarelin protocol protects a human heart from anything. Buying it for that reason is buying a hypothesis. Fourth, the short-cycle requirement makes hexarelin a poor fit for the way most people actually use peptides, which is to start something and keep taking it.

Bloodwork worth running

MarkerWhenWhy it matters
ProlactinBaseline and at the end of a two-to-three-week block, particularly above 200 mcg per day.Hexarelin raises prolactin dose-dependently and, unlike the GH response, the prolactin response does not fade with repeated dosing. On a compound run in two-to-three-week blocks this is the marker that decides whether you can do it again.Act if: Prolactin above the reference range, or any nipple sensitivity or libido change, means stop rather than add cabergoline. Treating a side effect with a second drug is a signal the dose is wrong.
Morning cortisolBaseline (08:00 fasted) and at the end of a run if fatigue develops.The AVP-mediated HPA activation is specific to this compound and is the likely explanation for the lethargy people report on it.Act if: A morning cortisol above the reference range on hexarelin is a stop signal, not a dose-reduction signal - the tachyphylaxis means you are getting the cortisol without the GH by that point anyway.
IGF-1Baseline and at the end of each two-to-three-week block.The only way to know whether the GH response has already desensitised. On hexarelin this is not a routine efficacy check - it is a test of whether the compound is still doing anything at all.Act if: A flat or falling IGF-1 at the end of a block confirms tachyphylaxis. Do not respond by increasing the dose; take the break.
Fasting glucoseBaseline and end of a run.Class effect. Less of a concern than with continuous-exposure compounds because runs are short by necessity.Act if: Crossing 100 mg/dL is a reason to reconsider running further blocks.

Pharmacokinetics

Tmax
0.5 h
Crosses blood-brain barrier
partial
Metabolism
Peptidase hydrolysis. The 2-methyl-tryptophan at position 2 confers substantial protease resistance relative to GHRP-6, which is where its higher potency and longer duration come from.
Elimination
Proteolysis with renal handling of fragments.

Receptor targets

  • GHS-R1a (ghrelin receptor), pituitary somatotroph — Higher potency than GHRP-6; the largest single GH pulse of the classical GHRPs. No specific Ki resolved here.

    Gq/PLC signalling, calcium-driven GH exocytosis. Rapid beta-arrestin-mediated desensitisation with repeated dosing.

  • CD36 scavenger receptor, cardiomyocytes and vascular tissue — Binds CD36 independently of GHS-R1a; affinity not quantified in the sources resolved here

    GH-independent cardioprotection in ischaemia-reperfusion models, with interleukin-1 signalling implicated in at least one rat study. This is the most distinctive property of hexarelin and the least well translated to humans.

  • Hypothalamo-pituitary-adrenal axis, via arginine vasopressin — Not applicable

    ACTH and cortisol elevation, mediated by AVP rather than CRH. Dose-dependent and the main reason hexarelin lost ground to ipamorelin.

  • Prolactin release — Not applicable

    Dose-dependent prolactin elevation, sustained even as the GH response desensitises.

  • Slow-wave sleep architecture — Not applicable

    Frieboes et al. found hexarelin decreased slow-wave sleep while stimulating GH, ACTH, cortisol and prolactin secretion during sleep in healthy volunteers - which is the opposite of what people expect from a GH secretagogue and is a good reason not to dose it at bedtime.

Trials

  • Imbimbo et al., growth hormone-releasing activity of hexarelin in humans - a dose-response study 1 · 1994

    Dose-dependent GH release in healthy volunteers. The primary human dose-response characterisation of hexarelin and the source of the saturating-dose figure.

  • Ghigo et al., GH-releasing activity of hexarelin after intravenous, subcutaneous, intranasal and oral administration in man 1 · 1994

    Demonstrated GH release by all four routes including intranasal and oral, establishing hexarelin as unusually route-flexible for a hexapeptide.

  • Maccario et al., impact of two or three daily subcutaneous injections of hexarelin on 24-hour GH, prolactin, ACTH and cortisol secretion 1 · 2002

    Characterised what actually happens on a repeated-dosing schedule: the GH response attenuates while prolactin, ACTH and cortisol responses persist. This is the study that most directly justifies short cycling.

  • Frieboes et al., hexarelin effects on sleep architecture and nocturnal hormone secretion in healthy volunteers 1 · 2004

    Hexarelin decreased slow-wave sleep while increasing GH, ACTH, cortisol and prolactin secretion during sleep - directly contradicting the common assumption that GH secretagogues improve sleep depth.

What to expect, and when

GH begins rising within 10 to 15 minutes and peaks at 20 to 30 minutes after subcutaneous injection, with the pulse over within about two hours. Head rush, flushing and transient sweating are immediate. Hunger, milder than GHRP-6 but present, arrives within 20 minutes. Cortisol and prolactin elevations follow the GH pulse and persist for a few hours. The important timeline is the desensitisation one: GH responsiveness is measurably reduced by around day 14 of continuous daily dosing, which is why runs are two to three weeks with at least two to four weeks off. Any IGF-1 change from a single block is small and should be measured at the end of the block, not later.

Stacking and comparisons

Hexarelin plus a GHRH analogue produces the largest acute GH pulse available from any common pairing, and that is a real and reproducible finding - Giustina's work in type 1 diabetic men combined GHRH and hexarelin specifically to probe hypothalamic control. If you want maximum acute GH for a short block, this is the combination. What you are buying with it is cortisol and prolactin on top of an already dirty compound, so it is a two-to-three-week tool rather than a stack you live on. Combining hexarelin with any other GHS-R1a agonist - ipamorelin, GHRP-2, GHRP-6, MK-677 - is pointless competition at one receptor. The cabergoline pairing deserves a specific comment: it is common enough that vendors mention it, and the fact that a compound routinely needs a dopamine agonist to manage its prolactin response is information about the compound rather than a clever protocol. If you are reaching for cabergoline, the correct move is a lower dose or a different GHRP.

Against ipamorelin: hexarelin gives a substantially bigger acute pulse and a substantially dirtier endocrine profile, and it stops working in a fortnight. For anything you intend to run for months, ipamorelin wins on every axis except peak GH. Against GHRP-2: hexarelin is more potent and desensitises faster; GHRP-2 is the middle option, and it has an actual regulatory approval in Japan as a diagnostic. Against GHRP-6: same parent molecule with one methyl group, roughly double the potency, less hunger. Against MK-677: MK-677 raises 24-hour GH and IGF-1 far more effectively and can be run for months; hexarelin's only advantages are that it is injectable, short-acting and has the CD36 story. The honest summary is that hexarelin's unique selling point is not GH release at all - other compounds do that better and for longer - it is the CD36 cardiac pharmacology, and that pharmacology has not been demonstrated to do anything for a human.

Rough cost

$25–$70/month. Approximate grey-market pricing. A 5 mg vial typically runs 25 to 50 USD, and because runs are two to three weeks at 100 to 200 mcg a day, a single vial covers a whole block with plenty left over. Cost is not the limiting factor with this compound - tachyphylaxis is. Figures are observed and approximate.

Genuinely uncertain

  • The 55-minute half-life quoted in the Core record has no primary human source that this session could resolve.
  • No bioavailability, clearance or volume of distribution figures exist in the resolved literature, including for the intranasal route despite its documented activity.
  • The sequence His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2 is consistent with the confirmed molecular formula C47H58N12O6 and molecular weight 887.0 (PubChem CID 6918297) but was not independently resolved residue by residue, so it is flagged unverified.
  • The CD36 binding affinity and its relationship to GHS-R1a affinity were not quantified from any resolved source.
  • Whether the cardioprotective effect occurs in humans at any dose is unknown. The human cardiac studies are small and old, and the strong claims circulating online rest on rodent ischaemia-reperfusion models.
  • The exact time course of tachyphylaxis is described as roughly two weeks, but no study resolved here mapped the dose-response of desensitisation or how long a washout is needed to restore full responsiveness.
  • The 50 to 100 mcg 'cardiac-interest' protocol has no human basis at all and is extrapolated from animal dosing.

Papers