Hexarelin

Examorelin; GHRP-His-D-2-MeTrp-Ala-Trp-D-Phe-Lys-NH2; EP-23905

Checked Oct 28, 2026

The short answer

Early human data for raising growth hormone in healthy adults, the effect people are after

Grade C for raising growth hormone: small 1990s human studies show it raises GH, but the response fell about 45% over 16 weeks of twice-daily use and IGF-I did not change.

Approved?: Not approved for any use.
Safety: D, uncharacterized: Each dose raises ACTH and cortisol, the longest human study ran 16 weeks in small groups, and nothing is known about long-term use or tumor growth.

Do we take it? Our read

Here is the deal with hexarelin. It is probably the most potent GHRP you can actually buy, and the 1990s Italian group did real human pharmacology, which puts it ahead of most of this space. But the tachyphylaxis is brutal. GH response was down about 45% by week 16 in the desensitization study and already significantly lower at week 4, so anyone telling you to run it daily for months is burning their own receptors. What is funny is the cortisol spike per injection is the most documented thing about it, and yet the chronic-dosing study found it did not accumulate into sustained hypercortisolism. So the per-shot cortisol hit is real, the chronic pituitary damage people worry about apparently is not, based on what little data exists. The cardiac stuff is interesting but this needs randomized trials before you build a heart protocol around it.

The full answer: what it is for, the dose, the units

What people take it for: People take it to raise growth hormone, hoping for leaner body composition and faster recovery. It is not approved for any use.

Does it work for raising growth hormone in healthy adults, the effect people are after? C, early human data. Result: mixed.

Grade C for raising growth hormone: small 1990s human studies show it raises GH, but the response fell about 45% over 16 weeks of twice-daily use and IGF-I did not change. No human trial tested body composition or recovery.

No approval for any use.

Safety: D, uncharacterized. Each dose raises ACTH and cortisol, the longest human study ran 16 weeks in small groups, and nothing is known about long-term use or tumor growth.

Do not use if: Active malignancy (GHS-R1a expressed in some cancers).

Could it be placebo? No controlled trial tested body composition or recovery, so a placebo effect cannot be ruled out for those outcomes; the acute GH rise itself is a measured blood result.

The dose people use, and the units to draw

No verified dose statement found for use outside research; human trials gave single doses of 1 to 2 mcg/kg IV and 1.5 to 3 mcg/kg under the skin, and one trial gave 1.5 mcg/kg twice daily for 16 weeks.

Source	Dose	How often and how	Who it was for	Link
Ghigo et al., J Clin Endocrinol Metab 1994	1 and 2 mcg/kg IV; 1.5 and 3 mcg/kg SC; 20 mcg/kg intranasal; 20 and 40 mg oral	Single doses, compared with IV saline and IV GHRH 1 mcg/kg; GH response measured as area under the curve	12 healthy young volunteers	Abstract: doses and routes; SC response dose-dependent, estimated SC bioavailability about 77%, oral about 0.3%
Rahim, O'Neill and Shalet, J Clin Endocrinol Metab 1998	1.5 mcg/kg	SC twice daily for 16 weeks, GH response retested at week 20 after 4 weeks off; no placebo arm mentioned in the abstract	Adults including older adults; sample size not stated in the abstract (the companion report of the same schedule, PMID 10990150, lists 12 healthy elderly people)	Abstract: GH AUC 19.1 at baseline, 10.5 at week 16, 19.4 at week 20; IGF-I and IGFBP-3 unchanged
Rahim, O'Neill and Shalet, Clin Endocrinol 1999	1.5 mcg/kg	SC twice daily for 16 weeks; cortisol also measured 4 weeks after stopping; no placebo arm mentioned in the abstract	Adults; number not stated in the abstract	Abstract: cortisol AUC 1506 at baseline, 1222 at week 16; prolactin AUC unchanged
Arvat et al., Neuroendocrinology 1997	2.0 mcg/kg	Single IV dose, alone and with human CRH 2.0 mcg/kg IV and/or vasopressin 0.17 U/kg IM	7 healthy young volunteers	Abstract: methods and results
Broglio et al., Endocrine 2001	2.0 mcg/kg	Single IV dose; ejection fraction measured every 15 minutes for up to 60 minutes	7 normal adults, 7 adults with severe GH deficiency, 12 adults with severe dilated cardiomyopathy	Abstract: design and results
Huberman Lab with Dr. Craig Koniver (Oct 7, 2024)	No dose from a non-seller source	Hexarelin is discussed in the growth-hormone secretagogue dosing chapter; the only figure given is the guest's own prescribing dose, which is not used	Podcast discussion	Chapter 01:19:32 (Hexarelin; Growth Hormone Secretagogues Dosing); auto-transcript segment near 4843 s, verify by ear. The guest runs a clinic that sells peptide therapies, so his stated dose is excluded

Human trials gave single doses from 1 mcg/kg IV (Ghigo 1994) to 3 mcg/kg SC (Ghigo 1994), and the one chronic trial gave 1.5 mcg/kg SC twice daily for 16 weeks (Rahim 1998).

No label, Dr. Abud Bakri episode, Examine page or Attia statement giving a hexarelin dose was found. The Huberman Lab episode with Dr. Koniver gives a prescribing dose, but he runs a clinic that sells peptide therapies, so it is excluded. The earlier per-injection range and on-off cycling had no named non-seller source and are removed.

Reported by the named source, never prescribed by us.

How many units do I draw?

Use the calculator: units on the syringe equal the dose in mcg divided by the mcg per unit of your mixed vial (mg per mL times 10 gives mcg per unit on a U-100 syringe). Open the dose calculator

Why it might work

Subcutaneous injection
Hexarelin (a synthetic hexapeptide
High-potency GHS-R1a activation
Hexarelin binds the GHS-R1a receptor w
GH and cortisol/prolactin co-release
As with GHRP-2
Rapid tachyphylaxis
Hexarelin's GH-releasing effect dimini
Assumed cardioprotective and downstream anabolic effects
CD36 binding on cardiomyocytes and end

Assumed pathway, not shown in people.

Assumed (largely confirmed in animal/cell models, partially confirmed in humans): Hexarelin binds GHS-R1a (the ghrelin receptor) at both pituitary somatotrophs and hypothalamic GHRH neurons, triggering pulsatile GH release via IP3/DAG signaling. It also binds a second, as-yet-incompletely-characterized receptor in cardiac tissue (possibly CD36 or adenosine A2 receptor) that mediates GH-independent cardioprotective effects. The dual receptor profile is better established mechanistically in rodents than in humans.

The trials, claim by claim

More actual human data than almost any grey-market GHRP, small 1990s studies showing it demonstrably raises GH, but the response halves within a few weeks of daily dosing.
The GH-independent cardioprotection angle is real in rodents and has two small human signals, but the studies were acute IV challenges with no placebo arm and n=5 in the most-cited one.
The catch: hexarelin hits cortisol and ACTH alongside GH at every dose, and the GH response fades with repeated use.

Hexarelin robustly raises GH levels in healthy adults

Result: worked

Multiple small human studies (1994-2001) consistently show significant IV or SC hexarelin raises serum GH above GHRH-alone in healthy volunteers, GH-deficient patients, and acromegalic patients. Effect is dose-dependent and replicated across labs.

Ghigo et al., JCEM 1994, GH-releasing activity of hexarelin after IV, SC, intranasal and oral administration (PMID 8126144)

GH response desensitizes substantially within weeks of daily dosing

PMID 10990150 directly examined desensitization and found partial but real attenuation. PMID 10341859 (Rahim et al. 1999, 16 weeks, twice-daily SC dosing) specifically examined chronic HPA and prolactin burden: it found NO significant progressive prolactin elevation over 16 weeks and concluded over-stimulation of the pituitary-adrenal axis and prolactin secretion do not occur at the studied dosing regimen. The acute per-injection cortisol/ACTH rise is real and well-documented, but the Rahim chronic study found ACTH/cortisol AUC decreased during the study period, not persisted. Pattern of GH desensitization is consistent across labs.

Does desensitization to hexarelin occur? PubMed 10990150

Hexarelin has acute GH-independent cardioprotective effects in ischemic cardiomyopathy but not dilated cardiomyopathy in humans

Result: mixed

Imazio et al. 2002 (EJHF, PMID 11959048) found LVEF improved in ischemic cardiomyopathy patients (n=5, peak LVEF 26.2+/-2.5%, p<0.05) but NOT in dilated cardiomyopathy patients (n=8, LVEF unchanged, p=NS) after acute IV hexarelin. GH rose similarly in both groups. This was an acute IV challenge, not a treatment study, and it lacked a randomized placebo arm. The n=5 for ischemic CM is too small to draw firm conclusions. Moretti et al. 2001 (PMID 11322491) reported small measurable ejection fraction changes in GH-deficient subjects. Sample sizes across all cardiac studies are very small and findings should be considered preliminary.

Imazio et al. 2002, European Journal of Heart Failure, PMID 11959048

Hexarelin raises cortisol and ACTH alongside GH at standard acute doses

PMID 9430449 (Arvat et al., Neuroendocrinology 1997) tested whether hexarelin's ACTH/cortisol-releasing effect operates via CRH or vasopressin. Its title and conclusion are explicitly 'hexarelin shows NO INTERACTION with corticotropin-releasing hormone and vasopressin on ACTH and cortisol secretion in humans.' The study confirms hexarelin does raise ACTH and cortisol acutely, but shows this occurs via a CRH/AVP-independent pathway, not by synergizing with the classical axis mediators. PMID 10341859 (Rahim et al. 1999) established that while the acute per-injection ACTH/cortisol rise is real, chronic twice-daily SC dosing over 16 weeks did NOT produce progressive sustained HPA axis overstimulation. The acute cortisol co-elevation is a class effect of potent GHRPs, strongest with hexarelin, but it does not translate to chronic hypercortisolism at studied doses.

Arvat et al. 1997, Neuroendocrinology, PubMed 9430449

Hexarelin improves cardiac function and reduces fibrosis in rodent myocardial infarction models

Result: not tested in humans

Multiple rodent studies (PMID 10614623, PMC5949285, PMC7018219) consistently show improved ejection fraction and reduced fibrosis post-MI. Animal data is internally consistent and mechanistically plausible via GHS-R1a and adenosine A2 receptor pathways. Does not establish human efficacy.

Hexarelin preserves myocardial function in mouse MI model, PMC5949285

Risks and the label warnings

Adverse events

Consistent acute cortisol and ACTH elevation at each GH-releasing dose. Acute prolactin rise per injection is documented in short-term studies. Importantly, PMID 10341859 (Rahim et al. 1999, 16 weeks, twice-daily SC dosing) found NO significant progressive prolactin elevation over the study period and concluded that over-stimulation of the pituitary-adrenal axis and prolactin secretion do not occur with chronic dosing at the studied regimen. Water retention and fatigue reported by users. Tachyphylaxis: in a 16-week trial of 12 healthy older adults on twice-daily injections the GH response was significantly lower by week 4 and about 45% lower by week 16, and it recovered 4 weeks after stopping (PMID 9589671). No serious adverse events documented in controlled studies, but sample sizes are all under 30 and maximum study duration was 16 weeks.

Contraindications

Active malignancy (GHS-R1a expressed in some cancers). Active acromegaly. Pregnancy and lactation (no data). Prolactin-sensitive conditions (prolactinoma, prolactin-driven breast cancer history). Co-administration with other GHRPs compounds cortisol/prolactin burden.

Theoretical concerns

Sustained prolactin elevation carries gynecomastia risk in men and menstrual irregularity risk in women. Chronic cortisol co-elevation is metabolically counterproductive when the goal is body composition. GHS-R1a is expressed in tumor tissue; unknown whether chronic stimulation promotes proliferation. No carcinogenicity studies in humans.

What nobody knows yet

No long-term human safety data exists beyond ~6 months. Oral bioavailability in humans is not established from RCT data. Interaction with GLP-1 receptor agonists (now widely used) has not been studied. Compounding purity and dose accuracy from grey-market sources is unverified.

What else could explain the result

Hexarelin is almost always stacked with GHRH analogs (CJC-1295, sermorelin) or other GHRPs (ipamorelin), making solo attribution impossible. Many users are also on TRT, which independently improves body composition and recovery. GLP-1 agonists (tirzepatide, semaglutide) now common in the same user cohort and produce dramatic fat loss attributable to the GLP-1 drug, not the peptide. Resistance training and caloric protocols are strong confounders for any body-composition claim.

Is the vial what it says?

Cross-checked against the cited sources below. The grade reflects the absence of formal human safety and efficacy data. Hexarelin raises ACTH and cortisol through a CRH/AVP-independent pathway (Arvat et al., PMID 9430449: no interaction with CRH and vasopressin), not by synergizing with the classical axis. In chronic dosing (Rahim et al., PMID 10341859) there was no significant progressive prolactin elevation, and ACTH/cortisol AUC decreased. The Imazio 2002 cardiac study was an acute IV challenge without a randomized placebo arm, not a controlled treatment study.

Half-life and storage

Half-life: 55-70 minutes (subcutaneous). Substantially longer than GHRP-6 due to D-amino acid substitutions that resist proteolytic degradation.

Once mixed: Moderate. Lyophilized powder reconstituted with bacteriostatic water (BAC water). Stable refrigerated for approximately 4 weeks post-reconstitution. Light and heat sensitive; avoid freeze-thaw cycles. Standard GHRP reconstitution rules apply.

What I noticed, and what people report

What people report

Volume of reports: mixed. Reports exist but contradict each other.

Moderate. Hexarelin has a real user community on peptide forums (r/Peptides, evolutionary.org), smaller than ipamorelin but more than obscure compounds. Discussed specifically for GH pulse strength.

Low-moderate. GH pulse strength gets consistent reports. Body composition results are inconsistent and highly confounded. Cardiac benefits are rarely the user motivation and not well tracked.

Low. Most reports come from grey-market users stacking multiple compounds with no controls. The few who try hexarelin solo consistently note strong but short-lived GH flushing and fatigue, which aligns with the cortisol co-elevation seen in studies.

Anecdote: strong warmth and flushing within 10-20 minutes of injection, described as noticeably more intense than ipamorelin at equivalent doses.
Anecdote: fatigue and hunger spike within 30-60 minutes post-injection, consistent with the cortisol and ghrelin-pathway activation documented in studies.
Anecdote: GH-related effects (morning pump, sleep quality improvement, finger tingling) reportedly fade within weeks.
Anecdote: some users report better acute response when combining with a GHRH analog (CJC-1295), consistent with the synergistic pituitary mechanism, though this muddies attribution entirely.

Reports are anecdote, not proof.

Can you tell if it is working?

Partly trackable

No non-blood readout is validated for hexarelin; the only defensible objective signal is a brief early-window blood IGF-1 rise that fades within weeks as the GH response desensitizes.

Bloodwork

Partly measurableConfidence: Weak

A lab moves, but it's noisy, indirect, or off-target, treat it as a hint, not proof.

Hexarelin is a GHS-R1a (ghrelin-receptor) agonist that triggers ACUTE pituitary GH pulses, and GH drives hepatic IGF-1, so serum IGF-1 (a standard LabCorp/Quest test) is the theoretically correct routine readout of GH-axis activity. BUT hexarelin desensitizes within days-to-weeks, and the best human chronic-dosing study found IGF-1 did NOT change significantly, so in real-world use it often will NOT show up durably in routine bloodwork.

IGF-1IGF-1 serum (standalone LabCorp/Quest order)

An early within-person rise above the personal baseline is suggestive of acute GH action. Critically, a FLAT IGF-1 is the common and expected result: the definitive human study (Rahim & Shalet, 20 weeks) found no significant IGF-1 change, so absence of movement does NOT indicate an inactive or bad product. Interpret asymmetrically, a rise can confirm acute action, a flat value refutes nothing.

IGF-1 is the standard integrated readout of GH-axis activity, but hexarelin's rapid tachyphylaxis blunts any sustained elevation, making it a noisy and unreliable efficacy proxy for this specific compound rather than a clean confirmatory marker.

Draw baseline

Before first dose, a single fasting morning IGF-1 draw to establish the personal baseline.

Retest

3-4 weeks, drawn on the early side. Any transient IGF-1 rise fades as GHS-receptor desensitization sets in within days-to-weeks; human data show IGF-1 is commonly flat by later weeks, so an early retest is the only realistic window to catch a signal.

Read this before you spend on labs

Honest caveat: the best available human evidence (Rahim & Shalet, JCEM 1998, PMID 9589671; 16-20 week twice-daily dosing) found serum IGF-1 and IGFBP-3 did NOT change significantly, and the authors concluded the biological impact on the GH-IGF-I axis was "minimal," driven by rapid, partial, reversible desensitization of the GH response. So IGF-1 cannot be treated as a reliable confirmation for hexarelin, a rise is weakly suggestive of acute action, but a flat result is the expected outcome and does not mean the peptide is inactive or the product bad. Separately, hexarelin acutely spikes cortisol, ACTH, and prolactin per injection; those are off-target effects, not efficacy readouts, and must not be used to "verify" the peptide is working.

Bottom line

Hexarelin has no validated objective efficacy readout in humans, and no consumer wearable or standard scan can prove it is "working." Blood IGF-1 is only a short early-window signal because the GH response undergoes rapid tachyphylaxis (chronic IGF-1/IGFBP-3 run flat), which is why blood is partial, not direct. Wearable deep-sleep was removed: the supporting evidence is ghrelin/GHRH-class and contested, there is no hexarelin-specific human data, and consumer wearables cannot reliably measure true slow-wave sleep. DEXA lean/fat mass was removed: no human body-composition data exists for hexarelin, the anabolic driver is not sustained due to desensitization, and any change is fully confounded by training, diet, TRT, or GLP-1 use. Cortisol, ACTH, and prolactin move with each injection but are off-target pituitary-adrenal effects, not efficacy. The cardiac/LVEF signal is preliminary, uncontrolled, and only in ischemic-cardiomyopathy patients, so a healthy user cannot track it as proof. Treat any signal as suggestive at best, never confirmation.

Logging baseline vs retest is the whole game. The Truth Tracker is our free log for bloodwork, DEXA, genetics, and wearable data, bring your own numbers.

How to track it

History

First documented human use: 1994, Ghigo et al., University of Turin. Acute IV/SC dosing in healthy men; GH-releasing activity confirmed in the first controlled human pharmacology paper (Journal of Clinical Endocrinology and Metabolism, 1994).

1993Romano Deghenghi and colleagues at Europeptides (Milan) synthesize hexarelin as a potency-optimized GHRP-6 analog. Structure: His-D-2-MeTrp-Ala-Trp-D-Phe-Lys-NH2.
1994First human pharmacology published by Ghigo, Arvat, Deghenghi et al. (Turin group) in the Journal of Clinical Endocrinology and Metabolism, confirming robust GH secretion in healthy men.
1999-2002Italian research groups publish small human cardiac studies showing GH-independent effects on LVEF in ischemic cardiomyopathy, generating brief interest in hexarelin as a cardioprotective agent.
2005-presentNo pharmaceutical sponsor advances hexarelin to Phase 3. Compound remains research-only; ghrelin itself and synthetic ghrelin analogs absorb most cardiovascular research focus. Hexarelin enters grey-market peptide trade as a research chemical.

All sources

Ghigo et al., JCEM 1994, first human pharmacology (IV, SC, intranasal and oral routes), PMID 8126144(Establishes that hexarelin raises GH in healthy men; foundational human paper by the Turin group.)
Imazio et al. 2002, cardiac study, European Journal of Heart Failure, PMID 11959048(Human cardiac study with the fewest design controls: acute IV challenge only, not a treatment study, no randomized placebo arm. Small n (n=5 ischemic CM, n=8 dilated CM). LVEF improved in ischemic CM patients (p<0.05) but was unchanged in dilated CM (p=NS). Cited as the primary human cardiac evidence but its acute, uncontrolled design limits conclusions substantially.)
Does desensitization to hexarelin occur? PubMed 10990150(Directly addresses tachyphylaxis question in humans. Confirms partial reversible attenuation.)
Chronic hexarelin and pituitary-adrenal axis, PubMed 10341859(Rahim et al. 1999. 16-week twice-daily SC hexarelin (1.5 mcg/kg). Key safety-relevant finding: the study found NO significant progressive prolactin elevation and concluded over-stimulation of the pituitary-adrenal axis and prolactin secretion do NOT occur at this chronic dosing regimen. ACTH/cortisol AUC decreased during the study period. Acute per-injection responses are real, but this chronic study found they do not accumulate into sustained hyperprolactinemia or hypercortisolemia.)
Ghigo E et al. Growth hormone-releasing activity of hexarelin, a new synthetic hexapeptide, after intravenous, subcutaneous, intranasal, and oral administration in man. J Clin Endocrinol Metab 1994;78:693-8. PMID 8126144(dose table)
Rahim A, O'Neill PA, Shalet SM. Growth hormone status during long-term hexarelin therapy. J Clin Endocrinol Metab 1998;83:1644-9. PMID 9589671(dose table)
Rahim A, O'Neill PA, Shalet SM. The effect of chronic hexarelin administration on the pituitary-adrenal axis and prolactin. Clin Endocrinol (Oxf) 1999;50:77-84. PMID 10341859(dose table)
Arvat E et al. Hexarelin, a synthetic growth-hormone releasing peptide, shows no interaction with corticotropin-releasing hormone and vasopressin on adrenocorticotropin and cortisol secretion in humans. Neuroendocrinology 1997;66:432-8. PMID 9430449(dose table)
Broglio F et al. 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;14:105-8. PMID 11322491(dose table)
Huberman Lab, Dr. Craig Koniver: Peptide and Hormone Therapies for Health, Performance and Longevity, Oct 7, 2024(dose table)

Not medical advice. Grades reflect the evidence as of the date above and will change as data arrives. Reports from users are anecdote, not proof. Talk to a licensed clinician before you act on anything here.