Hexarelin: the complete research guide.

Hexarelin is a six-amino-acid growth hormone secretagogue, the most potent of the older GHRPs, with preclinical signals across heart, kidney and inflammation. Its evidence stops at rodents. It also has a documented limit: tachyphylaxis, meaning the response fades with repeated dosing, which is why the field moved to ipamorelin.

What is hexarelin?

Hexarelin is a synthetic peptide with six amino acids. The sequence is His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH₂. Three of those amino acids are D-stereoisomers, meaning mirror-image versions that resist normal enzyme breakdown. This structural feature contributes to greater metabolic stability relative to natural ghrelin.

Hexarelin belongs to the family called growth hormone-releasing peptides (GHRPs). It came in the second wave of this class, after GHRP-2 and GHRP-6. In head-to-head dose-response studies, hexarelin produced a higher peak GH response per unit dose than either older GHRP. That profile made it briefly attractive in the 1990s as a candidate for short-stature diagnostics and therapy.

The drug development never materialized. Hexarelin stalled at Phase II in every indication, and academic interest shifted to effects that don't run through the growth hormone pathway at all.

Specifically, hexarelin binds CD36, a scavenger receptor involved in cardiovascular biology, immune signaling and lipid metabolism. That gives hexarelin a research story no other GHRP has: heart protection that doesn't depend on GH. We'd argue it's what drove most of the 2020–2026 literature.

One academic site dominates the field: the University of Milano-Bicocca, and specifically the Meanti, Rizzi, Bresciani and Locatelli group. They've published on hexarelin in neuroprotection, cardiology and pulmonology since the 2010s, and they're still the most productive program on the molecule in 2026.

How it works.

The GH pathway: binding the ghrelin receptor.

Hexarelin's classical mechanism is binding GHS-R1a, the ghrelin receptor. It sits on somatotrophs, the GH-producing cells in the anterior pituitary, and binding triggers a calcium signaling cascade that releases GH in a pulse.

The D-amino acid substitutions in the sequence confer metabolic stability. Natural ghrelin is degraded by enzymes within minutes; hexarelin's modifications extend circulating half-life sufficiently to evoke a measurable GH spike in pharmacological studies. The GH response has been reproduced across multiple published protocols.

The cardiovascular side door: CD36 binding.

Here's the part that makes hexarelin scientifically interesting. It also binds CD36, a scavenger receptor on immune cells, platelets, small blood vessels, and heart muscle cells. CD36 has multiple jobs: fatty-acid uptake, clearing oxidized LDL, thrombospondin-1 signaling, immune recognition.

GHRP-6 also binds CD36. Ipamorelin doesn't. The CD36 pathway is what gives hexarelin cardiovascular effects independent of GH release.

Take CD36 binding away and the cardioprotection story mostly disappears. That fits: ipamorelin, the cleaner GHRP, has no cardioprotective preclinical literature at all.

Survival signaling.

A 2021 study in mouse nerve-cell cultures by Meanti and colleagues found hexarelin blocked cell death caused by hydrogen peroxide, shifting cells toward survival.

The 2023 kidney-injury work from Guan and colleagues shows the same pattern. Hexarelin lowered death-signaling proteins and raised survival-signaling ones.

Anti-inflammation.

A 2021 mouse aortic aneurysm study from Jiang and colleagues showed hexarelin suppressed inflammatory signaling and shut down the NLRP3 inflammasome, a cellular alarm complex. Aortic wall integrity held.

That NLRP3 effect ties hexarelin's heart, kidney and lung findings together. The same alarm complex fires in atherosclerosis, kidney injury and lung injury, so suppressing it in any of them fits the pattern we keep seeing.

Autonomic balance.

A 2020 mouse heart-attack study by McDonald and colleagues showed hexarelin shifted autonomic balance toward the parasympathetic, rest-and-digest side. It also dropped inflammation markers and reduced interstitial collagen.

That parasympathetic shift lines up with older clinical pharmacology reports on heart-rate variability. It's a second candidate mechanism for cardioprotection, one that doesn't need CD36 at all.

Preclinical dosing summary.

We list the dose ranges below straight from the published preclinical literature, as context for reading the cited studies. No human therapeutic dose has ever been established or approved. Hexarelin is a research-use-only reference compound.

• Rodent injury models (subcutaneous): Published protocols report 0.1–0.3 mg/kg/day over 7–21 days. The 2020 McDonald cardiac study used 0.3 mg/kg/day for 21 days; the 2023 Guan kidney study used 0.1 mg/kg/day for 7 days prior to injury induction.
• Acute lung injury model (intraperitoneal): The 2021 Zambelli ARDS study administered 320 µg/kg as a single intraperitoneal dose pre- or post-injury.
• Historical pharmacology studies: Early-phase human pharmacology work examined single-bolus GH-stimulation protocols. The GH response was documented as non-linear, and tachyphylaxis was observed with repeated administration over days to weeks.

Administration routes studied.

Subcutaneous (preclinical standard route).

Subcutaneous delivery is the predominant route used across the published preclinical literature. Pharmacokinetic studies document that serum GH rises within 15–30 minutes of administration, with peak concentrations measured at 30–60 minutes in these models.

Intraperitoneal (rodent models).

Several rodent studies used intraperitoneal delivery, including the 2021 Zambelli ARDS study. This route is specific to the rodent model context and is not translatable to human research applications.

Oral route: bioavailability studies.

Hexarelin has very low oral bioavailability. Several 2020–2023 studies tried permeation enhancers to improve intestinal absorption, including work by Dahlgren and colleagues. None produced a viable oral formulation, and sublingual and nasal routes have fared little better.

Observed pharmacodynamic timeline (preclinical models).

• Minutes 15–60: Published pharmacokinetic studies report measurable serum GH elevation following a single dose, with peak concentrations at 30–60 min.
• Hours 2–6: GH returns toward baseline in preclinical pharmacology data. Any cortisol and prolactin elevations follow a similar time course.
• Days 1–7 (in vivo injury models): Protective biomarker changes — including reductions in TGF-β1 and NLRP3 activation and elevated Bcl-2/Bax ratios — were reported within the first dosing week in published rodent studies.
• Weeks 1–3 (in vivo models): Structural endpoints (preserved cardiac function, attenuated aneurysm progression, preserved kidney function) became measurable over this window in the cited studies. Tachyphylaxis also emerges in this window in GH-response pharmacology data, with documented attenuation of the GH signal under repeated dosing.
• Beyond 3 weeks: Receptor desensitization is well-documented as the primary pharmacological ceiling for sustained hexarelin administration in the published literature.

Research evidence.

Hexarelin's 2020–2026 preclinical literature is unusually diverse for a compound with no clinical translation. The 7 indications below are ordered by mechanistic strength, from the strongest preclinical signal to the weakest.

• Cardioprotection (myocardial ischemia-reperfusion model): A 2020 mouse study reported improved left-ventricular function, reduced collagen deposition, decreased TGF-β1 expression, and less myofibroblast differentiation following hexarelin treatment (McDonald et al., 2020).
• Abdominal aortic aneurysm (elastase model): A 2021 mouse study reported smaller aortic diameter, improved elastin integrity, preservation of smooth muscle cell contractile phenotype, and NLRP3 suppression (Jiang et al., 2021).
• Acute kidney injury (ischemia-reperfusion): A 2023 rat study found that pre-treatment preserved kidney function, reduced apoptotic cell death, and downregulated the MDM2/p53 pathway (Guan et al., 2023).
• ALS / neurodegeneration: A 2023 cell-line study using SOD1-G93A SH-SY5Y cells (an ALS model) reported reduced hydrogen peroxide cytotoxicity mediated through apoptosis-regulatory and survival pathways (Meanti et al., 2023).
• Acute lung injury / ARDS: A 2021 mouse model study reported improved lung compliance, reduced neutrophil recruitment, and less pulmonary collagen at 14 days (Zambelli et al., 2021).
• Obesity / metabolic phenotype: A 2021 MC4R-KO mouse study reported increased pulsatile GH, elevated lipolysis, lower hepatic lipid production, reduced visceral adiposity, and improved insulin sensitivity (Huang et al., 2021).
• Morphine tolerance (rodent model): A 2020 rat study reported that hexarelin co-administered with morphine attenuated analgesic tolerance in the study model (Baser et al., 2020).

The translational gap is the story. Across the 2020–2026 window there are zero published Phase II or Phase III randomized controlled trials in humans, for any indication.

Older pre-2020 cardiovascular studies looked at hexarelin's acute GH and blood-pressure effects in small human cohorts. None produced an outcome signal strong enough to justify a pivotal trial.

That leaves 35+ preclinical papers and zero human RCTs. We can't think of another GH-axis compound with a wider gap between the two.

Hexarelin (roadmap)

Hexapeptide 6 aa GHS-R1a / CD36

Peptriva does not currently stock hexarelin. The catalog focuses on the GH-axis peptides with the cleanest pharmacodynamic profile and the strongest research signal — CJC-1295 (no DAC) on the GHRH-receptor side, and ipamorelin as the selective GHS-R1a agonist without the cortisol, prolactin, or tolerance buildup profile that limits hexarelin. See the catalog for the stocked GH-axis options.

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Co-administration literature.

Hexarelin turns up rarely in modern multi-compound protocols. Ipamorelin displaced it in repeat-dosing study designs. The combinations below come from pharmacology literature, not from controlled trial data.

• Hexarelin + GHRH analog (CJC-1295 or sermorelin): The literature rationale for this combination involves synergistic GH release through simultaneous stimulation of both the GHRH receptor and the GHS-R1a receptor on the somatotropic axis. Studies have examined whether peak GH responses exceed those of either compound alone. The contemporary literature has investigated the analogous CJC-1295 + ipamorelin combination, which offers a similar mechanistic rationale without the cortisol, prolactin, or tachyphylaxis profile associated with hexarelin.
• Hexarelin monotherapy cycling protocols: The pharmacology literature has noted that receptor desensitization under sustained dosing limits the utility of continuous hexarelin administration. Interrupted dosing schedules have been discussed in the research context; however, no controlled study has validated a specific cycling protocol for hexarelin.

For sustained GH-axis stimulation research, the literature points at the CJC-1295 and ipamorelin combination as the current field standard.

CJC-1295 no DAC activates the GHRH receptor. Ipamorelin selectively activates GHS-R1a, without the cortisol, prolactin or rapid desensitization documented for hexarelin.

Side effects.

Commonly reported in the pharmacology literature.

• Transient cortisol elevation at GH-stimulating doses. Published comparisons report lower cortisol elevation than GHRP-6 and higher than ipamorelin.
• Transient prolactin elevation, with a similar comparative dose-response profile.
• Injection-site reactions (redness, brief discomfort) in subcutaneous administration studies.
• Mild flushing or warmth, particularly at higher dose levels examined in pharmacology studies.

Less commonly reported.

• Headache.
• Mild appetite increase. Less pronounced than GHRP-6, which demonstrates the strongest appetite-driving effect in the class via the ghrelin pathway.
• Transient changes in heart-rate variability, consistent with the autonomic-rebalancing effects documented in animal models.

Rare, serious, or theoretical.

• Long-term cardiac effects with chronic dosing. Older clinical-pharmacology literature reported positive inotropic effects that raised long-term safety questions. No long-term human safety dataset exists to resolve this.
• Receptor downregulation / tolerance buildup. The GH response attenuates with repeat dosing. This is the dominant pharmacological limit documented in the literature.
• Unknown effects on the broader CD36 axis. CD36 has documented roles in lipid uptake, immune signaling, and platelet function. Sustained agonism of this scavenger receptor lacks a long-term human safety dataset.

Legal status.

You can buy hexarelin in the US as a research reference compound. It's not FDA-approved for any indication, and it's not EMA-approved either.

No completed Phase III trial exists, and no pivotal trial was enrolling as of May 2026. It sells legally labeled for laboratory use only. Marketing it as a therapeutic, or with human dosing instructions, draws FDA enforcement against the supplier.

The DEA doesn't schedule hexarelin. It's not a controlled substance.

Sports and WADA.

Hexarelin is on the WADA 2026 Prohibited List under section S2, which covers peptide hormones, growth factors, related substances and mimetics.

It's classified as a growth hormone secretagogue. The S2 category names GH-releasing peptides explicitly, and hexarelin sits there alongside GHRP-2, GHRP-6, ipamorelin, ibutamoren and tabimorelin.

Prohibition window: in-competition and out-of-competition for all athletes governed by WADA-compliant sports bodies.

Detection: reliable in athlete urine with modern LC-MS/MS assays. The window for the parent peptide is short, a matter of hours. Metabolite tracking and the biological-passport approach, which monitors IGF-1 and bone markers over time, stretch the practical window well past that.

Hexarelin vs. the rest of the GHRP class.

The published literature frequently positions hexarelin relative to the broader GHRP class. The comparative profiles below are summarized from pharmacology studies and published head-to-head data.

• vs. GHRP-2: Hexarelin has higher GH-release potency. Both elevate cortisol and prolactin transiently. Hexarelin's elevations are reported as similar or slightly lower than GHRP-2 at equipotent GH doses. GHRP-2 has a Japan diagnostic-use approval (KP-102, short-stature testing). Hexarelin has no comparable regulatory pathway.
• vs. GHRP-6: Hexarelin has higher GH potency and lower appetite-driving effect. GHRP-6 is the strongest ghrelin-pathway appetite stimulator in the class. GHRP-6 also elevates cortisol and prolactin more than hexarelin.
• vs. ipamorelin: Ipamorelin is the selective option in the class. Studies report similar GH-release potency to GHRP-2 with minimal cortisol, prolactin, or appetite effects and no notable tolerance buildup at research-protocol doses. This selectivity profile is the basis for ipamorelin becoming the field-standard pairing for CJC-1295 in modern research.
• vs. tesamorelin (the only FDA-approved GH-axis peptide): Tesamorelin is a GHRH analog (different receptor, different mechanism), FDA-approved for HIV-associated lipodystrophy. Two pivotal Phase III RCTs (n=410, n=404) support the approval. Hexarelin has zero comparable evidence in any indication.

CJC-1295 + Ipamorelin (in stock)

5 mg ≥99% pure Lyophilized

The modern GH-axis combination studied in the published literature is CJC-1295 (no DAC) + ipamorelin — GHRH-receptor activation paired with selective GHS-R1a agonism, without the cortisol, prolactin, or rapid desensitization characteristics documented for hexarelin. third-party tested reference compound; COA available per lot.

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Frequently asked questions

What is hexarelin?

Hexarelin is a synthetic six-amino-acid peptide from the 1990s, built as a growth hormone secretagogue. It binds GHS-R1a, the ghrelin receptor, on the anterior pituitary to stimulate GH release.

It also binds CD36, a scavenger receptor, which is the basis of its cardioprotective preclinical signal. It isn't FDA-approved, no Phase III trial has completed, and WADA prohibits it under S2. The University of Milano-Bicocca runs the most consistent academic program on it.

Hexarelin vs. GHRP-2 vs. GHRP-6 vs. ipamorelin: how do they compare in the research literature?

All four are growth hormone secretagogues acting on GHS-R1a. What separates them is the off-target profile.

Hexarelin has the highest GH-release potency, and it also raises cortisol and prolactin, less than GHRP-6 but more than ipamorelin. Tachyphylaxis is documented with repeat dosing, and hexarelin alone binds CD36.

GHRP-2 also raises cortisol and prolactin. GHRP-6 adds strong appetite stimulation through the ghrelin pathway.

Ipamorelin has emerged as the field-standard choice. Published studies report GH release similar to GHRP-2, with minimal cortisol, prolactin or appetite effects and no notable tolerance buildup. That's why it became the standard GHS-R1a pairing for CJC-1295.

Is hexarelin FDA-approved?

No. The FDA, the EMA and every other major regulator have approved hexarelin for nothing, and no Phase III trial has completed.

It sells legally in the US as a research reference compound labeled for laboratory use only, and it can't be marketed or used as a therapeutic. Tesamorelin is the only FDA-approved peptide in the wider GH-axis category, and that approval covers HIV-associated lipodystrophy specifically.

Why does hexarelin tolerance build so fast?

Chronic stimulation of GHS-R1a desensitizes and downregulates the receptor. That happens to most G-protein-coupled receptors under sustained agonism.

Hexarelin's high potency is documented as speeding that process up, compared with a more selective agonist like ipamorelin. Published pharmacology reports the GH response fading with daily dosing over days to weeks.

That's the main pharmacological reason ipamorelin displaced it in repeat-dosing protocols. Interrupted dosing schedules get discussed as a workaround, and no controlled trial has validated one for hexarelin.

Hexarelin cardiac effects: are they real?

The cardioprotection signal in acute ischemic-injury models is real but narrow. A 2020 mouse heart-attack study from McDonald and colleagues showed improved LV function, less collagen and lower TGF-β1 expression.

The mechanism runs through CD36 binding, NF-κB and NLRP3 inflammasome suppression, and a shift toward parasympathetic tone. A 2021 mouse aneurysm study and a 2023 rat kidney study showed similar tissue-protective signals.

Then the negative side. A 2022 synchrotron-imaging study in a chronic pulmonary hypertension rat model, from Waddingham and colleagues, found hexarelin did not prevent right-ventricular hypertrophy or relaxation impairment. Cardioprotection here is condition-specific, not universal, and no human RCT has tested it.

What is hexarelin's WADA status?

Hexarelin is on the WADA 2026 Prohibited List under section S2, covering peptide hormones, growth factors, related substances and mimetics. It's prohibited in and out of competition for every athlete under a WADA-compliant body. Detection in urine is reliable with modern LC-MS/MS assays.

How much does third-party tested hexarelin cost?

Hexarelin is six amino acids with no lipid modifications, so it sits at the cheap end of synthesis complexity. Longer GH-axis peptides like tesamorelin at 44 residues or retatrutide at 39 cost much more to make.

Third-party tested material has typically run $45–$80 for 5 mg vials and $75–$140 for 10 mg vials, depending on supplier and purity tier.

Anything well below that is worth verifying on identity. Even simple peptides carry a real synthesis-cost floor, and credible suppliers absorb the cost of third-party CoA testing.