TL;DR
The 1984 ancestor of every GHRP. Biggest hunger kick of the family. Cuban labs run the clinical work.
What is it? Cyril Bowers' founding GH-releasing peptide. Six amino acids, GHS-R1a agonist. Its existence predicted the 1996 receptor cloning and the 1999 discovery of ghrelin.
What does it do? Fires a GH pulse at pituitary somatotrophs. Also mimics ghrelin at the arcuate nucleus, so hunger lands within 15–30 min. Binds CD36 on cardiomyocytes for a separate cardioprotective signal.
Does the evidence hold up? Four decades of GH-release pharmacology. Pandya 1998 nailed the GHRH synergy. Berlanga's Cuban group ran 2007 and 2024 cardioprotection papers. Zero Western Phase 3.
Who uses it? Endocrinologists doing GHRH+GHRP stim tests. A small community crowd using it for the hunger signal.
Bottom line? Historically important. Dirtier than ipamorelin. Best modern case is CD36.
What It Is
GHRP-6 (Growth Hormone-Releasing Peptide-6, developmental code SKF-110679) is the original synthetic growth hormone secretagogue (GHS) — a hexapeptide with the sequence His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 that stimulates pulsatile GH release from the anterior pituitary by activating the ghrelin receptor (GHS-R1a). It is the founding member of the GHRP family from which GHRP-1, GHRP-2, hexarelin, and (less directly) ipamorelin were all derived. GHRP-6 has a molecular weight of approximately 872 g/mol.
GHRP-6 was developed and characterized in 1984 by American endocrinologist Cyril Y. Bowers and colleagues at Tulane University, who had observed in the late 1970s that certain D-amino-acid modifications of met-enkephalin produced unexpected GH-releasing activity in cultured pituitary cells. Through systematic structure-activity work, Bowers' team designed GHRP-6 as the first synthetic peptide to specifically and dose-dependently release GH both in vitro and in vivo through a mechanism entirely distinct from growth hormone-releasing hormone (GHRH). The 1984 Endocrinology paper from Bowers, Momany, Reynolds, and Hong is the foundational reference. This discovery had two enormous downstream consequences: it led to Howard et al.'s 1996 Science paper cloning the growth hormone secretagogue receptor (GHS-R1a), and it set up the 1999 Kojima et al. discovery of ghrelin — the natural endogenous ligand of the same receptor — which had been waiting to be found ever since the synthetic ligand was characterized.
For users in the optimization community, GHRP-6 sits in a particular niche: it is the original, the cheapest (off-patent and commoditized), and the most appetite-stimulating of the commonly used GH-releasing peptides. Its defining clinical feature compared to second-generation analogs (GHRP-2, ipamorelin) is the prominent ghrelin-mimetic hunger response — many users describe a strong, hard-to-ignore hunger pang within 15–30 minutes of injection that can be useful (in lean-bulking or appetite-stimulation contexts) or unwanted (in fat-loss contexts). It also has a more notable cortisol and prolactin signal than ipamorelin, which makes ipamorelin the preferred "clean" GHRP for most modern community protocols.
Outside the optimization community, GHRP-6 has been studied seriously by Cuban research groups (notably Berlanga-Acosta and colleagues at the Center for Genetic Engineering and Biotechnology in Havana) for a separate non-GH indication — cytoprotection and cardioprotection in myocardial ischemia and doxorubicin-induced cardiotoxicity — through a CD36-mediated mechanism distinct from the GH-secretion pathway. This second mechanism is the most clinically interesting aspect of GHRP-6 in 2026 and gives it a potential clinical future independent of its endocrine pedigree.
Mechanism of Action
GHRP-6 has at least two distinct, well-characterized receptor systems through which it acts: the ghrelin receptor (GHS-R1a) for endocrine effects, and CD36 for cardioprotective and cytoprotective effects. Understanding both is essential for understanding the full pharmacology.
- Ghrelin receptor (GHS-R1a) agonism — dominant endocrine mechanism — GHRP-6 binds and activates GHS-R1a, a Gαq-coupled G-protein-coupled receptor expressed densely in the anterior pituitary somatotroph and the hypothalamic arcuate nucleus. Activation triggers IP3 / DAG-mediated calcium release and downstream GH secretion. The receptor was cloned by Howard et al. in 1996 (Science 273:974-977) and the natural ligand ghrelin was isolated by Kojima et al. in 1999.
- Synergy with GHRH — GHRP-6 and GHRH (or GHRH analogs) act synergistically on GH release. Pandya et al. (1998, J Clin Endocrinol Metab; PMID 9543138) showed using a GHRH antagonist that endogenous GHRH is required for the maximal GH response to GHRP-6 — the two pathways converge at the somatotroph and the response is multiplicative rather than additive. This is the mechanistic basis for the standard GHRP + GHRH combination protocols.
- Ghrelin-mimetic appetite stimulation — Because GHS-R1a is the ghrelin receptor, GHRP-6 acts as a ghrelin mimetic in the hypothalamic arcuate nucleus where ghrelin normally signals hunger. The result is the prominent appetite-stimulating effect that distinguishes GHRP-6 from selective GHRPs like ipamorelin.
- Modest cortisol and prolactin elevation — GHRP-6 produces dose-related elevations in ACTH / cortisol and prolactin via GHS-R1a activation in the corticotroph and lactotroph respectively. The cortisol and prolactin signal is meaningfully smaller than seen with full ghrelin and substantially smaller than with hexarelin, but is not zero. Ipamorelin is the GHS family's "cleanest" agonist with essentially no cortisol / prolactin signal at typical doses.
- CD36 binding — cytoprotective mechanism — Hexarelin and GHRP-6 bind CD36, a scavenger receptor expressed on cardiomyocytes, vascular endothelium, and macrophages. CD36 binding mediates anti-apoptotic and cytoprotective effects in models of myocardial ischemia / reperfusion injury that are independent of the GH axis. CD36-null mice show enhanced myocardial vulnerability to ischemia / reperfusion, and the cytoprotective effect of GHRP-6 is lost in those animals — demonstrating that CD36 (not GHS-R1a) is the relevant cardioprotective receptor (Bodart, Febbraio, Demers et al. 2002, Circ Res).
- Anti-apoptotic and antioxidant effects in cardiomyocytes — Berlanga-Acosta and colleagues have characterized GHRP-6's preservation of cardiomyocyte mitochondrial function, reduction of oxidative stress, modulation of Bcl-2 / Bax ratio, and reduction in infarct size in animal AMI models — all CD36-mediated and largely independent of GH release.
- Inotropic effect — Cabrales / Berlanga group echocardiography studies in mice show GHRP-6 increases left ventricular ejection fraction without elevating heart rate, an inotropic effect that persists during chronic beta-blocker (metoprolol) administration. Also independent of the GH axis and likely CD36-mediated.
- Gastric prokinetic effect — As a ghrelin mimetic, GHRP-6 increases gastric emptying rate and gastrointestinal motility (Depoortere et al. 2005, Eur J Pharmacol). Part of its acute "feeling hungry" phenotype.
- What it does not do — GHRP-6 does not directly increase IGF-1 production (IGF-1 elevation is downstream of GH release, mediated by hepatic GH receptor activation). It does not bypass the somatotroph; if the somatotroph is depleted or non-functional, GHRP-6 will not produce GH release. It does not reset endogenous GH pulsatile architecture; it superimposes a pulse on the existing rhythm.
What the Research Shows
GHRP-6 has the most extensive preclinical research base of the original first-generation GHRPs, plus a meaningful (if smaller-than-modern) clinical literature in GH stimulation testing and a separate cardioprotection arc developed primarily by Cuban groups.
- Foundational GH-release characterization (Bowers 1984) — Bowers CY, Momany FA, Reynolds GA, Hong A. On the in vitro and in vivo activity of a new synthetic hexapeptide that acts on the pituitary to specifically release growth hormone. Endocrinology 1984;114(5):1537-1545. Discovery paper establishing GHRP-6 as the first specific GH secretagogue acting on the pituitary somatotroph.
- Receptor cloning (Howard 1996) — Howard AD et al. A receptor in pituitary and hypothalamus that functions in growth hormone release. Science 1996;273(5277):974-977. Cloned GHS-R1a using GHRP-6 as the radioligand.
- Ghrelin discovery (Kojima 1999) — Kojima M et al. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature 1999;402(6762):656-660. The natural endogenous ligand of GHS-R1a — discovered by tissue-screening for activity that the synthetic GHRP-6 had predicted must exist.
- GHRH synergy in humans (Pandya 1998) — Pandya N, DeMott-Friberg R, Bowers CY, Barkan AL, Jaffe CA. GH-releasing peptide-6 requires endogenous hypothalamic GH-releasing hormone for maximal GH stimulation. J Clin Endocrinol Metab 1998;83(4):1186-1189. PMID 9543138. Established the GHRP-GHRH synergy underpinning all modern combination protocols.
- Diagnostic GH stimulation testing — GHRP-6 has been used as a GH stimulation test in pediatric and adult endocrinology, particularly in combination with GHRH. The combined GHRH + GHRP-6 stimulation test is more sensitive than insulin tolerance testing for GH deficiency diagnosis.
- Comparison with ghrelin (Arvat 2001, 2002) — Arvat E et al. compared GHRP-6 and ghrelin head-to-head in human volunteers. Ghrelin produced larger GH responses than GHRP-6 at equivalent dosing, with a similar pattern of cortisol / prolactin / ACTH elevation.
- Cardioprotection in AMI models (Berlanga 2007) — Berlanga J, Cibrian D, Guevara L, et al. Growth-hormone-releasing peptide 6 (GHRP-6) prevents oxidant cytotoxicity and reduces myocardial necrosis in a model of acute myocardial infarction. Clin Sci (Lond). 2007;112(4):241-250. PMID 17034365. Foundational cardioprotection paper.
- CD36 mediation (Bodart, Demers et al. 2002) — Established that hexarelin and GHRP-6 cytoprotective effects are mediated through CD36, not GHS-R1a. CD36-null mice fail to show the cardioprotective benefit.
- Inotropic / echocardiography studies (Cabrales 2013, Biotecnología Aplicada) — In vivo echocardiography in mice showed GHRP-6 increases LVEF without HR elevation, dose-dependently, and the effect persists during beta-blocker therapy.
- Doxorubicin cardiotoxicity prevention (Berlanga-Acosta 2024, PMID 38873418) — GHRP-6 administered concomitantly with doxorubicin in rats prevented chemotherapy-induced cardiomyopathy, cardiomyocyte demise, and ventricular dilation; reduced multi-organ damage.
- Multi-organ cytoprotection (Cibrián 2006) — GHRP-6 extends tissue viability during acute ischemia / reperfusion in small bowel, liver, and kidneys in addition to heart.
- Pharmacokinetics in healthy volunteers (Cabrales 2013, Eur J Pharm Sci) — 9 male healthy volunteers; characterized plasma concentration kinetics with LC-MS using ¹³C-labeled internal standard. Biliary excretion hypothesized as one elimination route.
Critical Context — Mature Pharmacology, Limited Modern Clinical Trials
GHRP-6 has been studied for over 40 years and the GH-release pharmacology is extremely well-characterized. The cardioprotection arc is smaller, almost entirely driven by Cuban groups, and has not progressed to large Western Phase 3 trials. The compound has not been advanced through modern pharmaceutical regulatory pathways because more selective second-generation GHRPs (GHRP-2, ipamorelin) and small-molecule analogs (ibutamoren) have largely replaced it in the GH stimulation use case, while the cardioprotection use case has not had a Western sponsor.
Human Data
GHRP-6 has been studied in dozens of small human trials over four decades, primarily for GH stimulation testing, GH-deficiency assessment, and (more recently) cardioprotective applications.
- GH stimulation testing — Numerous human studies have validated GHRP-6 (alone and in combination with GHRH) as a GH-stimulation diagnostic test. Bowers' combined GHRH + GHRP-6 test is more sensitive than ITT for GH deficiency. Healthy adults receiving 1–2 mcg/kg IV GHRP-6 show robust GH peaks within 15–30 minutes.
- Pandya 1998 (PMID 9543138) — 8 healthy male volunteers; GHRP-6 1 mcg/kg IV ± GHRH antagonist. Endogenous GHRH required for maximal GH response.
- Arvat et al. — comparative human studies — Multiple studies comparing GHRP-6, hexarelin, ghrelin, and GHRH. GHRP-6 produces significantly smaller GH peaks than ghrelin at equivalent doses and smaller cortisol / prolactin peaks.
- Aging studies — GHRP-6 has been studied for whether it can restore youthful GH pulsatility in elderly subjects with reduced spontaneous GH secretion. Modest but measurable effects in some protocols; not advanced to large outcomes trials.
- Cabrales 2013 PK study (Eur J Pharm Sci) — 9 male healthy volunteers; characterized GHRP-6 plasma kinetics after subcutaneous administration. Biliary excretion suggested as one elimination route.
- Cuban cardioprotection clinical work — Cuban research groups (CIGB Havana) have advanced GHRP-6 toward cardioprotection clinical applications. Publications in regional journals (Biotecnología Aplicada, Revista Cubana de Investigaciones Biomédicas) have not advanced to large Western Phase 3 trials.
- Body composition / aging studies — Smaller studies have evaluated GHRP-6 ± GHRH for body composition outcomes in elderly subjects. Effects are typically modest and require chronic dosing.
- No large modern Phase 3 RCT — Despite 40 years of research, no major Western pharmaceutical sponsor has advanced GHRP-6 through Phase 3 for an FDA-approval-targeted indication. This reflects the commercial difficulty of advancing a 1984-vintage peptide that lacks composition-of-matter patent protection.
Dosing from the Literature
Dosing guidance below is compiled from clinical-research and community use. Not medical advice. No FDA-approved dose exists for therapeutic use.
| Indication / Context | Dose | Frequency | Notes |
|---|
| GH stimulation testing (research) | 1–2 mcg/kg IV | Single dose | Diagnostic context; peak GH at 15–30 min. |
| Combined GHRH + GHRP-6 stim test | 1 mcg/kg each, IV | Single dose | More sensitive than ITT for GH deficiency. |
| Community SubQ (typical) | 100 mcg per dose | 2–3x daily | Standard hyperphysiologic GH-pulse community dose. Often pre-bed + upon waking + post-workout. |
| Community SubQ (weight-adjusted) | 1 mcg/kg per dose | 2–3x daily | Some users dose at 1 mcg/kg per pulse — ~75 mcg for a 75 kg person, close to the 100 mcg round-number standard. |
| Cardioprotection (preclinical models) | ~100–400 mcg/kg | Daily | Cuban preclinical and small clinical work; no FDA-approved dose. |
| Cycle length (community) | 8–12 weeks | — | Receptor desensitization is plausible with chronic GHS-R1a agonism; cycling is community convention rather than evidence-derived. |
Dosing Disclaimer
GHRP-6 is investigational. Doses above are taken from research papers and community use; no FDA-approved dosing exists. Combining GHRP-6 with GHRH analogs produces synergistic GH release — community protocols routinely combine the two, but this combination has not been formally dose-finding-studied for community use. Dose timing matters: GHRP-6 should be administered on an empty stomach (food, particularly high-carbohydrate meals, blunts the GH pulse via insulin-mediated suppression).
Reconstitution & Storage
GHRP-6 is supplied as a lyophilized powder, typically in 5 mg or 10 mg vials.
| Vial Size | BAC Water | Concentration | 100 mcg Dose | 200 mcg Dose |
|---|
| 5 mg | 2 mL | 2,500 mcg/mL | 4 units (0.04 mL) | 8 units (0.08 mL) |
| 10 mg | 2 mL | 5,000 mcg/mL | 2 units (0.02 mL) | 4 units (0.04 mL) |
- Reconstitution — Inject bacteriostatic water slowly down the inside wall of the vial at 45°. Swirl gently — never shake. Solution should be clear and colorless.
- Storage — Lyophilized stable at room temperature for 12+ months out of light; refrigerated (2–8°C) for longer storage. Reconstituted: refrigerated at 2–8°C, used within 28 days. Do not freeze reconstituted.
- Inspection — Discard if cloudy, particulate, discolored, or with unusual odor.
- Empty-stomach administration — Dose 30+ minutes before food or 2+ hours after. Insulin spike from food blunts the GH pulse via somatostatin-mediated negative feedback.
→ Use the Kalios Dosing Calculator for exact syringe units
Side Effects & Risks
Important
GHRP-6 elevates cortisol and prolactin and mimics ghrelin at the hunger center. Western regulators have not advanced it through Phase 3. WADA-banned under S2. Talk to someone licensed before deciding if GHRP-6 is the right GHRP for your goal.
GHRP-6 has the most thoroughly characterized side-effect profile of the GHRP family due to its long use history, but modern selective alternatives (ipamorelin) often have a cleaner profile for community use.
- Hunger — defining acute side effect — GHRP-6 produces a marked, fast-onset hunger pang within 15–30 minutes of injection that is much more prominent than with GHRP-2 or ipamorelin. For users targeting appetite stimulation (lean bulking, recovery from cachexia, post-illness weight regain) this is a feature; for users targeting fat loss it is the dose-limiting toxicity. Tolerance can develop over several weeks of continuous use.
- Cortisol and prolactin elevation — Modest dose-related elevations vs placebo; substantially smaller than with hexarelin, slightly larger than with GHRP-2, and meaningfully larger than with ipamorelin. Chronic high doses may produce clinically meaningful cortisol elevation.
- Water retention — Some users report mild fluid retention in the first 1–2 weeks, attributable to GH's effect on sodium and water handling. Usually resolves with continued use.
- Tingling / numbness / carpal-tunnel-like symptoms — At higher chronic doses, GH-mediated water retention can produce nerve compression symptoms — most commonly mild morning hand tingling. Dose-related; resolves with dose reduction.
- Insulin sensitivity reduction — Elevated GH (and IGF-1) reduces insulin sensitivity. Sustained chronic high-dose GHRP-6 use can produce mild glucose intolerance. Periodic fasting glucose and HbA1c monitoring is reasonable.
- Injection-site reactions — Mild local erythema common; significant reactions uncommon.
- Drug interactions — Synergy with GHRH analogs (intentionally exploited). Insulin and high-carbohydrate meals blunt the GH pulse. Glucocorticoids blunt the GH response. Beta-blockers do not blunt and may enhance.
- WADA banned (S2) — All GH secretagogues including GHRP-6 are explicitly prohibited at all times for tested athletes. Detection methods for GHRP-6 and its metabolites are well-established by WADA-accredited laboratories.
- Theoretical cancer concern (GH / IGF-1 axis) — Chronic elevation of GH and IGF-1 has been epidemiologically associated with increased risk of certain cancers. Applies to all GH-elevating compounds and is the central long-term safety consideration. Age-appropriate cancer screening before initiation is reasonable.
- Sourcing risk — Research-chemical channel quality varies. Independent COA (HPLC purity + mass spec) is the practical floor for due diligence.
Bloodwork & Monitoring
The GH / IGF-1 axis warrants more careful baseline and follow-up monitoring than many other peptide protocols.
- Baseline IGF-1 — Most important single marker. Establishes individual baseline and tracks effective GH elevation. Repeat at 8 weeks.
- Fasting glucose and HbA1c — GH reduces insulin sensitivity. Baseline and at 8–12 weeks.
- Fasting insulin — Sensitive marker for glucose-handling changes.
- Lipid panel — GH affects lipid handling; baseline and at 12 weeks.
- Cortisol (AM) — Particularly relevant for higher-dose chronic GHRP-6 use given the modest cortisol signal.
- Prolactin — Same rationale; modest signal warrants tracking on extended cycles.
- CBC and CMP — Baseline and at 8 weeks; routine endocrine-protocol monitoring.
- Cancer screening (age-appropriate) — Given the GH / IGF-1 epidemiology, age-appropriate screening before chronic use.
- Sleep tracking — Subjective sleep-quality changes are common and useful to track.
Commonly Stacked With
The standard pairing. CJC-1295 (GHRH analog) + GHRP-6 (GHS-R1a agonist) produces synergistic GH release — multiplicative rather than additive at the somatotroph. With-DAC CJC-1295 has ~8 day half-life; without DAC has ~30 min half-life and is dosed alongside each GHRP pulse for saturation-dosing protocols.
The 1-29 amino-acid fragment of GHRH. Cleaner than CJC-1295 in some practitioner protocols, with shorter half-life. Combined with GHRP-6 for the same synergistic GH-release rationale.
FDA-approved GHRH analog (Egrifta), originally for HIV-associated lipodystrophy. Used in physician-supervised contexts as the GHRH partner for GHRP-6 in users who want a regulated-quality GHRH alongside research-grade GHRP-6.
Not a stack but the modern selective alternative. Most users picking between the two GHRPs choose ipamorelin for a cleaner side-effect profile, GHRP-6 for the appetite-stimulating context.
For tissue-repair-plus-GH protocols. BPC-157 local repair signaling complements the systemic GH / IGF-1 elevation from GHRP-6 + GHRH. Common in injury recovery contexts.
→ Check compound compatibility in the Stack Builder
Regulatory Status
Current Status — April 2026
GHRP-6 is not FDA-approved for any indication. It is currently classified as an FDA Category 2 bulk drug substance — meaning it is not eligible for use by 503A or 503B compounding pharmacies under sections 503A or 503B of the Federal Food, Drug, and Cosmetic Act. It is a research chemical for the U.S. market.
On February 27, 2026, HHS Secretary Robert F. Kennedy Jr. publicly announced an intention to reclassify approximately 14 of the 19 Category 2 peptides — GHRP-6 and the GHRP family among the candidates — back to Category 1, which would make them available through licensed compounding pharmacies with a prescription. As of April 2026, the FDA has not published a formal update reflecting that announcement, and the Pharmacy Compounding Advisory Committee (PCAC) has not completed review. Practically, GHRP-6 still cannot be legally compounded by 503A pharmacies as of this publication date.
WADA: GHRP-6 is explicitly banned at all times under category S2 (peptide hormones, growth factors, related substances and mimetics). Detection methods are established; GHRP-6 and its metabolites are routinely tested by WADA-accredited laboratories. Any tested athlete using GHRP-6 faces sanction under the WADA Code.
Outside the United States: GHRP-6 has been the subject of clinical research programs by Cuban and other Latin American groups for cardioprotection indications. It has not received marketing authorization from EMA, MHRA, PMDA, or any other major regulator for either GH-stimulation or cardioprotection use.
Cost & Access
GHRP-6 is not approved for human use. It is available through research suppliers for laboratory research purposes only.
U.S. compounding pharmacies cannot legally compound GHRP-6 under current FDA bulk-substance rules. The compound is among the cheapest peptides in the GH-secretagogue family due to its 1984 vintage and absence of composition-of-matter patent protection; it has been supplied through research-chemical channels for over two decades. Quality and purity vary substantially between vendors; independent COA (HPLC + mass spec) is the practical floor for due diligence.
If GHRP-6 is reclassified back to Category 1 under HHS Secretary Robert F. Kennedy Jr.'s February 2026 announcement (subject to PCAC review and FDA implementation), 503A compounded GHRP-6 would become available to clinician-prescribed patients for off-label use with regulatory legitimacy and quality assurance. As of April 2026, this reclassification remains pending. Kalios does not sell compounds.
Access and regulatory status as of April 2026. Actual availability varies by provider, location, and prescription status. Kalios does not sell compounds.
Related Compounds
Peptides GHRP-6 users weigh against the original:
Second-generation growth hormone releasing peptide. Stronger GH pulse than ipamorelin with mild prolactin rise.
Potent ghrelin-receptor agonist with cardioprotective signaling but rapid receptor desensitization.
Ibutamoren — oral nonpeptide ghrelin-receptor agonist producing 24-hour GH/IGF-1 elevation.
CJC-1295 + ipamorelin — the classic GHRH + GHRP combination for natural growth-hormone pulse amplification.
Key References
- Bowers CY, Momany FA, Reynolds GA, Hong A. On the in vitro and in vivo activity of a new synthetic hexapeptide that acts on the pituitary to specifically release growth hormone. Endocrinology. 1984;114(5):1537-1545. PMID: 6142782. (Foundational GHRP-6 discovery paper.)
- Howard AD, Feighner SD, Cully DF, Arena JP, Liberator PA, Rosenblum CI, et al. A receptor in pituitary and hypothalamus that functions in growth hormone release. Science. 1996;273(5277):974-977. PMID: 8688086. (Cloning of GHS-R1a using GHRP-6 as the radioligand.)
- Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 1999;402(6762):656-660. PMID: 10604470. (Discovery of the natural endogenous ligand of GHS-R1a.)
- Pandya N, DeMott-Friberg R, Bowers CY, Barkan AL, Jaffe CA. Growth hormone (GH)-releasing peptide-6 requires endogenous hypothalamic GH-releasing hormone for maximal GH stimulation. J Clin Endocrinol Metab. 1998;83(4):1186-1189. PMID: 9543138. (GHRH-GHRP synergy in humans.)
- Bowers CY. Unnatural growth hormone-releasing peptide begets natural ghrelin. J Clin Endocrinol Metab. 2001;86(4):1464-9. PMID: 11297568. (Bowers' personal review of the discovery arc from synthetic to natural ligand.)
- Berlanga J, Cibrian D, Guevara L, Dominguez H, Alba JS, Seralena A, et al. Growth-hormone-releasing peptide 6 (GHRP-6) prevents oxidant cytotoxicity and reduces myocardial necrosis in a model of acute myocardial infarction. Clin Sci (Lond). 2007;112(4):241-250. PMID: 17034365. (Foundational cardioprotection paper.)
- Berlanga-Acosta J, Cibrian D, Valiente-Mustelier J, Suárez-Alba J, García-Ojalvo A, Falcón-Cama V, Jiang B, Wang L, Guillén-Nieto G. Growth hormone releasing peptide-6 (GHRP-6) prevents doxorubicin-induced myocardial and extra-myocardial damages by activating prosurvival mechanisms. PMID: 38873418. 2024. (Most recent comprehensive cardioprotection paper.)
- Cabrales A, Gil J, Fernández E, Valenzuela C, Hernández F, García I, Hernández A, Besada V, Reyes O, Padrón G, Berlanga J, Guillén G, González LJ. Pharmacokinetic study of Growth Hormone-Releasing Peptide 6 (GHRP-6) in nine male healthy volunteers. Eur J Pharm Sci. 2013;48(1-2):40-46. PMID: 23159700. (Human PK in healthy volunteers.)
- Bowers CY, Sartor AO, Reynolds GA, Badger TM. On the actions of the growth hormone-releasing hexapeptide, GHRP. Endocrinology. 1991;128(4):2027-2035. PMID: 2004616.
- Bowers CY. Growth hormone-releasing peptide (GHRP). Cell Mol Life Sci. 1998;54(12):1316-1329. PMID: 9893708.
- Hataya Y, Akamizu T, Takaya K, et al. A low dose of ghrelin stimulates growth hormone (GH) release synergistically with GH-releasing hormone in humans. J Clin Endocrinol Metab. 2001;86(9):4552. PMID: 11549709.
- Bodart V, Febbraio M, Demers A, McNicoll N, Pohankova P, Perreault A, Sejlitz T, Escher E, Silverstein RL, Lamontagne D, Ong H. CD36 mediates the cardiovascular action of growth hormone-releasing peptides in the heart. Circ Res. 2002;90(8):844-849. PMID: 11988484. (CD36 cardioprotective receptor characterization.)
- Depoortere I, De Winter B, Thijs T, De Man J, Pelckmans P, Peeters T. Comparison of the gastroprokinetic effects of ghrelin, GHRP-6 and motilin in rats in vivo and in vitro. Eur J Pharmacol. 2005;515(1-3):160-168. PMID: 15890335. (Gastric prokinetic mechanism.)
- Granado M, Priego T, Martín AI, Villanúa MA, López-Calderón A. Anti-inflammatory effect of the ghrelin agonist growth hormone-releasing peptide-2 (GHRP-2) in arthritic rats. Am J Physiol Endocrinol Metab. 2005;288(3):E486-492. PMID: 15507534. (GHRP family anti-inflammatory mechanism.)
- Cabrales A, Berlanga J, et al. Cardiotropic effect of GHRP-6: in vivo characterization by echocardiography. Biotecnología Aplicada. 2013;30(4):285-289. (Inotropic effect characterization.)
- Berlanga-Acosta J, et al. Synthetic Growth Hormone-Releasing Peptides (GHRPs): A Historical Appraisal of the Evidences Supporting Their Cytoprotective Effects. Medicc Rev. 2017. PMC5392015. (Comprehensive cytoprotection review.)
- Arvat E, Maccario M, Di Vito L, et al. Endocrine activities of ghrelin, a natural growth hormone secretagogue (GHS), in humans: comparison and interactions with hexarelin, a nonnatural peptidyl GHS, and GH-releasing hormone. J Clin Endocrinol Metab. 2001;86(3):1169-1174. PMID: 11238504. (Comparative human endocrine study.)
- FDA. Bulk Drug Substances That Raise Significant Safety Risks (Category 2) Under Section 503A / 503B. FDA.gov. Updated 2025-2026.
- WADA Prohibited List 2026. World Anti-Doping Agency. wada-ama.org. (GHRP family banned under S2.)
Last updated: April 2026 | Profile authored by Kalios Peptides research team