GHRP-6

GHRP-6 is a synthetic hexapeptide consisting of six amino acids (His-D-Trp-Ala-Trp-D-Phe-Lys-NH₂) with a molecular weight of 872.44 Da. First synthesized in 1977, GHRP-6 was the first growth hormone-releasing peptide to demonstrate significant in vivo activity, establishing the foundation for an entire class of GH secretagogues. The compound functions as a ghrelin mimetic, binding to and activating the growth hormone secretagogue receptor (GHS-R, also known as the ghrelin receptor) expressed in hypothalamic neurons and pituitary somatotroph cells.

The development of GHRP-6 originated from research into opiate-like peptides and their potential to stimulate GH release. Scientists discovered that certain synthetic peptides could “stimulate growth hormone without any analgesic effect and was not addictive,” leading to the GHRP class. Critically, researchers found that GHRPs work through a secretagogue receptor separate from the GHRH receptor, explaining the synergistic GH release observed when GHRPs and GHRH analogs are coadministered.

GHRP-6 demonstrates several pharmacological characteristics that limit its clinical utility:

Poor Oral Bioavailability: As a peptide, GHRP-6 is susceptible to gastrointestinal degradation, requiring parenteral (injectable) administration for systemic effects.

Short Half-Life: Rapid enzymatic degradation results in a brief duration of action, with GH levels returning toward baseline within 2-4 hours following single administration. This necessitates multiple daily injections (typically 2-3 times daily) to maintain elevated GH secretory capacity.

Frequency-Dependent Efficacy: Due to the circadian rhythm of GH secretion involving multiple “peaks and troughs throughout the day,” optimal effects require multiple daily doses timed to physiological GH pulses. This makes in-office administration impractical, requiring patient self-administration at home.

Despite being the founding member of the GHRP class with decades of research, GHRP-6 has never received FDA approval for any indication. A comprehensive 2021 systematic review conducted by the University of Maryland for the FDA found zero clinical trials meeting inclusion criteria for GHRP-6 therapeutic use—the most profound evidence gap among all peptides examined in the FDA’s 503B Bulks List evaluation. The compound is not available in any of the 13 countries/regions surveyed, including the United States, Canada, EU, UK, Ireland, Belgium, Latvia, Australia, New Zealand, Saudi Arabia, Abu Dhabi, Hong Kong, or Namibia.

Mechanism of Action

GHRP-6 operates through the ghrelin receptor (GHS-R) signaling pathway, distinct from and complementary to GHRH:¹ ² ³

Ghrelin Receptor Activation: GHRP-6 binds to and activates GHS-R1a receptors on hypothalamic neurons and pituitary somatotrophs.¹ ² Upon ligand binding, the receptor activates Gq proteins, leading to phospholipase C (PLC) activation, inositol trisphosphate (IP₃) production, and intracellular calcium mobilization.² This calcium flux triggers GH secretion from stored granules while activating protein kinase C (PKC) and signaling cascades that enhance GH gene transcription.²

Dual Hypothalamic and Pituitary Action: Unlike GHRH which acts solely at the pituitary, evidence suggests GHRP-6 exerts effects at both the pituitary (direct somatotroph stimulation) and hypothalamic (modulation of GHRH and somatostatin secretion) levels.⁵ This dual mechanism contributes to GHRP-6’s efficacy and explains why it can release GH even in some conditions where GHRH responsiveness is impaired.⁵

Increased Somatotroph Recruitment: Rather than increasing the amount of GH secreted per cell (GHRH’s primary mechanism), GHRP-6 increases the number of somatotrophs participating in each secretory event, amplifying GH pulse amplitude.¹ ² This mechanism is independent of GHRH, though GHRH receptor presence potentiates the stimulus.¹

Somatostatin Suppression: Evidence suggests GHRPs partially work by suppressing somatostatin, the hypothalamic peptide that tonically inhibits GH release.¹ ⁵ By reducing inhibitory tone, GHRP-6 permits more robust GH secretion in response to stimulatory signals.¹

Dose-Dependent GH Release: The foundational Bowers 1990 study demonstrated dose-dependent GH release with GHRP-6 doses ranging from 0.1 to 3.2 µg/kg IV, with peak GH responses occurring 15-30 minutes post-administration.³ At the highest dose, mean peak GH reached 52.0±11.0 µg/L, substantially greater than typical baseline levels (<5 µg/L).³

Synergy with GHRH: When GHRP-6 and GHRH are coadministered, they produce synergistic GH release substantially exceeding the arithmetic sum of either compound alone.¹ ³ ⁵ The Bowers study found that GHRH 1 µg/kg + GHRP-6 1 µg/kg produced mean peak GH of 61.7±10.8 µg/L, while the arithmetic sum of individual responses would predict only 32.7 µg/L—demonstrating true synergy rather than simple additivity.³ This complementary mechanism—GHRH increasing GH synthesis and secretion per cell, GHRP-6 increasing the number of cells releasing GH and suppressing somatostatin—explains why combination protocols are frequently used despite lack of controlled trials validating them.¹ ³

Preserved Feedback Regulation: Unlike exogenous GH administration which provides constant, non-physiological hormone levels and suppresses endogenous production, GHRP-6 stimulates the body’s own pulsatile GH secretion subject to negative feedback via somatostatin and IGF-I.¹ ² This “restores the growth hormone to what it should be and secreted, and that’s really important for normal growth,” according to SME interviews.¹ The intact feedback mechanism makes it “very hard to overshoot” and difficult to “overtreat patients,” offering a safety advantage over recombinant GH.¹

IGF-I Production: Pulsatile GH elevation stimulates hepatic and peripheral tissue production of insulin-like growth factor-I (IGF-I), the primary mediator of GH’s anabolic effects.¹ ² Due to GH’s extremely short half-life (2-3 minutes), IGF-I serves as a surrogate marker to assess GH pathway activation and treatment efficacy.¹ ² SMEs noted that IGF-I levels below 150 ng/mL suggest potential benefit from GH secretagogue therapy.¹

Physiological Effects

The downstream effects of GH and IGF-I elevation include:¹ ²

• Body Composition: Increased lean body mass and reduced fat mass through enhanced protein synthesis and lipolysis
• Growth: Increased height velocity in children with growth impairment (theoretical application)
• Metabolic Effects: Complex effects on glucose and lipid metabolism; GH antagonizes insulin, potentially affecting glucose tolerance²
• Bone Metabolism: Enhanced bone turnover and potential improvements in bone mineral density
• Recovery and Tissue Repair: Potential improvements in wound healing and connective tissue health
• Physical Appearance: SMEs noted patients seek GH secretagogues for improvements in “skin, hair, or body” appearance¹

Comprehensive Systematic Review

University of Maryland Center of Excellence in Regulatory Science and Innovation (M-CERSI), 2021 –

*Comprehensive scoping review examining clinical use of GHRP-6 to assist FDA in evaluating inclusion on the 503B Bulks List for compounding.*¹

**Systematic Literature Review Methodology:**¹

• Comprehensive search of Ovid MEDLINE and Embase databases through December 2, 2019
• PRISMA-compliant systematic review process
• Inclusion criteria: Studies using GHRP-6 in nominated dosage forms/routes to diagnose, prevent, or treat any condition
• Two independent reviewers screened 345 titles/abstracts after deduplication
• 29 full-text articles reviewed

**Results:**¹

• Total studies included: 0 (zero)
• Reasons for exclusions: Wrong study design (14 studies); wrong dosage form or ROA (5); wrong indication (4); wrong substance (2); GHRP-6 used as brand/proprietary product (2); GHRP-6 not used clinically (1); language other than English (1)
• Total patients treated with GHRP-6 in qualifying studies: 0
• Key finding: Zero clinical trials met inclusion criteria despite nomination for GH deficiency, wasting syndrome, and anorexia nervosa

**Pharmacology and Historical Use (from excluded studies):**¹

The review identified several studies that didn’t meet therapeutic use criteria but provided context on GHRP-6’s pharmacology and diagnostic applications:

Diagnostic Testing for GH Deficiency: Multiple excluded studies examined GHRP-6 (1 µg/kg IV), often combined with GHRH (1 µg/kg IV), as an alternative to the insulin tolerance test (ITT) for diagnosing GH deficiency.¹ ⁶ ⁷ ⁸ These studies found that GHRP-6 alone or combined with GHRH “compared favorably to the ITT for the diagnosis of GH deficiency,” was “convenient, safe, and reliable,” and correctly identified patients with GH deficiency while avoiding the risks associated with induced hypoglycemia.¹ ⁶ ⁷

Traumatic Brain Injury (TBI) Screening: One study found that a single GH measurement 30 minutes after GHRH + GHRP-6 administration was sufficient to diagnose GH deficiency in TBI patients, suggesting potential use for population screening given the convenience, cost, and rapid results.¹

Combination Therapy in Hypogonadal Men: The Sigalos 2017 retrospective review examined GHRP-2 100 µg / GHRP-6 100 µg / sermorelin 100 µg administered subcutaneously three times daily in 14 hypogonadal men on testosterone therapy.¹ ⁹ The combination significantly increased IGF-I levels, but no functional outcomes (body composition, strength, quality of life) were measured.¹ ⁹ This study represents the only published data on the triple-combination protocol frequently mentioned by SMEs.¹

**Subject Matter Expert Interviews (N=4 SMEs):**¹

Clinical Context:

• Three of 4 SMEs had used GHRP-6; one had used the GHRP-2 / GHRP-6 / sermorelin combination¹
• GHRP-6 “rarely used as monotherapy”; more commonly prescribed in combination with GHRP-2 and/or sermorelin¹
• Primary applications: “Lifestyle medications” for patients seeking improvements in physical appearance (skin, hair, body composition) rather than medical necessity¹
• Typical patients: Often prescribed after testosterone replacement therapy in hypogonadal men who desire additional body composition improvements¹

Historical Development:

• “In the 1970’s there was interest in the synthesis of opiate-like peptides” and their potential to stimulate GH¹
• Discovery that GHRPs “stimulate growth hormone without any analgesic effect and was not addictive”¹
• Researchers found GHRPs work on a “secretagogue receptor separate from GHRH,” explaining synergistic effects¹

Dosing Practices:

• Typical dosing: 100-500 µg/day subcutaneously, up to 1,000 µg/day when combined with sermorelin¹
• Requires multiple daily doses (2-3 times daily) due to short half-life and circadian GH rhythm¹
• Patients started on low doses and titrated up based on tolerance and desired outcomes¹
• Dosing based on clinical experience rather than evidence-based protocols: “limited literature” on optimal combinations and doses¹

Rationale for Combination Therapy:

• “When GH secretagogues are used together they have a synergistic effect”¹
• GHRP-2 or GHRP-6 combined with sermorelin produces a “stronger growth hormone response, or growth hormone secretary response”¹
• “Receptor interactions in the growth pathway that will accentuate the response”—GHRPs and GHRH analogs “interact at different receptors, stimulating different methods of releasing growth hormone”¹
• By combining hormones with “different molecular effects on the pathways, a synergistic effect can be achieved”¹

Monitoring and Outcomes:

• IGF-I levels used as surrogate for GH due to GH’s 2-3 minute half-life; “it’s very difficult to do a growth hormone assay”¹
• Treatment considered if baseline IGF-I <150 ng/mL¹
• “It takes a while for IGF-1 to actually go up”¹
• Some clinicians monitor progress by physical changes since they “prescribe these types of medications for patients who want a desired physical outcome” instead of IGF-1 levels¹

Safety Perspective:

• “Much safer than growth hormones, because they’re stimulating the natural pathway” instead of shutting it down and overriding natural feedback¹
• Feedback mechanism intact, making it “very hard to overshoot” and difficult to “overtreat patients”¹
• “Few side effects” and dose response effect beyond which the body won’t respond to more medication¹
• “Anecdotally over the years…they [GH secretagogues] seem to work as advertised, and they seem to be quite safe, but we don’t have the peer review literature to prove that, just yet”¹

Evidence Gaps Acknowledged:

• “Limited literature” about specific dose and/or combination of GHRPs to use¹
• “Limited outcomes-based human research on the clinical use of GH and GH secretagogues, making it difficult to know the ideal combination and dose of medication to use, and the effects of long-term use”¹
• Most literature focused on “what’s the impact going to be on the growth hormone pathway” rather than downstream effects (muscle growth, fat loss, other measurable functional effects)¹
• One SME who did not use GH secretagogues cited “lack of evidence-based research” as a reason¹

**Survey Results:**¹

• Zero respondents from professional medical associations
• Complete absence of survey responses suggests extremely limited adoption in mainstream medical practice

**Conclusion:**¹
“GHRP6 was nominated for inclusion on the 503B Bulks List as an injection to treat growth hormone deficiency (including adult onset), wasting syndrome, and anorexia nervosa… Zero studies were included from the literature review. However, several studies that did not meet the inclusion criteria described the use of GHRP6 in the diagnosis of GH deficiency… Three SMEs had used GHRP6 and 1 had used the GHRP2 / GHRP6 / sermorelin combination… Several SMEs stated that there was limited outcomes-based human research on the clinical use of GH and GH secretagogues, making it difficult to know the ideal combination and dose of medication to use, and the effects of long-term use.”

Significance: This FDA-commissioned review reveals the most profound evidence gap of any peptide examined—zero qualifying clinical trials for therapeutic use despite nomination for three indications and decades since GHRP-6’s synthesis.¹ The stark contrast between complete absence of therapeutic evidence and widespread off-label use as “lifestyle medication” represents the ultimate disconnect between clinical practice and evidence-based medicine.¹

Foundational Pharmacology Study

**Study Protocol:**³

• GHRP-6 administered IV at doses of 0.1, 0.3, 1.0, and 3.2 µg/kg
• GHRH administered IV at 1.0 µg/kg
• Combined administration of GHRH 1.0 µg/kg + GHRP-6 1.0 µg/kg
• Serial GH measurements at 15-minute intervals

*Results:*³

• Dose-dependent GH release: GHRP-6 produced dose-dependent increases in GH:
  • 0.1 µg/kg: Mean peak GH 8.9±2.0 µg/L
  • 0.3 µg/kg: Mean peak GH 16.0±3.5 µg/L
  • 1.0 µg/kg: Mean peak GH 22.2±6.2 µg/L
  • 3.2 µg/kg: Mean peak GH 52.0±11.0 µg/L
• GHRH response: GHRH 1.0 µg/kg produced mean peak GH of 10.5±2.7 µg/L³
• Synergistic combination: GHRH 1.0 µg/kg + GHRP-6 1.0 µg/kg produced mean peak GH of 61.7±10.8 µg/L³
  • Arithmetic sum of individual responses: 10.5 + 22.2 = 32.7 µg/L
  • Observed combined response: 61.7 µg/L
  • Synergistic effect: ~1.9× greater than expected additive effect

Significance: This foundational study established that GHRP-6 releases GH in a dose-dependent manner and produces striking synergistic GH release when combined with GHRH—substantially exceeding the arithmetic sum of either alone.³ This demonstration of complementary mechanisms provided the pharmacological rationale for combination protocols, though the study did not examine functional outcomes or long-term effects.³

Broader GH Secretagogue Context

*Systematic review of GH secretagogues providing context for GHRP-6 within the broader class.*²

**Key Points:**²

• GH secretagogues preserve pulsatile GH release subject to negative feedback, theoretically avoiding supratherapeutic levels associated with recombinant GH
• GHRP-6 was the first GHRP with significant in vivo activity; served as scaffold for GHRP-1, GHRP-2, hexarelin, and ipamorelin development
• Must be administered parenterally (injection) due to poor oral bioavailability and short half-life
• Combination of GHRPs with GHRH analogs produces synergistic GH elevation
• Evidence base focuses predominantly on biomarker changes (GH, IGF-I elevation) rather than functional outcomes
• Long-term safety data insufficient across the GH secretagogue class
• Glucose metabolism concerns: GH elevation can increase insulin resistance, elevating blood glucose and HbA1c

Research Status

As of January 2026, GHRP-6 is not FDA-approved for any medical indication and is not approved in any of the 13 countries/regions surveyed by the University of Maryland review.¹ Despite being synthesized in 1977 and serving as the founding member of the GHRP class, GHRP-6 has never progressed to regulatory approval anywhere in the world.¹ ²

The FDA-commissioned systematic review found zero clinical trials meeting inclusion criteria for therapeutic use—the most striking evidence gap among all peptides examined in the 503B Bulks List evaluation project.¹ This complete absence of qualifying studies contrasts sharply with SME reports of widespread use in “lifestyle medicine” practices, revealing perhaps the ultimate disconnect between clinical practice and evidence-based medicine.¹

All clinical use occurs outside approved indications, typically in specialized practices (urology, naturopathy, anti-aging clinics) focused on “patient demand-based medicine” for physical appearance improvements rather than medical necessity.¹ The zero survey responses from professional medical associations confirms that GHRP-6 use is essentially absent from mainstream medical practice.¹

Potential Research Applications

Growth Hormone Deficiency: GHRP-6 was nominated for GH deficiency treatment, but the University of Maryland review found zero therapeutic trials for this indication.¹ Multiple excluded studies examined GHRP-6 for diagnostic testing (identifying GH deficiency) rather than treatment, finding it comparable to the insulin tolerance test for diagnostic purposes.¹ ⁶ ⁷ However, diagnostic utility does not establish therapeutic efficacy. For documented GH deficiency, FDA-approved recombinant GH remains the evidence-based standard of care.²

Body Composition Optimization: SME interviews revealed this as the primary current application—prescribed to patients (often already on testosterone therapy) seeking lean mass gains and fat loss.¹ However, the University of Maryland review found zero clinical trials examining GHRP-6 for body composition in any population.¹ The single study in hypogonadal men examined a triple-combination (GHRP-2 / GHRP-6 / sermorelin), demonstrated IGF-I elevation but measured no functional outcomes, and suffered from significant methodological limitations.¹ ⁹

Combination Protocols: SME interviews consistently cited combination therapy (GHRP-6 + GHRP-2 + sermorelin, or GHRP-6 + CJC-1295 + ipamorelin) as common practice based on synergistic GH release mechanisms.¹ While the Bowers 1990 study demonstrated synergistic GH elevation with GHRP-6 + GHRH, no controlled trials have systematically evaluated clinical efficacy, optimal combinations, doses, or schedules for any therapeutic application.¹ ³ All combination rationale derives from pharmacological theory and acute GH measurements, not functional outcome trials.¹

Wasting Syndrome and Anorexia Nervosa: GHRP-6 was nominated for these indications, but the University of Maryland review found zero qualifying studies.¹ The theoretical rationale—GH’s anabolic effects plus appetite stimulation through ghrelin receptor activation—has not been tested in clinical trials.¹

Diagnostic Testing: While excluded from therapeutic review, multiple studies found GHRP-6 (1 µg/kg IV) alone or combined with GHRH comparable to insulin tolerance testing for diagnosing GH deficiency, with advantages including safety (no hypoglycemia risk), convenience, and rapid results.¹ ⁶ ⁷ However, this diagnostic application remains investigational and is not FDA-approved.¹

Safety Profile Summary

The University of Maryland review found zero therapeutic trials, providing no safety data for the nominated indications and dosing regimens:¹

**Known from Foundational Studies:**³

• Well-tolerated in acute pharmacology studies at doses up to 3.2 µg/kg IV
• Dose-dependent GH release without reported serious adverse events
• Brief duration studies (single doses) insufficient to assess chronic use safety

**SME Safety Perspectives:**¹

• “Much safer than growth hormones, because they’re stimulating the natural pathway”
• Intact feedback mechanism makes it “very hard to overshoot”
• “Few side effects” reported in clinical experience
• “Anecdotally over the years…they seem to be quite safe, but we don’t have the peer review literature to prove that, just yet”

**Critical Safety Gaps:**¹ ²

• No long-term safety data: Maximum exposure in published studies measured in hours to days; chronic use safety completely unknown
• No therapeutic trial safety data: Zero qualifying studies means no safety assessment for nominated indications or typical use scenarios
• IGF-I and cancer risk: Theoretical concerns about sustained IGF-I elevation and malignancy risk unaddressed by available evidence
• Glucose metabolism: GH antagonizes insulin; long-term effects on glucose tolerance and diabetes risk unknown
• Multiple daily injections: Required dosing frequency (2-3× daily) increases injection site reaction risk and compliance challenges

Important Considerations

Zero Therapeutic Evidence: The University of Maryland FDA review’s finding of zero qualifying clinical trials is unprecedented among commonly used peptides.¹ This means that all therapeutic use of GHRP-6—for GH deficiency, body composition, wasting syndrome, anorexia nervosa, or any other indication—occurs without supporting clinical trial evidence.¹ The compound has been used for decades based entirely on pharmacological reasoning (GH-releasing activity), acute biomarker changes (GH elevation), and anecdotal clinical experience.¹

“Lifestyle Medicine” Context: SME interviews revealed GHRP-6 is prescribed primarily for “patient demand-based medicine” seeking physical appearance improvements (skin, hair, body) rather than medical necessity.¹ Patients “want a desired physical outcome,” and clinicians monitor progress by physical changes rather than objective outcome measures.¹ This patient demand-driven prescribing occurs outside evidence-based medicine and mainstream medical practice.¹

Synergy Based on Theory, Not Trials: While the Bowers study demonstrated synergistic acute GH release with GHRP-6 + GHRH, SMEs acknowledged “limited literature” on optimal combinations, doses, and whether acute GH elevation translates to functional benefits.¹ ³ The widely-used GHRP-2 / GHRP-6 / sermorelin triple-combination has only one small retrospective study showing IGF-I elevation without functional outcomes.¹ ⁹ All combination prescribing occurs based on mechanistic reasoning rather than efficacy trials.¹

Rarely Used Alone: SMEs indicated GHRP-6 is “more commonly prescribed in combination” with other secretagogues than as monotherapy.¹ This practice complicates attribution of effects or adverse events to specific components, increases complexity and cost, and multiplies injection burden for patients.¹

Diagnostic vs. Therapeutic Confusion: Multiple studies examined GHRP-6 for diagnostic testing (identifying GH deficiency), finding it useful for this purpose.¹ ⁶ ⁷ However, diagnostic utility does not establish therapeutic efficacy. The ability to stimulate acute GH release does not prove that chronic GHRP-6 administration produces clinically meaningful functional benefits.¹

Multiple Daily Injections Required: GHRP-6’s short half-life necessitates 2-3 daily subcutaneous injections to maintain GH secretory capacity, timed to circadian GH rhythm.¹ This creates substantial compliance burden compared to weekly alternatives (CJC-1295 with DAC), makes in-office administration impractical, and requires patient self-administration skills.¹

Dosing Based on Anecdote: SMEs acknowledged “limited literature” on optimal dosing, with patients started on low doses (100-500 µg/day) and titrated based on tolerance and desired outcomes rather than evidence-based protocols.¹ Typical community-used doses derive from clinical experience, not dose-finding trials.¹

Product Quality Variability: As an unapproved compound available only through research suppliers and compounding pharmacies, GHRP-6 product quality, purity, and dosage accuracy vary substantially.¹ No regulatory oversight ensures product consistency or safety. The peptide structure makes it susceptible to degradation if not properly stored.¹

Not Approved Anywhere Globally: Unlike some peptides approved in select countries, GHRP-6 is not approved in any of the 13 countries/regions surveyed—representing a complete global absence of regulatory approval despite 47+ years since synthesis.¹ This universal rejection by regulatory agencies worldwide is notable and suggests fundamental limitations in risk-benefit profile or development challenges.

Superseded by Newer GHRPs: GHRP-6 served as the scaffold for developing more potent (GHRP-2, hexarelin) and more selective (ipamorelin) GHRPs.² These second-generation compounds offer pharmacological advantages (greater potency, improved selectivity, longer half-life variants), yet none have achieved FDA approval for therapeutic use.² The collective failure of the entire GHRP class to achieve approval raises questions about the therapeutic utility of this approach.²

Preclinical Cardioprotection Not Validated: Excluded studies demonstrated potent cardioprotective effects of GHRP-6 in animal models of myocardial ischemia, reducing infarct size by 78% and preserving cardiac function.¹⁰ While scientifically interesting, preclinical cardioprotection has not translated to human clinical trials or regulatory approval.¹ The disconnect between promising preclinical effects and absence of clinical development suggests either translational failure, safety concerns, or commercial challenges.

Regulatory and Legal Status: GHRP-6 is not FDA-approved for any indication and is prohibited by WADA for competitive athletes.¹ Use outside approved clinical trials may carry legal and professional consequences. Prescribing occurs in regulatory gray zones without established clinical guidelines or professional society endorsement.¹

Alternative Approaches Exist: For documented GH deficiency, FDA-approved recombinant GH provides evidence-based treatment with established safety and efficacy.² For body composition and performance enhancement, no peptide-based secretagogue has sufficient evidence to recommend over proven interventions (progressive resistance training, adequate protein intake, sleep optimization) with established efficacy and safety profiles.²

1. University of Maryland Center of Excellence in Regulatory Science and Innovation (M-CERSI).
2. Sigalos JT, Pastuszak AW. Sexual Medicine Reviews. 2018;6(1):45-53.
3. Bowers CY, Reynolds GA, Durham D, Barrera CM, Pezzoli SS, Thorner MO. Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone. Journal of Clinical Endocrinology & Metabolism. 1990;70(4):975-982.
4. Pharmacokinetic study of Growth Hormone-Releasing Peptide 6 (GHRP-6) in nine healthy male participants. Clinical Trials. 2013.
5. Casanueva FF, Dieguez C. Growth hormone secretagogues: Physiological role and clinical utility. Trends in Endocrinology and Metabolism. 1999;10(1):30-38.
6. Popovic V, Leal A, Micic D, et al. GH-releasing hormone and GH-releasing peptide-6 for diagnostic testing in GH-deficient adults. Lancet. 2000;356(9236):1137-1142.
7. Petersenn S, Jung R, Beil FU. Diagnosis of growth hormone deficiency in adults by testing with GHRP-6 alone or in combination with GHRH: Comparison with the insulin tolerance test. European Journal of Endocrinology. 2002;146(5):667-672.
8. Alaioubi B, Mann K, Petersenn S. Diagnosis of growth hormone deficiency in adults: provocative testing with GHRP6 in comparison to the insulin tolerance test. Hormone & Metabolic Research. 2009;41(3):238-243.
9. Sigalos JT, Pastuszak AW, Allison A, et al. Growth hormone secretagogue treatment in hypogonadal men raises serum insulin-like growth factor-1 levels. American Journal of Men’s Health. 2017;11(6):1752-1758.
10. Berlanga J, Cibrian D, Guillén I, et al. Growth-hormone-releasing peptide 6 (GHRP6) prevents oxidant cytotoxicity and reduces myocardial necrosis in a model of acute myocardial infarction. Clinical Science. 2007;112(4):241-250.

Comprehensive Systematic Review

University of Maryland Center of Excellence in Regulatory Science and Innovation (M-CERSI).

Foundational Study

Journal of Clinical Endocrinology & Metabolism. PMID: 2180977.

Broader GH Secretagogue Reviews

Sexual Medicine Reviews. PMID: 28400207.

Casanueva FF, Dieguez C. Growth hormone secretagogues: Physiological role and clinical utility. Trends in Endocrinology and Metabolism..

Diagnostic Testing Studies

Lancet. PMID: 11030302.

European Journal of Endocrinology. PMID: 11980622.

Alaioubi B, Mann K, Petersenn S. Diagnosis of growth hormone deficiency in adults: provocative testing with GHRP6 in comparison to the insulin tolerance test. Hormone & Metabolic Research.

Additional Studies

Sigalos JT, Pastuszak AW, Allison A, et al. Growth hormone secretagogue treatment in hypogonadal men raises serum insulin-like growth factor-1 levels. American Journal of Men’s Health.

Berlanga J, Cibrian D, Guillén I, et al. Growth-hormone-releasing peptide 6 (GHRP6) prevents oxidant cytotoxicity and reduces myocardial necrosis in a model of acute myocardial infarction. Clinical Science.

This content is for educational and research purposes only and does not constitute medical advice. GHRP-6 is not FDA-approved for any medical indication and is not approved in any country surveyed by comprehensive regulatory review. A 2021 FDA-commissioned systematic review identified zero human clinical trials meeting inclusion criteria for therapeutic use, despite nomination for growth hormone deficiency, wasting syndrome, and anorexia nervosa. All current clinical use occurs without supporting clinical trial evidence. Subject matter experts acknowledge “limited outcomes-based human research” and that evidence is lacking to determine “the ideal combination and dose of medication to use, and the effects of long-term use.” Current evidence does not support efficacy for any therapeutic application. All products are intended strictly for laboratory research and development purposes only.