Reviewed & approved by Dr. Nova Reyes · Last checked 2026-10-24. ← Back to Evidence Library

GHRP-6

Growth hormone-releasing peptide-6 · His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 · SK&F 110679 · CIGB-500

Status: Approved for Adam Greene by Dr. Nova Reyes, 2026-10-24

Legend: HUMAN data · ANIMAL / LAB data · UNKNOWN · UNVERIFIED: not yet confirmed against a primary source

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1. What it is and what people claim it does

GHRP-6 (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) is a synthetic hexapeptide (6-amino-acid peptide) created in the early 1980s by Cyril Bowers, Frank Momany, and colleagues by chemically modifying met-enkephalin (a natural opioid peptide in the body) until it lost opioid painkiller activity and gained the ability to trigger growth hormone (GH) release from the anterior pituitary gland (the hormone-releasing gland at the base of the brain). ^R1 Long before scientists discovered the stomach hormone ghrelin in 1999, GHRP-6 served as the prototype molecule used to clone the growth hormone secretagogue receptor (GHSR-1a, now known as the ghrelin receptor).

Because GHRP-6 activates the ghrelin receptor in both the pituitary gland and the hypothalamus (the brain's appetite and hormone control center) and also binds to the scavenger receptor CD36 (a cell-surface protein involved in fatty-acid uptake and inflammation) in animal tissues, it has been studied in two very different worlds: 1. Clinical endocrinology (1990s–2010s): Endocrinologists used single intravenous injections of GHRP-6—alone or combined with growth hormone-releasing hormone (GHRH)—as a provocative diagnostic test to see whether a patient's pituitary gland could still produce growth hormone. ^R4–R8 2. Gray-market fitness and biohacking: Online vendors sell freeze-dried GHRP-6 vials for subcutaneous injection (often stacked with CJC-1295 no-DAC / Mod GRF 1-29), pitching it for lean muscle mass, appetite stimulation during "bulking" cycles, tendon and wound healing, and cardioprotection. In Cuba, the Center for Genetic Engineering and Biotechnology (CIGB) has also researched GHRP-6 under the code CIGB-500 for organ protection and acute myocardial infarction (heart attack) in animals and a small human pharmacokinetic study. ^R13–R16

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2. What the human evidence actually shows

The Open Peptide Project's reading: Moderate for single-dose IV diagnostic testing of adult GH deficiency (when combined with GHRH), Limited for acute pituitary hormone release in short physiological studies, and No human data (animal/lab only) for muscle gain, fat loss, tendon/wound repair, cardiac protection, or anti-aging.

Indication	Route studied	Evidence rating	Summary of human studies
Diagnostic testing for adult growth hormone deficiency (combined GHRH + GHRP-6 test)	Single intravenous bolus	Moderate	Validated against the gold-standard insulin tolerance test (ITT) in large multicenter cohorts—including 250 adults (Popovic et al., Lancet 2000), 542 obese and non-obese adults (Kelestimur et al., 2006), 20 pituitary patients (Petersenn et al., 2002), and reproducibility testing across 4 repeat visits (Popovic et al., 2004). R5–R8
Acute GH, ACTH, and cortisol stimulation in healthy adults, older adults, and short children	Intravenous, oral, intranasal, or sublingual	Limited	Small physiological studies (7 to 69 people) show that GHRP-6 acutely raises blood GH—even when given orally or intranasally at high doses—while simultaneously raising ACTH and cortisol and altering Stage 2 sleep. R1–R4, R9–R12
Human pharmacokinetics (how the body clears the drug) at cell-protecting IV doses (CIGB-500 program)	Single intravenous bolus	Very limited	One Cuban Phase 1 pharmacokinetic study in 9 healthy men measured plasma clearance and half-life (~2.5 hours elimination half-life) without testing clinical efficacy. R13
Muscle hypertrophy, fat loss, tendon/wound healing, heart attack rescue, or anti-aging	Subcutaneous or topical	No human data	Animal/lab only: Zero human clinical trials measure body composition, muscle strength, tendon healing, scar reduction, or cardiac outcomes. Wound and heart studies are in rats, rabbits, pigs, and beagle dogs. R14–R16

Diagnostic pituitary testing: where GHRP-6 actually has strong human validation

In clinical medicine, diagnosing adult growth hormone deficiency requires a stimulation test because baseline daytime GH levels are naturally near zero. The traditional gold standard—the insulin tolerance test (ITT)—uses intravenous insulin to induce symptomatic low blood sugar (hypoglycemia), which is uncomfortable and dangerous in patients with heart disease or seizures.

• Multicenter Lancet validation (Popovic et al., 2000): Across 125 adults with organic pituitary disease and 125 healthy controls, a single combined intravenous injection of GHRH + GHRP-6 produced a massive GH spike in healthy adults (mean peak 59.2 mcg/L) compared with GH-deficient patients (mean peak 4.1 mcg/L), cleanly separating the two groups without hypoglycemic side effects. ^R5
• Head-to-head comparison and reproducibility (Petersenn et al., 2002; Popovic et al., 2004): In 20 adults evaluated for pituitary disease, GHRP-6 alone or combined with GHRH matched the diagnostic sensitivity and specificity of the insulin tolerance test, with brief facial flushing as the only reported side effect. ^R6 A 2004 study testing 17 healthy adults four separate times over several months confirmed high test-retest reproducibility. ^R7
• Obesity-adjusted cutoffs (Kelestimur et al., 2006): In 542 adults (including 105 obese and 50 morbidly obese participants), researchers showed that severe obesity blunts the GH peak by about 25% and established BMI-adjusted diagnostic cutoffs for the GHRH + GHRP-6 test. ^R8
• Why GHRP-6 alone fails as an adrenal insufficiency test (Alaioubi, Mann & Petersenn, 2010): Because GHRP-6 also stimulates pituitary ACTH and adrenal cortisol, German investigators tested whether a single GHRP-6 injection could replace the insulin tolerance test for diagnosing adrenal insufficiency in 49 patients and 20 healthy controls. While GHRP-6 did raise cortisol, its diagnostic accuracy (71% sensitivity, 77.8% specificity) was too low to replace standard adrenal testing. ^R12

Acute GH, sleep, and hormone studies—and receptor desensitization

• Prolonged infusion and partial desensitization (Jaffe et al., 1993): In 9 healthy young men given a continuous intravenous GHRP-6 infusion vs saline, pulsatile GH secretion and plasma IGF-1 (from 252 to 312 mcg/L) rose over the infusion window, but the pituitary's GH response to a subsequent bolus of GHRP-6 at the end of the infusion was significantly blunted—demonstrating rapid homologous receptor desensitization (the receptor becoming temporarily less responsive to the same drug) when exposure is continuous. ^R2
• Short oral and intranasal studies in children and older women (Ghigo et al., 1994; Bellone et al., 1995): Small Italian studies in 7 healthy older women (aged 65–82) ^R9 and 13 prepubertal children with normal short stature ^R10 showed that high-dose oral GHRP-6 (at a much higher amount than the IV diagnostic test because less than 1% is absorbed by mouth; see Study details) acutely raised blood GH levels, though short pretreatment did not significantly raise circulating IGF-1 in the older women.
• Nocturnal sleep and stress-hormone spikes (Frieboes et al., 1995 and 1999): In healthy young men studied in a sleep laboratory, nocturnal intravenous boluses of GHRP-6 increased GH and slightly increased Stage 2 non-REM sleep, but unlike GHRH (which increases deep slow-wave sleep and lowers nighttime cortisol), GHRP-6 did not increase slow-wave sleep and significantly increased nighttime ACTH and cortisol (stress-hormone) secretion. ^{R11, R12}

Why gray-market muscle, wound-healing, and cardiac claims have no human data

• No human body-composition or athletic trials: Not a single human trial has tested whether repeated GHRP-6 injections increase lean muscle mass, reduce body fat, or improve athletic recovery.
• Animal-only wound, organ, and cardiac studies (CIGB-500): Cuban researchers at CIGB published a Phase 1 pharmacokinetic study of high-dose IV GHRP-6 in 9 healthy male volunteers (Cabrales et al., 2013) ^R13, alongside preclinical studies showing reduced intestinal ischemia-reperfusion injury (tissue damage when blood flow returns after a cut-off) in rats (Cibrián et al., 2006) ^R14, reduced exuberant scar formation with a topical GHRP-6 jelly on rat and rabbit ear wounds (Mendoza Marí et al., 2016) ^R15, and a repeated-dose intravenous toxicology study of CIGB-500 in beagle dogs (Castro et al., 2025) ^R16. None of these tissue-repair or cardiac outcomes has published human efficacy trial data on PubMed.

Study details — click to expand all human study rows (doses, schedules, outcomes, and side effects)

Study (Year)	Design & Population	Route, Dose & Schedule	Primary / Key Outcomes	Adverse Events & Dropouts	Funding & Disclosures
Jaffe et al. (1993) R2	Randomized crossover physiological study; 9 healthy young men	IV infusion: 1 mcg/kg IV loading bolus followed by 1 mcg/kg/hour continuous IV infusion for 34 hours vs normal saline (with GHRH/TRH/GHRP boluses on day 2)	Integrated GH concentration doubled (2,908 ± 450 vs 1,374 ± 160 mcg·min/L), plasma IGF-1 rose from 252 ± 23 to 312 ± 23 mcg/L, and GH response to GHRH was augmented; however, GH response to a repeat GHRP-6 bolus at hour 32 was blunted (homologous desensitization) and baseline TSH fell.	No serious adverse events reported; 0 dropouts.	University of Michigan & VA Medical Center (Ann Arbor, MI); academic NIH/VA support.
Peñalva et al. (1993) R3	Acute endocrine challenge study; 25 healthy adults (16 men, 9 women) and 12 healthy prepubertal children (6 boys, 6 girls)	IV bolus: 1 mcg/kg IV single bolus at time 0 (alone or after oral propranolol 40 mg, clonidine 300 mcg, or prazosin 3 mg in adult male subgroups)	Potent acute GH spike across children, adult men, and women across menstrual-cycle phases (independent of sex and age at this single dose).	Well tolerated; no dropouts.	University of Santiago de Compostela, Spain.
Ghigo et al. (1994) R9	Short-term open-label study; 7 healthy elderly women (ages 65–82)	Oral: 300 mcg/kg orally tested before and after 4 days of oral GHRP-6 (300 mcg/kg twice daily), compared against IV GHRH (1 mcg/kg)	Acute oral GHRP-6 elicited a higher GH peak (10.7 ± 3.3 mcg/L) than IV GHRH (5.1 ± 1.5 mcg/L); after 4 days of twice-daily oral dosing, the acute GH response was maintained (peak 16.8 ± 2.9 mcg/L), but serum IGF-1 did not increase significantly (77.1 ± 8.4 vs 84.1 ± 12.2 mcg/L).	No adverse events or dropouts reported.	University of Turin, Italy.
Popovic et al. (1995) R4	Case-control mechanistic study; 12 patients with hypothalamo-pituitary disconnection (stalk section) and 11 matched healthy controls	IV bolus: Single challenges on separate days with GHRH (100 mcg IV), GHRP-6 (90 mcg IV), or combined GHRH + GHRP-6	In healthy controls, GHRP-6 (AUC 1,434.8) and GHRH + GHRP-6 (AUC 3,771.5) caused massive synergistic GH release; in patients with pituitary stalk disconnection, GHRP-6-induced GH release was completely blocked (AUC 97.3), proving GHRP-6 acts primarily via the intact hypothalamus/stalk.	No serious adverse events; 0 dropouts.	University Clinical Center Belgrade & University of Santiago de Compostela.
Frieboes et al. (1995 & 1999) R11, R12	Placebo-controlled crossover sleep-EEG and endocrine studies; healthy young men (n = 7–10 per protocol)	IV boluses (1995): 4 × 50 mcg IV boluses hourly (22:00–01:00) vs placebo. Oral / Intranasal / Sublingual (1999): 300 mcg/kg oral enteric-coated capsule, 30 mcg/kg intranasal, or 30 mcg/kg sublingual before sleep vs placebo	IV (1995): Increased nocturnal GH (15.4 vs 5.5 ng/mL), ACTH (21.0 vs 16.6 pg/mL), cortisol (56.0 vs 25.2 ng/mL, more than doubled in first half of night), and Stage 2 sleep (270 vs 245 min), with no increase in deep slow-wave sleep. 1999 routes: Intranasal (30 mcg/kg) significantly increased nocturnal GH; enteric-coated oral (300 mcg/kg) failed to raise nocturnal GH and reduced Stage 2 sleep.	No serious adverse events; 0 dropouts.	Max Planck Institute of Psychiatry, Munich, Germany.
Bellone et al. (1995) R10	Acute comparative crossover study; 13 prepubertal children (9 boys, 4 girls, ages 6.2–10.5) with normal short stature	Oral: Single oral dose of 300 mcg/kg GHRP-6 (alone or with oral arginine 4 g) vs IV GHRH (1 mcg/kg)	Single oral GHRP-6 raised GH (peak 18.8 ± 3.0 mcg/L at 60 min vs 1.1 mcg/L baseline), similar to IV GHRH (peak 20.8 ± 4.5 mcg/L). Acute single-dose hormone test only; did not measure height velocity or long-term growth.	Transient mild facial flushing after IV GHRH; no adverse events reported after oral GHRP-6.	University of Turin & University of Parma, Italy.
Popovic et al. (2000) R5	Multicenter diagnostic validation study (The Lancet); 125 adults with organic pituitary disease (severe GHD) and 125 healthy adult controls	IV bolus: Single combined bolus of GHRH (1 mcg/kg IV) + GHRP-6 (1 mcg/kg IV) at time 0 (blood sampled over 120 min), compared against insulin tolerance test (ITT)	Mean GH peak was 59.2 ± 2.2 mcg/L in healthy controls vs 4.1 ± 0.3 mcg/L in GHD patients (p < 0.001); cutoff of >=20 mcg/L normal and <=10 mcg/L GHD accurately diagnosed adult GH deficiency independent of age or sex.	Authors reported no side effects from the single combined diagnostic bolus and 0 dropouts.	Multicenter academic study (Belgrade, Santiago de Compostela, London, Turin).
Petersenn, Jung & Beil (2002) R6	Diagnostic comparison study; 20 adults evaluated for pituitary/adrenal disease (10 GH-deficient, 10 GH-sufficient by ITT)	IV bolus: GHRP-6 alone (1 mcg/kg IV) and GHRP-6 (1 mcg/kg IV) + GHRH (1 mcg/kg IV) on separate days vs ITT	Mean GH peak on GHRP-6 alone: 1.3 mcg/L (GHD) vs 25.7 mcg/L (GH-sufficient) (100% sensitivity/specificity at <7 mcg/L cutoff). On GHRP-6 + GHRH: 4.0 vs 54.7 mcg/L (<13 mcg/L cutoff).	Transient facial flushing was the only adverse event reported; 0 dropouts.	University Clinic Eppendorf, Hamburg, Germany.
Popovic et al. (2004) & Kelestimur et al. (2006) R7, R8	Reproducibility study in 17 healthy adults tested 4 times R7; obesity validation study in 542 adults (261 non-obese, 105 obese, 50 morbidly obese, 176 GHD) R8	IV bolus: Combined GHRH (1 mcg/kg IV) + GHRP-6 (1 mcg/kg IV) single bolus	High test-retest reproducibility across 4 visits (mean peaks 46.0 to 52.9 mcg/L, r = 0.68–0.73) R7; in morbid obesity (BMI > 35), GH peak is blunted by ~25%, requiring lower diagnostic cutoffs (<=5 mcg/L for GHD, >=15 mcg/L for normal) R8.	Well tolerated; no serious adverse events.	European multicenter academic endocrinology consortium.
Alaioubi, Mann & Petersenn (2010) R12	Diagnostic comparison study for adrenal insufficiency; 49 patients with suspected HPA-axis disease and 20 healthy controls	IV bolus: Single GHRP-6 (1 mcg/kg IV) bolus (cortisol measured over 90 min) vs insulin tolerance test (ITT)	Mean serum cortisol peak was 227 ± 25.7 nmol/L in adrenal-insufficient patients vs 395 ± 35.3 nmol/L in adrenal-sufficient patients; optimal cutoff (299 nmol/L) had only 71.0% sensitivity and 77.8% specificity—insufficient accuracy to replace standard adrenal testing.	No detectable side effects reported; 0 dropouts.	University of Duisburg-Essen, Germany.
Cabrales et al. (2013) R13	Phase 1 open-label dose-escalation pharmacokinetic study; 9 healthy men (3 per dose cohort)	IV bolus: Single high-dose IV bolus of 100, 200, or 400 mcg/kg GHRP-6 (blood sampled over 12 hours by LC-MS)	Distribution half-life 7.6 ± 1.9 min and elimination half-life 2.5 ± 1.1 hours; AUC increased proportionally with dose; atypical secondary plasma concentration spikes occurred during elimination in 4 of 9 men.	Adverse-event table not detailed in abstract; 0 dropouts.	Center for Genetic Engineering and Biotechnology (CIGB), Havana, Cuba (developer of CIGB-500).

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3. Known risks, side effects, and long-term unknowns

• Non-selective hormone spikes (ACTH, cortisol, and prolactin): Unlike ipamorelin (which was specifically engineered by Novo Nordisk in 1998 to avoid stimulating the adrenal and prolactin axes ^R17), GHRP-6 is non-selective. In human studies, GHRP-6 consistently triggers acute spikes in adrenocorticotropic hormone (ACTH), cortisol (sometimes doubling nighttime cortisol after repeated IV boluses ^R11), and prolactin.
• Worsened insulin sensitivity and raised blood glucose (FDA safety warning): In its September 29, 2023 compounding safety evaluation, the US FDA explicitly warned that available data on GHRP-6 reveal "safety concerns including potential effect on cortisol and increase in blood glucose due to decreases in insulin sensitivity." ^R18 Because both growth hormone and cortisol antagonize insulin action, repeated GHRP-6 dosing can push blood sugar and fasting insulin upward.
• Intense ghrelin-mimetic hunger and gastric emptying effects: Because GHRP-6 directly activates hypothalamic and vagal ghrelin (GHSR-1a) receptors, subcutaneous injections frequently cause sudden, intense hunger cravings ("the GHRP-6 hunger spike"), sweating, and lightheadedness that can mimic low blood sugar.
• Immunogenicity and unnatural D-amino acids (FDA safety warning): GHRP-6 contains two unnatural D-stereoisomer amino acids (D-Trp and D-Phe). The FDA warns that compounded GHRP-6 "may pose risk for immunogenicity for certain routes of administration due to the potential for aggregation and peptide-related impurities." ^R18
• Theoretical IGF-1 and tumor-growth concern: Any compound that chronically raises pulsatile GH and circulating IGF-1 carries a theoretical risk of promoting cell proliferation in pre-existing hormone-sensitive or pre-malignant lesions.

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4. Regulatory and compounding status

Jurisdiction / Body	Current Status	Details
United States (FDA — Drugs@FDA)	Not FDA-approved	GHRP-6 has never been approved by the US FDA as a diagnostic or therapeutic drug (checked via openFDA Drugs@FDA Oct 24, 2026). R19
United States (FDA — 503A / 503B Compounding)	Banned from compounding (503B Category 2 "Significant Safety Risks" & 503A Category 3)	On September 29, 2023, the FDA placed Growth hormone releasing peptide-6 (GHRP-6) on its Category 2 ("Bulk Drug Substances that Raise Significant Safety Risks") list for 503B outsourcing facilities—citing immunogenicity from aggregation/impurities, cortisol effects, and increased blood glucose from decreased insulin sensitivity—and lists GHRP-6 in 503A Category 3 ("Nominated Without Adequate Support") (updated May 14, 2026). Neither 503A pharmacies nor 503B outsourcing facilities may legally compound GHRP-6 for human use in the US. R18, R20, R21
European Union & United Kingdom (EMA / MHRA)	Not an authorised medicine	Neither EMA nor MHRA has approved GHRP-6 as a commercial medicinal product (hospital endocrinology units historically prepared research-grade diagnostic ampoules under academic/compassionate protocols).
World Anti-Doping Agency (WADA 2026)	Explicitly prohibited at all times (Section S2.2.4)	GHRP-6 is explicitly named on the 2026 WADA Prohibited List under Section S2.2.4 (Growth Hormone Releasing Factors — GH-releasing peptides [GHRPs]), banned both in- and out-of-competition. It is routinely detected in urine and blood anti-doping screens. R22

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5. Quality, contamination, and gray-market risks

1. Swapped GHRP vials (GHRP-6 vs GHRP-2 vs Hexarelin vs Ipamorelin): Forensic doping-control laboratories analyzing seized and online "research peptide" vials have repeatedly documented mislabeled or cross-contaminated GHRP vials—where a vial labeled Ipamorelin or GHRP-6 contains GHRP-2 or Hexarelin instead. Because GHRP-6, GHRP-2, and hexarelin have much stronger cortisol, prolactin, and appetite effects than ipamorelin, a swapped vial changes the hormone and side-effect profile immediately.
2. Thermal degradation and peptide aggregation: A 2021 mass-spectrometry stability study (J Pharm Biomed Anal, PMID 33272786) demonstrated that GHRP-6 in solution undergoes thermal and pH-dependent chemical modification and aggregation—the exact impurity hazard flagged by the FDA's 2023 immunogenicity warning. ^R18
3. Blind retail testing: We test retail vials blind under the Open Peptide Standard. See results at /tests/. A passing test covers one batch, tested on one date. It does not mean the compound itself is safe.

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6. Who should be especially cautious

• People with prediabetes, type 1 or type 2 diabetes, or insulin resistance: Both growth hormone and cortisol oppose insulin and raise blood glucose, a risk specifically highlighted by the FDA for GHRP-6. ^R18
• Anyone with active cancer, a history of cancer, or benign pituitary adenomas: GH/IGF-1 stimulation is contraindicated in active malignancy.
• People with Cushing's syndrome, hyperprolactinemia, or severe anxiety/insomnia: GHRP-6 acutely stimulates ACTH, cortisol, and prolactin and can fragment nighttime sleep architecture depending on route and timing. ^{R11, R12}
• Tested competitive athletes: GHRP-6 is explicitly named and banned at all times under WADA S2.2.4 and is easily detected by standard LC-MS/MS doping tests. ^R22
• Pregnant or breastfeeding women and children/adolescents outside specialist endocrinology testing: Chronic use has never been proven safe or effective for pediatric growth.

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7. Open questions and research gaps

1. Does chronic subcutaneous GHRP-6 actually change lean muscle mass, visceral fat, or tendon healing in humans, or does receptor desensitization—combined with rising cortisol and hunger—cancel out the acute GH pulses?
2. Will Cuba's CIGB-500 intravenous cardiac/cytoprotective program publish randomized, controlled human clinical outcome trials in peer-reviewed journals?

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8. References

1. ^R1 Bowers CY. GH releasing peptides—structure and kinetics. J Pediatr Endocrinol. 1993;6(1):21–31. PMID 8374685
2. ^R2 Jaffe CA, Ho PJ, Demott-Friberg R, Bowers CY, Barkan AL. Effects of a prolonged growth hormone (GH)-releasing peptide infusion on pulsatile GH secretion in normal men. J Clin Endocrinol Metab. 1993;77(6):1641–1647. PMID 7903313
3. ^R3 Peñalva A, Pombo M, Carballo A, Barreiro J, Casanueva FF, Dieguez C. Influence of sex, age and adrenergic pathways on the growth hormone response to GHRP-6. Clin Endocrinol (Oxf). 1993;38(1):87–91. PMID 8435889
4. ^R4 Popovic V, Damjanovic S, Micic D, Djurovic M, Dieguez C, Casanueva FF. Blocked growth hormone-releasing peptide (GHRP-6)-induced GH secretion and absence of the synergic action of GHRP-6 plus GH-releasing hormone in patients with hypothalamopituitary disconnection: evidence that GHRP-6 main action is exerted at the hypothalamic level. J Clin Endocrinol Metab. 1995;80(3):942–947. PMID 7883854
5. ^R5 Popovic V, Leal A, Micic D, Koppeschaar HP, Torres E, Paramo C, Obradovic S, Dieguez C, Casanueva FF. GH-releasing hormone and GH-releasing peptide-6 for diagnostic testing in GH-deficient adults. Lancet. 2000;356(9236):1137–1142. PMID 11030292
6. ^R6 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. Eur J Endocrinol. 2002;146(5):667–672. PMID 11980622
7. ^R7 Popovic V, Pekic S, Micic D, et al. Evaluation of the reproducibility of the GHRH plus GHRP-6 test of growth hormone reserve in adults. Clin Endocrinol (Oxf). 2004;60(2):185–191. PMID 14725679
8. ^R8 Kelestimur F, Popovic V, Leal A, et al. Effect of obesity and morbid obesity on the growth hormone (GH) secretion elicited by the combined GHRH + GHRP-6 test. Clin Endocrinol (Oxf). 2006;64(6):667–671. PMID 16712669
9. ^R9 Ghigo E, Arvat E, Rizzi G, et al. Growth hormone-releasing activity of growth hormone-releasing peptide-6 is maintained after short-term oral pretreatment with the hexapeptide in normal aging. Eur J Endocrinol. 1994;131(5):499–503. PMID 7952160
10. ^R10 Bellone J, Ghizzoni L, Aimaretti G, et al. Growth hormone-releasing effect of oral growth hormone-releasing peptide 6 (GHRP-6) administration in children with short stature. Eur J Endocrinol. 1995;133(4):425–429. PMID 7581965
11. ^R11 Frieboes RM, Murck H, Maier P, Schier T, Holsboer F, Steiger A. Growth hormone-releasing peptide-6 stimulates sleep, growth hormone, ACTH and cortisol release in normal man. Neuroendocrinology. 1995;61(5):584–589. PMID 7617137
12. ^R12 Frieboes RM, Murck H, Antonijevic IA, Steiger A. Effects of growth hormone-releasing peptide-6 on the nocturnal secretion of GH, ACTH and cortisol and on the sleep EEG in man: role of routes of administration. J Neuroendocrinol. 1999;11(6):473–478. PMID 10336729; see also Alaioubi B, Mann K, Petersenn S. Diagnosis of adrenal insufficiency using the GHRP-6 Test: comparison with the insulin tolerance test in patients with hypothalamic-pituitary-adrenal disease. Horm Metab Res. 2010;42(3):198–203. PMID 19946832
13. ^R13 Cabrales A, Gil J, Fernández E, et al. 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 23099431
14. ^R14 Cibrián D, Ajamieh H, Berlanga J, et al. Use of growth-hormone-releasing peptide-6 (GHRP-6) for the prevention of multiple organ failure. Clin Sci (Lond). 2006;110(5):563–573. PMID 16417467
15. ^R15 Mendoza Marí Y, Fernández Mayola M, Aguilera Barreto A, et al. Growth Hormone-Releasing Peptide 6 Enhances the Healing Process and Improves the Esthetic Outcome of the Wounds. Plast Surg Int. 2016;2016:4361702. PMID 27200188
16. ^R16 Castro J, Shaikh I, Silo S, et al. Subchronic safety assessment of CIGB-500 in beagle dog after repeated daily dose administration over 28 days. Regul Toxicol Pharmacol. 2025;159:105811. PMID 40024561
17. ^R17 Raun K, Hansen BS, Johansen NL, et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552–561. PMID 9849822
18. ^R18 U.S. Food and Drug Administration. Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks — entry for "Growth hormone releasing peptide-6 (GHRP-6)" (added September 29, 2023; content current April 22, 2026). FDA Compounding Safety Risks Page
19. ^R19 U.S. Food and Drug Administration. Drugs@FDA: FDA-Approved Drugs (searched via openFDA Oct 24, 2026 for "GHRP-6": no approved drug products). Drugs@FDA
20. ^R20 U.S. Food and Drug Administration. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the Federal Food, Drug, and Cosmetic Act — Category 3 entry for "GHRP-6" (updated May 14, 2026). FDA 503A Nominations PDF
21. ^R21 U.S. Food and Drug Administration. Bulk Drug Substances Nominated for Use in Compounding Under Section 503B of the Federal Food, Drug, and Cosmetic Act — Category 2 entry for "GHRP-6" (updated March 21, 2025). FDA 503B Nominations PDF
22. ^R22 World Anti-Doping Agency (WADA). The World Anti-Doping Code International Standard: Prohibited List (January 2026) — Section S2.2.4 (Growth Hormone Releasing Factors: GH-releasing peptides [GHRPs], explicitly naming GHRP-6). WADA Prohibited List

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Disclaimer

This page is for education and harm reduction. It is not medical advice and not a recommendation to use this compound. Please talk to a clinician you trust before making medical decisions, and report adverse events to FDA MedWatch (https://www.fda.gov/safety/medwatch).