Dashnaiv Peptides
Compounds·ghrelin mimetics·ghrelin receptor (GHS-R1a) agonist

GHRP-6 peptide: what the endocrine studies and the Cuban stroke trial measured, why it makes you hungry, and what was never tested

What 738 indexed publications and 22 randomized trials actually state about ghrp-6, sentence by sentence, each tied to its source and labeled by the kind of evidence it is.

Human clinical trial Reviewed 48 sources Updated

At a glance

Evidence availability
Human clinical evidence
Strongest tier in the indexed literature
Indexed publications
738
Europe PMC, title or abstract, 2026-09-14
Human studies in ledger
12
5 randomized; study count, not efficacy proof
Approval
none found
no registered development programme
Routes reported
intranasal, intravenous, oral, subcutaneous
from studies in this ledger
Studied in
Dogs, Humans, Mice, Rats
24 primary studies in the evidence table
Reviewed by Adam Mirando, PharmD, on . What changed

What GHRP-6 is, and what the endocrine studies actually measured

GHRP-6 is a peptide in the ghrelin mimetics class (ghrelin receptor (GHS-R1a) agonist). Europe PMC indexes 738 publications naming it or a listed alias in a title or abstract, including 22 randomized controlled trials and 41 clinical trials of any design, as of . The strongest evidence tier in that literature is human clinical trials.

This page reports what those studies state, sentence by sentence, with each statement tied to its source and labeled by the kind of evidence it is. It does not recommend use, and it does not translate study doses into anything personal.

What the evidence level means

Publication counts show what is indexed, not how strong the evidence is. The ledger below separates human clinical records from preclinical, analytical, and in-vitro work.

Human clinical studies in this ledger125 randomized · 7 other human clinical
Evidence strengthNot yet assessedSeparate from evidence availability
Efficacy signalNot yet assessedRead the study result, not the tier alone

Interpretation boundary: An indexed publication count is a discovery measure. It does not establish efficacy, safety, approval, or a personal treatment plan.

GHRP-6 in two minutes

What it is. The first growth hormone releasing peptide, a six-amino-acid ghrelin mimic from 1984 whose receptor search discovered ghrelin itself. It makes the pituitary release a pulse of growth hormone and makes people hungry, by the same mechanism.

What the research actually shows. 738 indexed publications, most of them 1990s endocrinology: single intravenous doses raise growth hormone within an hour, far more when combined with GHRH, and also raise ACTH, cortisol and prolactin. The GHRH plus GHRP-6 test was validated as a diagnostic for growth hormone deficiency in 250 people. A Cuban phase 3 trial gave GHRP-6 with EGF to 95 stroke patients for seven days and found no difference in disability.

What was never measured. Muscle, fat, strength or recovery in people, by any route, over any period. No human study in the ledger used subcutaneous injection.

Status. Never approved. Named on the WADA list under S2. Its cousin GHRP-2 is a Japanese diagnostic; its cousin ipamorelin is the one people switched to for less cortisol and hunger.

Where the evidence is thinnest. Everything about the way it is used: subcutaneous, three times a day, for months.

Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.

How it works

Written from general pharmacology and the development record, and marked as editorial synthesis; the measurements behind it are quoted in the biomarker section.

  • GHRP-6 is the hexapeptide His-D-Trp-Ala-Trp-D-Phe-Lys-NH2, built by Cyril Bowers' group in 1984 from an enkephalin analogue that happened to release growth hormone. It was the first growth hormone releasing peptide and the founder of the family that includes GHRP-2, hexarelin and ipamorelin. Its importance to science is larger than its use: the search for its receptor found the growth hormone secretagogue receptor in 1996, and the search for that receptor's natural ligand found ghrelin in 1999. GHRP-6 is, in effect, a synthetic ghrelin that came first.Editorial synthesis
    Editorial synthesis from general knowledge
  • It acts at two sites. In the pituitary it makes somatotrophs release growth hormone directly; in the hypothalamus it acts on the same neurons ghrelin does, which is why it releases far more growth hormone with GHRH than either does alone, why it does nothing in children whose pituitary stalk was severed at birth, and why it drives hunger. The same hypothalamic action releases ACTH and, downstream, cortisol, and it raises prolactin; those are the effects the later, more selective GHRPs were made to reduce.Editorial synthesis
    Editorial synthesis from general knowledge
  • What the endocrine literature established is the response, not the outcome: a growth hormone pulse that peaks within an hour after intravenous or intranasal dosing, larger with GHRH, blunted by high blood sugar, preserved in old age, absent after stalk transection. Nothing in the ledger measured body composition, strength or recovery in people after GHRP-6, by any route or over any period.Editorial synthesis
    Editorial synthesis from general knowledge

What happened in the human studies?

This record's ledger holds 12 primary human studies, of which 12 are trials. Few enough to show in full: each card quotes what its abstract reported about GHRP-6. Read them before any other section on this page.

  • Randomized controlled trial humans n = 95 2026 Human clinical trial
    In the intention-to-treat population, no differences were found in mRS, Barthel index nor survival.
    Source pmid-42462342 · quoted verbatim from the abstract
  • Phase 1 clinical trial humans 2013 Human clinical trial
    Disposition of GHRP-6 best fitted a bi-exponential function with R(2) higher than 0.99, according to a mathematic modeling and confirmed by an Akaike index (AIC) lower than that of the corresponding one-compartment model for all subjects.
    Source pmid-23099431 · quoted verbatim from the abstract
  • Randomized controlled trial humans n = 9 2010 Human clinical trial
    When analyzing Δ area under the curve (ΔAUC) GH values after ghrelin, GHRP-6, and GHRH, no significant differences were observed in T1DM compared with controls.
    Source pmid-20189610 · quoted verbatim from the abstract
  • Randomized controlled trial humans 2010 Human clinical trial
    GHRP-6-induced ACTH release also increased (before: 60.7 +/- 17.2; 6th month: 78.5 +/- 12.1), although not significantly.
    Source pmid-19453623 · quoted verbatim from the abstract
  • Clinical trial humans 2004 Human clinical trial
    Peak GH response to GHRH+GHRP-6 during the hyperglycemic clamp was lower than in the englycemic clamp (112.45+/-14.45 mU/l versus 151.06+/-16.87 mU/l; P<0.05).
    Source pmid-14693411 · quoted verbatim from the abstract
  • Clinical trial humans 2000 Human clinical trial
    Inclusion criteria were severe GH deficiency--ie, a GH peak after ITT of Findings GH peaks seen after the GHRH/GHRP-6 test did not result in any side-effects and were not affected by age, sex, amount of adipose tissue, or by the GH assay system used.
    Source pmid-11030292 · quoted verbatim from the abstract
  • Randomized controlled trial humans 1999 Human clinical trial
    The association of the two peptides markedly increased GH levels (peak: 172.4 +/- 34.2; AUC: 10393.0 +/- 1894.8) compared with the isolated administration of GHRP-6 or GHRH.
    Source pmid-10583306 · quoted verbatim from the abstract
  • Clinical trial humans 1999 Human clinical trial
    GHRP-6 i.n. prompted a significant increase in GH concentration during the total night and a trend toward an increase in ACTH secretion during the first half of the night, whereas cortisol secretion remained unchanged.
    Source pmid-10336729 · quoted verbatim from the abstract
  • Controlled clinical trial humans 1995 Human clinical trial
    In normal subjects, GH secretion was 1029 +/- 202 after GHRH treatment, 1221 +/- 345 after GHRP-6, and 3542 +/- 650 after GHRH plus GHRP-6; the latter value was significantly (P < 0.05) higher than the secretion elicited by GHRH or GHRP-6 alone.
    Source pmid-7593423 · quoted verbatim from the abstract
  • Controlled clinical trial humans n = 7 1995 Human clinical trial
    Growth hormone-releasing peptide 6 (GHRP-6) is a synthetic hexapeptide with a potent GH-releasing activity after intravenous, subcutaneous, intranasal and oral administration in man.
    Source pmid-7581965 · quoted verbatim from the abstract
  • Randomized controlled trial humans n = 9 1995 Human clinical trial
    In the group of young adult subjects the combined administration of GHRH and GHRP-6 elicited a greater GH increase than GHRH alone (F = 21.9, P Conclusions These data show that GH responses to GHRP-6 are much greater than to GHRH in late adulthood.
    Source pmid-7734029 · quoted verbatim from the abstract
  • Clinical trial humans n = 8 1993 Human clinical trial
    Small transient increases in cortical and PRL were observed (increases in cortical averaged 182.1 +/- 33.1 nmol/L and peak PRL was 21 +/- 2.6 micrograms/L after 1.0 mg/kg L-692,429, respectively), whereas no significant changes occurred in LH, FSH, TSH, insulin, or glucose concentrations.
    Source pmid-8077339 · quoted verbatim from the abstract

Study by study: what GHRP-6 did in people

Every human study in the ledger, with what was given and what was measured. The pattern is hormones after one dose.

Human studies of GHRP-6 in the ledger.
StudyParticipantsDose and routeWhat was measuredResult
Popovic 2000 (diagnostic validation)125 adults with pituitary disease, 125 healthy controlsGHRH 1 mcg/kg + GHRP-6 1 mcg/kg IVPeak GH over 120 min vs insulin tolerance testThe combined test separated deficient from healthy as well as the standard test, more conveniently
Hernández-Bernal 2026 (COURAGE-2, phase 3)188 acute stroke patients (95 treated, 93 standard care)EGF 75 mcg + GHRP-6 5 mg IV, twice daily, 7 daysDisability at 3 and 6 monthsNo difference in Rankin or Barthel scores in the intention-to-treat analysis
Cabrales 2013 (pharmacokinetics)9 healthy men100, 200, 400 mcg/kg IV bolusPlasma GHRP-6 over 12 hoursTwo-phase decline; measurable at 12 hours
Frieboes 1999 (sleep and routes)Healthy young men300 mcg/kg oral; 30 mcg/kg intranasal or sublingualOvernight GH, ACTH, cortisol, sleep EEGOral did nothing; intranasal raised GH all night; earlier IV boluses had raised ACTH and cortisol
Pinto 199916 healthy adults1 mcg/kg IV, with or without GHRH and dexamethasoneGH responseAcute dexamethasone enhanced the GH response to GHRP-6
Micic 1995Healthy young and older adults90 mcg IV alone or with GHRH 100 mcgGH responseThe response did not decline with age when GHRP-6 was given, alone or combined
Micic 200412 men with type 2 diabetesGHRH + GHRP-6, 100 mcg each, IVGH under euglycaemic and hyperglycaemic clampsHigh glucose blunted the GH peak
Bellone 199513 children with short stature300 mcg/kg oral, with or without arginineGH responseOral GHRP-6 released GH; the abstract compares it with IV GHRH
Pombo 1995Children with neonatal pituitary stalk transectionGHRH, GHRP-6 or bothGH responseNo GH release by any route: GHRP-6 needs an intact hypothalamus
Correa-Silva 20108 patients with Cushing's disease, 11 controlsGHRP-6 and ghrelin, before and after ketoconazoleACTH and cortisolExaggerated ACTH response, larger after six months of ketoconazole
de Sá 20109 patients with type 1 diabetes, 9 controlsGhrelin, GHRP-6 and GHRHGH, ACTH, cortisolGhrelin released more GH than GHRP-6 or GHRH in both groups
Gertz 199324 healthy menL-692,429, a non-peptide GHRP-6 mimic, IVGH, cortisol, prolactinDose-dependent GH; small transient cortisol and prolactin rises

Nothing in this table is a body-composition result. The literature that made GHRP-6 famous is about how growth hormone is regulated, and it used the peptide as a probe.

Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.

What the evidence shows

One row per primary study in this record's ledger. Fields are read from each paper's indexing and abstract. "Analytical method" marks papers about detecting or measuring the compound rather than about its effects.

24 primary studies in this record's ledger, strongest evidence first. A dash means the abstract did not state the value.
StudyDesignnSpeciesDoseRouteDurationReported outcomeTier
Hernández-Bernal 2026 Randomized controlled trial 95 Humans——7 days; 3 years In the intention-to-treat population, no differences were found in mRS, Barthel index nor survival. Human clinical trial
Cabrales 2013 Phase 1 clinical trial — Humans——— Disposition of GHRP-6 best fitted a bi-exponential function with R(2) higher than 0.99, according to a mathematic modeling and confirmed by an Akaike index (AIC) lower than that of the corresponding one-compartment… Human clinical trial
de 2010 Randomized controlled trial 9 Humans——— When analyzing Δ area under the curve (ΔAUC) GH values after ghrelin, GHRP-6, and GHRH, no significant differences were observed in T1DM compared with controls. Human clinical trial
Correa-Silva 2010 Randomized controlled trial — Humans——6 months GHRP-6-induced ACTH release also increased (before: 60.7 +/- 17.2; 6th month: 78.5 +/- 12.1), although not significantly. Human clinical trial
Micic 2004 Clinical trial — Humans100 mcgintravenous— Peak GH response to GHRH+GHRP-6 during the hyperglycemic clamp was lower than in the englycemic clamp (112.45+/-14.45 mU/l versus 151.06+/-16.87 mU/l; P<0.05). Human clinical trial
Popovic 2000 Clinical trial — Humans—intravenous— Inclusion criteria were severe GH deficiency--ie, a GH peak after ITT of Findings GH peaks seen after the GHRH/GHRP-6 test did not result in any side-effects and were not affected by age, sex, amount of adipose tissue,… Human clinical trial
Pinto 1999 Randomized controlled trial — Humans—intravenous, oral— The association of the two peptides markedly increased GH levels (peak: 172.4 +/- 34.2; AUC: 10393.0 +/- 1894.8) compared with the isolated administration of GHRP-6 or GHRH. Human clinical trial
Frieboes 1999 Clinical trial — Humans—intravenous, oral— GHRP-6 i.n. prompted a significant increase in GH concentration during the total night and a trend toward an increase in ACTH secretion during the first half of the night, whereas cortisol secretion remained unchanged. Human clinical trial
Pombo 1995 Controlled clinical trial — Humans—intravenous— In normal subjects, GH secretion was 1029 +/- 202 after GHRH treatment, 1221 +/- 345 after GHRP-6, and 3542 +/- 650 after GHRH plus GHRP-6; the latter value was significantly (P < 0.05) higher than the secretion… Human clinical trial
Bellone 1995 Controlled clinical trial 7 Humans—intranasal, intravenous, oral, subcutaneous— — Human clinical trial
Micic 1995 Randomized controlled trial 9 Humans—intravenous— In the group of young adult subjects the combined administration of GHRH and GHRP-6 elicited a greater GH increase than GHRH alone (F = 21.9, P Conclusions These data show that GH responses to GHRP-6 are much greater… Human clinical trial
Gertz 1993 Clinical trial 8 Humans—intravenous— Small transient increases in cortical and PRL were observed (increases in cortical averaged 182.1 +/- 33.1 nmol/L and peak PRL was 21 +/- 2.6 micrograms/L after 1.0 mg/kg L-692,429, respectively), whereas no… Human clinical trial
Risco-Acevedo 2026 Animal study 6 Mice——— In aged animals, EGF + GHRP6 treatment increased step length (p = 0.04). Animal, preclinical
Rodríguez-Ulloa 2026 Animal study 12 Rats——— At 24 h post-treatment, proteins associated with reactive oxygen species (ROS) detoxification, heat shock factor 1 (HSF1) activation, and negative regulation of cellular hypoxia response were significantly modulated. Animal, preclinical
Yunjia 2026 Animal study — Mice——— YJP improved cardiac dysfunction and myocardial fibrosis and markedly ameliorated depressive behaviors. Animal, preclinical
Wang 2026 Animal study — Rats——7 days Here, we show that GHRP-6 attenuated myocardial tissue demise, reduced myocardial interstitial fibrosis/scarring, and integrally improved left ventricle physiology. Animal, preclinical
Zhao 2025 Animal study — Mice——— — Animal, preclinical
Zhu 2025 Animal study — Mice——— Compared with the E. granulosus (Eg) group, the GHSR-KO group presented a significant reduction in the number of liver infection foci. Animal, preclinical
Castro 2025 Animal study — Dogs——— Hypersalivation, hypoactivity, reduced heart rate, changes in respiration, pale gums and erythema of the head region were observed in some animals administered at 1000 and 2000 μg/kg/day. Animal, preclinical
Ayman 2025 Animal study — Rats——— On the eighth day, in nicotine-treated rats a significant hyperactivity was observed, that was reduced significantly by ghrelin and GHRP-6. Animal, preclinical
Poelman 2025 Animal study — Mice5 mg/kgintranasal— Only GHRP-6 (5 mg/kg) increased food intake without adverse effects, prompting detailed analysis of meal patterns, neuronal activation in the arcuate nucleus (via Fos mapping) and neurochemical identification of c-fos… Animal, preclinical
Wu 2025 Animal study — Mice——— EM-1-DLS demonstrated the highest antinociceptive potency among the peptides, with an ED 50 approximately 8-fold greater than EM-1, while EM-2-DLS showed comparable effects to EM-2. Animal, preclinical
Elimam 2024 Animal study — Mice——— — Animal, preclinical
Zhu 2024 Animal study — Mice——— Serum Ghrelin levels were increased in E.g-infected 4- and 12-week mice, and reduced in 36-week mice. Animal, preclinical

Doses reported in studies

Each entry is a sentence quoted from the study's abstract, with the study's design, sample size and year in front of it. Comparator doses in the same sentence are not attributed to ghrp-6.

  • The diagnostic test gives GHRH 1 microgram per kilogram plus GHRP-6 1 microgram per kilogram intravenously, validated in 125 patients with pituitary disease and 125 healthy controls.Human clinical trial
    Source pmid-11030292
  • In a sleep study, healthy young men received 300 micrograms per kilogram orally in enteric-coated capsules, or 30 micrograms per kilogram intranasally or sublingually.Human clinical trial
    Source pmid-10336729
  • Intravenous GHRP-6 at 1 microgram per kilogram was compared with GHRH 100 micrograms and their combination in 16 healthy adults.Human clinical trial
    Source pmid-10583306
  • GHRP-6 90 micrograms or GHRH 100 micrograms, alone or combined, as an intravenous bolus in young and older adults.Human clinical trial
    Source pmid-7734029
  • GHRH plus GHRP-6, 100 micrograms each, intravenously in 12 men with type 2 diabetes under glucose clamps.Human clinical trial
    Source pmid-14693411
  • Children with short stature received 300 micrograms per kilogram orally.Human clinical trial
    Source pmid-7581965
  • Nine healthy men received single intravenous boluses of 100, 200 and 400 micrograms per kilogram for pharmacokinetics.Human clinical trial
    Source pmid-23099431
  • In the Cuban stroke trial, 95 patients received intravenous EGF 75 micrograms plus GHRP-6 5 mg twice daily for seven days.Human clinical trial
    Source pmid-42462342
  • Animal study mice 2025 Animal, preclinical
    Doses stated in the abstract: 5 mg/kg
    Only GHRP-6 (5 mg/kg) increased food intake without adverse effects, prompting detailed analysis of meal patterns, neuronal activation in the arcuate nucleus (via Fos mapping) and neurochemical identification of c-fos messenger RNA (mRNA)-expressing neurons using RNAscope.
    Source pmid-39813130 · quoted verbatim from the abstract, emphasis added
  • Animal study rats, rabbits 2016 Animal, preclinical
    Doses stated in the abstract: 400 μg
    Treatments for both species were based on a CMC jelly composition containing GHRP-6 400 μg/mL.
    Source pmid-27200188 · quoted verbatim from the abstract, emphasis added

Every GHRP-6 dose in the studies, in one table

Every figure here was given in a study, almost always as a single intravenous dose. No human study in the ledger injected it under the skin.

Doses of GHRP-6 administered in studies.
SettingRouteDoseSchedulePopulation
Diagnostic testIntravenous bolus1 mcg/kg, with GHRH 1 mcg/kgSingleAdults with suspected GH deficiency
Endocrine studiesIntravenous bolus1 mcg/kg; 90 to 100 mcg fixedSingleHealthy adults; diabetes; Cushing's disease
PharmacokineticsIntravenous bolus100, 200, 400 mcg/kgSingle9 healthy men
Sleep and route studyOral capsules; intranasal; sublingual300 mcg/kg oral; 30 mcg/kg nasal or sublingualSingle, eveningHealthy young men
ChildrenOral300 mcg/kgSingleShort stature
Stroke (COURAGE-2)Intravenous5 mg with EGF 75 mcgTwice daily, 7 daysAcute ischaemic stroke
Mice (2025)Intranasal5 mg/kgSingleFood-intake study
Rabbits and rats (2016)Local and systemic400 mcgRepeatedHypertrophic scar and wound models

Figures for subcutaneous GHRP-6 circulate on forums and vendor pages. None was given to a person in any study in the ledger, so none is reproduced here; the table holds every dose a study actually administered. Note that the stroke trial's 5 mg twice daily, by vein, is orders of magnitude above the endocrine doses and was a different use entirely.

Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.

Side effects: cortisol, prolactin, hunger, and what was never measured

Cortisol and prolactin rise with GHRP-6 in the studies that measured them, more than with ipamorelin; hunger is its signature. Beyond single-dose endocrine work and one 7-day stroke trial, no safety data exist for the way it is used. Events and their frequency as each study reported them, with the denominator where the abstract gives one.

  • Repeated intravenous GHRP-6 raised ACTH and cortisol as well as growth hormone in an earlier sleep study by the same group.Human clinical trial
    Source pmid-10336729
  • In Cushing's disease the ACTH and cortisol response to GHRP-6 is exaggerated, and it increased further after six months of ketoconazole.Human clinical trial
    Source pmid-19453623
  • A 1993 study of a non-peptide GHRP-6 mimic in 24 men saw small transient rises in cortisol and prolactin, the class effect the later peptides were designed to avoid.Human clinical trial
    Source pmid-8077339
  • In the stroke trial the combination with EGF was given for seven days with safety as a primary endpoint; the abstract reports no difference in disability and does not detail adverse events.Human clinical trial
    Source pmid-42462342
  • Hunger is not listed as an adverse event in the endocrine studies because it is the drug's mechanism, but it is the effect every user reports first. No study has measured what months of three-times-daily ghrelin-receptor stimulation does to cortisol, prolactin, glucose or weight; the studies are single doses, and the one seven-day trial measured stroke outcomes.Editorial synthesis
    Editorial synthesis from general knowledge
  • Animal study rats 2025 Animal, preclinical
    The present study aimed to investigate the impacts of ghrelin and GHRP-6 on the horizontal and vertical activity in rats exposed to chronic nicotine treatment followed by acute nicotine withdrawal.
    Source pmid-39857727 · quoted verbatim from the abstract
  • Animal study mice 2025 Animal, preclinical
    Only GHRP-6 (5 mg/kg) increased food intake without adverse effects, prompting detailed analysis of meal patterns, neuronal activation in the arcuate nucleus (via Fos mapping) and neurochemical identification of c-fos messenger RNA (mRNA)-expressing neurons using RNAscope.
    Source pmid-39813130 · quoted verbatim from the abstract

Who GHRP-6 is discussed for, and the cautions that recur

Studied: healthy adults and children in single-dose endocrine tests; adults with pituitary disease, diabetes and Cushing's disease as diagnostic or physiological probes; acute stroke patients in Cuba. Never studied: anyone dosed subcutaneously, anyone dosed for muscle or fat, anyone dosed for more than seven days. Community: bodybuilders, people wanting to gain weight, and people using it for sleep.

The cautions come from the mechanism and the endocrine data:

  • Cortisol and prolactin. Both rise with GHRP-6, more than with ipamorelin; the response is exaggerated in Cushing's disease. Anyone with a mood, adrenal or prolactin-related condition is on the wrong side of this compound's selectivity.
  • Blood sugar. High glucose blunts the GH response, and growth hormone itself raises glucose; no study measured glucose over repeated dosing.
  • Hunger and weight. The mechanism drives food intake; whether that becomes weight gain in people is unmeasured, and for many users it is the point.
  • Anyone without an intact hypothalamus. It does nothing after stalk transection, which also means its effects depend on a working axis that steroids and other drugs alter.
  • Cancer and growth-sensitive conditions. Repeated GH and IGF-1 stimulation is the class concern; no study of GHRP-6 addressed it.
  • Tested athletes. Named on the WADA list under S2; detection methods exist.

Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.

Biomarkers measured in studies

Laboratory and clinical measures the studies report tracking, including which hormones did and did not change.

  • Randomized controlled trial humans n = 95 2026 Human clinical trial
    Combined therapy of Epidermal Growth Factor (EGF) and Growth Hormone Releasing Peptide-6 (GHRP6) has shown potential benefits in stroke patients.
    Source pmid-42462342 · quoted verbatim from the abstract
  • Phase 1 clinical trial humans 2013 Human clinical trial
    GHRP-6 is a growth hormone secretagogue that also enhances tissue viability in different organs.
    Source pmid-23099431 · quoted verbatim from the abstract
  • Randomized controlled trial humans n = 9 2010 Human clinical trial
    Ghrelin is a GH secretagogue that also increases adrenocorticotropic hormone (ACTH) and cortisol levels, similarly to GH-releasing peptide-6 (GHRP-6).
    Source pmid-20189610 · quoted verbatim from the abstract
  • Randomized controlled trial humans 2010 Human clinical trial
    In Cushing's disease (CD), adrenocorticotrophic hormone (ACTH)/cortisol responses to growth hormone secretagogues (GHS), such as ghrelin and GHRP-6, are exaggerated.
    Source pmid-19453623 · quoted verbatim from the abstract
  • Clinical trial humans 2004 Human clinical trial
    The aim of this study was to investigate the effect of two different glucose levels on GH response to the combined administration of GHRH+GHRP-6 in patients with type 2 diabetes.
    Source pmid-14693411 · quoted verbatim from the abstract

Reported interactions

Sentences in which the compound is studied alongside another agent. Read the quotation: the word interaction can also be statistical.

  • Controlled clinical trial humans n = 7 1995 Human clinical trial
    As the GHRH-induced GH rise in children is potentiated by arginine (ARG), even when administered by oral route at low dose (4 g), we studied also the interaction of oral GHRP-6 and ARG administration.
    Source pmid-7581965 · quoted verbatim from the abstract
  • Randomized controlled trial humans n = 9 1995 Human clinical trial
    The marked increase of plasma GH levels observed after administration of GHRP-6 alone or in combination with GHRH indicates that impaired GH secretion in late adulthood is a functional and potentially reversible state.
    Source pmid-7734029 · quoted verbatim from the abstract

Reported timelines

Onset, peak and duration figures as each study reported them.

  • After intravenous boluses, GHRP-6 followed a two-phase decline and was still measurable at 12 hours.Human clinical trial
    Source pmid-23099431
  • Intranasal GHRP-6 raised growth hormone across the whole night; oral capsules did nothing.Human clinical trial
    Source pmid-10336729
  • The stroke trial measured disability at three and six months after seven days of treatment.Human clinical trial
    Source pmid-42462342
  • Animal study rats 2024 Animal, preclinical
    Here we examined whether GHRP-6 administration concomitant to Dox prevented the onset of DCM/HF and multiple organs damages in otherwise healthy rats.
    Source pmid-38873418 · quoted verbatim from the abstract
  • Animal study rats, rabbits 2016 Animal, preclinical
    Importantly, in the hypertrophic scars rabbit's model, GHRP-6 intervention dramatically reduced the onset of exuberant scars by activating PPARγ and reducing the expression of fibrogenic cytokines.
    Source pmid-27200188 · quoted verbatim from the abstract
  • Animal study 2016 Animal, preclinical
    Four different doses of rhEGF, GHRP-6 and these combined agents were intraperitoneally administered immediately after the onset of reperfusion.
    Source pmid-26311576 · quoted verbatim from the abstract
  • Animal study rats 2012 Animal, preclinical
    GHRP-6 was injected [intraperitoneal (IP) or intracerebroventricular (ICV)] 2 h before the onset of stress to observe its potential prevention of the mucosal lesion.
    Source pmid-22791951 · quoted verbatim from the abstract

What is measured over time, and what is not

The literature measures minutes and hours. A growth hormone pulse peaks within the first hour after an intravenous bolus and the diagnostic test samples for 120 minutes; the peptide itself was still measurable at 12 hours after large intravenous doses; intranasal dosing raised growth hormone across one night. The longest exposure in any human study is seven days, in the stroke trial, which measured disability at six months and found none of the hoped-for difference. Nothing has been measured over the weeks and months of use the community describes, and the three-times-daily pattern is an inference from the pulse duration, not a studied schedule.

Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.

Study durations

Treatment and follow-up periods as stated in each abstract.

  • Randomized controlled trial humans n = 95 2026 Human clinical trial
    Durations stated: 7 days; 3 years; 6 months
    Participants received the combined therapy (n=95; twice daily, 7 days) or standard care (n=93).
    Source pmid-42462342 · quoted verbatim from the abstract, emphasis added
  • Randomized controlled trial humans 2010 Human clinical trial
    Durations stated: 6 months
    Design/patients Eight untreated patients with CD (BMI: 28.5 +/- 0.8 kg/m(2)) were evaluated before and after 3 and 6 months of ketoconazole treatment and compared with 11 controls (BMI: 25.0 +/- 0.8).
    Source pmid-19453623 · quoted verbatim from the abstract, emphasis added
  • Animal study rats 2026 Animal, preclinical
    Durations stated: 7 days
    Treatments were initiated post-surgery and continued for 7 days.
    Source pmid-41901314 · quoted verbatim from the abstract, emphasis added
  • Animal study rats, rabbits 2016 Animal, preclinical
    Durations stated: 5 days; 30 days
    Excisional full-thickness wounds (6 mmØ) were created in the dorsum of Wistar rats and topically treated twice a day for 5 days.
    Source pmid-27200188 · quoted verbatim from the abstract, emphasis added

Routes: intravenous in the studies, oral and nasal once, subcutaneous only on vendor pages

Intravenous bolus in almost every human study; oral capsules and a nasal spray in one sleep study; intravenous in the stroke trial. No human study in the ledger gave GHRP-6 by subcutaneous injection, the route it is sold for. Routes of administration named in each study.

  • Clinical trial humans 2004 Human clinical trial
    administration by intravenous route reported
    GH response to i.v. bolus of GHRH+GHRP-6 (100 mcg, each) was measured in 12 male patients with type 2 diabetes (mean age: 53.9+/-1.59 years; BMI: 25.58+/-0.39 kg/m(2); mean HbA(1c): 8.7+/-0.42%), during a euglycemic (mean glucose: 4.92+/-0.08 mmol) hyperinsulinemic clamp (insulin infusion rate of 100 mU/kg/h) and a hyperglycemic clamp (mean glucose: 12.19+/-0.11 mmol/l).
    Source pmid-14693411 · quoted verbatim from the abstract
  • Clinical trial humans 2000 Human clinical trial
    administration by intravenous route reported
    All cases and controls were given GHRH 1 microg per kg bodyweight intravenously plus GHRP-6 1 microg per kg intravenously at 0 min and blood samples were obtained during a subsequent 120 min period.
    Source pmid-11030292 · quoted verbatim from the abstract
  • Randomized controlled trial humans 1999 Human clinical trial
    administration by intravenous, oral route reported
    One group of subjects received iv GHRP-6 (1 microg/kg), GH-releasing hormone (GHRH; 100 microg), GHRH plus GHRP-6 or saline 3.5 h after oral acute dexamethasone administration (4 mg; at 0600 h).
    Source pmid-10583306 · quoted verbatim from the abstract
  • Clinical trial humans 1999 Human clinical trial
    administration by intravenous, oral route reported
    After repeated intravenous (i.v.) boluses of growth hormone-releasing peptide-6 (GHRP-6) we found recently increases of growth hormone (GH), corticotropin (ACTH) and cortisol levels and of the amount of stage 2 sleep.
    Source pmid-10336729 · quoted verbatim from the abstract
  • Controlled clinical trial humans 1995 Human clinical trial
    administration by intravenous route reported
    The subjects underwent 3 different tests on separate occasions, being challenged with GHRH (1 microgram/kg, iv), GHRP-6 (1 microgram/kg, iv), or GHRH plus GHRP-6.
    Source pmid-7593423 · quoted verbatim from the abstract

Weight-normalized doses, as published

Per-kilogram figures exactly as each study published them, for the species it studied.

  • 1 microgram per kilogram intravenous, the diagnostic-test dose.Human clinical trial
    Source pmid-11030292
  • 100 to 400 micrograms per kilogram intravenous in the pharmacokinetic study; 300 micrograms per kilogram oral and 30 intranasal in the sleep study.Human clinical trial
    Source pmid-23099431
  • Animal study mice 2025 Animal, preclinical
    Weight-normalized doses as published: 5 mg/kg
    Only GHRP-6 (5 mg/kg) increased food intake without adverse effects, prompting detailed analysis of meal patterns, neuronal activation in the arcuate nucleus (via Fos mapping) and neurochemical identification of c-fos messenger RNA (mRNA)-expressing neurons using RNAscope.
    Source pmid-39813130 · quoted verbatim from the abstract, emphasis added

Weight-normalized figures above are reproduced exactly as each study published them, for the species it studied. Dose does not scale linearly with body mass between species: metabolic rate, clearance and receptor density differ, and regulatory guidance uses allometric, not proportional, conversion. A mg/kg figure from a rat study is a fact about that rat study and nothing else.

What people report outside the literature

Forum reports describe intense hunger within minutes, water retention, tiredness and a warm flush, with three-times-daily injection for months. None of the studies used that pattern, and none measured what months of ghrelin-receptor stimulation does. What circulates in user communities and clinic marketing, reported so a reader knows the figures and their origin. None of it has been tested in a trial, and none of it is a suggestion.

  • GHRP-6 circulates for muscle gain, recovery, sleep and, deliberately, appetite, injected subcutaneously two or three times a day for months, usually with a GHRH analogue such as CJC-1295 or sermorelin. Reports describe hunger within minutes of injection, water retention, tiredness, a warm flush, and vivid sleep; some report lethargy and low mood attributed to cortisol and prolactin. None of this comes from a study: no human study in the ledger used the subcutaneous route or dosed for longer than seven days. The microgram figures that circulate are not reproduced here; the table above holds every dose a study actually gave.Editorial synthesis
    Editorial synthesis from general knowledge
Method note · shared across compounds

Reconstitution mathematics

Lyophilised peptide is supplied as a mass in a vial and dissolved in a stated volume of diluent. Two figures follow from that and nothing else:

  • Concentration = mass in vial ÷ diluent volume. A 5 mg vial in 2 mL is 2.5 mg/mL, or 2,500 mcg/mL.
  • Volume for a given mass = that mass ÷ concentration. 250 mcg at 2,500 mcg/mL is 0.1 mL. On a U-100 insulin syringe, where 1 mL is 100 units, that is 10 units.

Study doses on this page are quoted as published, in the units the authors used. Converting between mcg, mg and IU, or between a mass and a syringe volume, is arithmetic; deciding a mass is not, and this page does not do it. The reconstitution calculator performs the conversion with the formula shown.

Method note · shared across compounds

Reading a certificate of analysis

A certificate of analysis is a laboratory report on one batch. Reading it means checking four things in order.

  1. Identity. Mass spectrometry should report an observed molecular mass matching the peptide's theoretical mass within the instrument's stated tolerance. A certificate with no mass spectrometry, or one that lists only the expected value, has not confirmed identity.
  2. Purity. HPLC purity is the area of the main peak as a share of all peaks, at a stated wavelength. It says nothing about what the other peaks are, and it is not a measure of quantity.
  3. Quantity. Net peptide content, by amino acid analysis or UV, is the fraction of the vial's mass that is peptide rather than counter-ions and water. A 5 mg vial at 80% net content holds 4 mg of peptide, and every concentration figure above changes accordingly.
  4. Provenance. The batch number on the certificate should match the vial, the laboratory should be named and independent of the seller, and the test date should be recent.

This page rates no supplier and links to none. It describes how to read the document.

Method note · shared across compounds

Equipment described in studies

Published human studies of injectable peptides report the same small set of materials: single-use insulin syringes with fixed needles, most often U-100 with 29 to 31 gauge needles; bacteriostatic water or sterile water for injection as diluent, with the choice stated in the methods; alcohol swabs; and refrigerated storage of reconstituted solution. Animal studies more often report intraperitoneal or intragastric administration and state the vehicle used. Where a study in this record's ledger names its materials or vehicle, that sentence appears under storage or routes above; where it does not, nothing is assumed here.

Storage and handling

Anti-doping laboratories have studied GHRP-6's stability in serum and its degradation products for detection purposes; the peptide degrades in liquid samples over days. That is analytical chemistry, not a vial instruction. Vendor sheets follow general lyophilised-peptide practice; contents are unverified.

Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.

Common mistakes in how GHRP-6 is discussed

  1. Reading the endocrine literature as efficacy data. Hundreds of papers used GHRP-6 as a probe of growth hormone regulation. None measured muscle or fat in people.
  2. Calling hunger a side effect. It is the mechanism: GHRP-6 is a ghrelin mimic, and ghrelin is the hunger hormone. A user who does not want to eat more has chosen the wrong GHRP.
  3. Assuming the subcutaneous schedule is studied. Every human study in the ledger dosed intravenously, orally or nasally, once. The three-times-daily pattern is community practice.
  4. Confusing it with its antagonist. [D-Lys3]-GHRP-6 blocks the ghrelin receptor and appears in many papers; it is a different molecule with the opposite effect, and automated searches pull it in.
  5. Treating GHRP-2's Japanese approval as GHRP-6's. Pralmorelin (GHRP-2) is approved in Japan as a diagnostic; GHRP-6 is approved nowhere.
  6. Missing the stroke trial. The only phase 3 of GHRP-6 was in acute stroke, with EGF, and it was negative on its primary endpoint.

Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.

GHRP-6 vs GHRP-2, ipamorelin, hexarelin and MK-677

GHRP-6 beside the other ghrelin-receptor agonists, from their own records where one exists.
CompoundWhat it isGH release and selectivityStatus
GHRP-6First GHRP (1984); hexapeptideStrong GH pulse; raises ACTH, cortisol and prolactin; strongest hungerNot approved; WADA S2
GHRP-2 (pralmorelin)Second-generation GHRPMore potent GH release than GHRP-6 in comparative studies; also raises cortisol and prolactinApproved in Japan as a diagnostic; no record on this site
IpamorelinPentapeptide designed for selectivity; 63 indexed publications, 2 randomized trialsGH release with little cortisol or prolactin effect and less hungerNot approved; WADA S2
HexarelinHexapeptide GHRP-6 analoguePotent GH release; desensitises with repeated dosing; cardiac studiesNot approved; no record on this site
MK-677 (ibutamoren)Oral non-peptide ghrelin mimeticSustained GH and IGF-1 rise over 24 hours; raises appetite and glucose; heart-failure signal in one trialNot approved; no record on this site
CJC-1295 (the usual stacking partner)GHRH analogue, a different receptor; 37 indexed publicationsSynergistic GH release with any GHRP, as the GHRH + GHRP-6 test demonstratesNot approved; WADA S2

The comparison that has actually been run in people is GHRP-6 against GHRH and against ghrelin, in the endocrine studies above; the comparisons among GHRPs come from separate studies and from the pharmacology that motivated each successor. This site's ipamorelin vs GHRP-6 page lines the two records up side by side, and the CJC-1295 and ipamorelin page holds the GHRH-plus-GHRP evidence.

Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.

Exclusion criteria in studies

Who each trial excluded, as stated in the abstract.

  • Clinical trial humans 2000 Human clinical trial
    Inclusion criteria were severe GH deficiency--ie, a GH peak after ITT of Findings GH peaks seen after the GHRH/GHRP-6 test did not result in any side-effects and were not affected by age, sex, amount of adipose tissue, or by the GH assay system used.
    Source pmid-11030292 · quoted verbatim from the abstract

Other compounds in its class

Same class in the registry: Ipamorelin. Each row shows what that compound's own record states; nothing is inferred across rows. Head-to-head evidence, where any exists, is on the comparison page: Ipamorelin vs GHRP-6.

2 compounds in the ghrelin mimetics class. Each row states what that compound's own record says; nothing is inferred across rows.
CompoundTierPublicationsRCTsRecord
GHRP-6 Human clinical trial 738 22 draft
Ipamorelin Human clinical trial 63 2 draft

Regulatory status: never approved, named by WADA, a diagnostic relative approved in Japan

Registry facts only. Jurisdiction-level status, compounding categories and sport prohibitions need their own cited documents before they appear here.

  • Not approved anywhere as a medicine. Its relative GHRP-2 (pralmorelin) is approved in Japan as a diagnostic agent for growth hormone deficiency; GHRP-6 has been used in the same way in research and in the multicentre validation study but never registered. In Cuba, the Center for Genetic Engineering and Biotechnology has taken GHRP-6 through trials for cardioprotection (CIGB-500) and, with EGF, for stroke, without a registration documented in the ledger. WADA names GHRP-6 on the Prohibited List under S2 as a growth hormone secretagogue, prohibited at all times, and detection methods and serum-stability studies exist for doping control. Not on FDA's 503A compounding lists as far as this record can determine.Editorial synthesis
    Editorial synthesis from general knowledge · primary document to be added to the ledger

Open questions and limitations

What is genuinely unknown, stated plainly. A missing field is not evidence that the outcome is safe, effective, or established.

  • No human study in the ledger gave GHRP-6 subcutaneously or for longer than seven days, and none measured body composition, strength or recovery.
  • The 2013 pharmacokinetic half-life figures and the 1980s and 1990s dose-response papers (Bowers 1984 onward) are not in the ledger.
  • The Cuban CIGB programme's earlier-phase results for cardioprotection and stroke are not indexed.

Questions people ask

Why does GHRP-6 cause hunger?

Because it is a ghrelin mimic. Ghrelin is the stomach's hunger hormone, and GHRP-6 was the compound that led to the discovery of its receptor; activating that receptor in the hypothalamus drives food intake, which is why a 2025 mouse study chose GHRP-6 as the tool to engage the brain's ghrelin system and why hunger is the first thing users report. The effect is the mechanism, not a side effect of it.

What is GHRP-6?

GHRP-6 is a six-amino-acid synthetic peptide (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) described by Cyril Bowers in 1984, the first growth hormone releasing peptide. It acts on the ghrelin receptor to make the pituitary release growth hormone, and its discovery led to the identification of that receptor and of ghrelin itself. It has been used as a research tool and a diagnostic test agent, never approved as a medicine, and is sold as a research chemical.

What is the half-life of GHRP-6?

Short. A 2013 pharmacokinetic study gave nine men single intravenous boluses of 100, 200 and 400 micrograms per kilogram and found a two-phase decline with the peptide still measurable at 12 hours; the half-life figures are in the full text, not the abstract. The growth hormone pulse it triggers lasts about an hour, which is why the community injects it several times a day.

Does GHRP-6 increase weight?

No human study has measured body weight or composition after GHRP-6. It increases hunger, which is why the community expects weight gain and why a 2025 mouse study found intranasal GHRP-6 increased food intake; whether the growth hormone pulses change body composition in people has never been tested.

Has GHRP-6 been tested in humans?

Extensively, but as a probe rather than a treatment: single intravenous doses in healthy adults, children and patients to study growth hormone regulation; a 250-person validation of the GHRH plus GHRP-6 diagnostic test; one oral and nasal sleep study; and a Cuban phase 3 trial of GHRP-6 with EGF in 188 stroke patients, which found no difference in disability. No study measured muscle, fat or recovery.

What dose was used in the studies?

One microgram per kilogram intravenously in the diagnostic test and most endocrine work, 90 to 100 micrograms as fixed boluses, 100 to 400 micrograms per kilogram in the pharmacokinetic study, 300 micrograms per kilogram orally and 30 intranasally in the sleep study, and 5 mg intravenously twice daily with EGF in the stroke trial. No human study in the ledger gave it subcutaneously.

Why does GHRP-6 make you hungry?

Because it is a synthetic ghrelin: it activates the receptor for the stomach's hunger hormone in the hypothalamus, the same action that releases growth hormone. Hunger is the mechanism working, not a side effect, and it is the trait the later GHRPs, especially ipamorelin, were designed to reduce.

Does GHRP-6 raise cortisol and prolactin?

Yes. Repeated intravenous boluses raised ACTH and cortisol alongside growth hormone in healthy men, the ACTH response is exaggerated in Cushing's disease, and a non-peptide mimic produced small transient cortisol and prolactin rises. This is the selectivity gap between GHRP-6 and ipamorelin.

What are the side effects of GHRP-6?

In the studies: hunger, cortisol and prolactin rises, and, from the class, water retention and tingling that the abstracts do not detail. Nothing has been measured beyond single doses and one seven-day trial, so the effects of months of use, including on glucose and weight, are unknown.

Is GHRP-6 FDA approved?

No, and it has never been approved anywhere. Its relative GHRP-2 is approved in Japan as a diagnostic for growth hormone deficiency; GHRP-6 has been used the same way in research without registration.

Is GHRP-6 banned in sport?

Yes. WADA names GHRP-6 on the Prohibited List under S2 as a growth hormone secretagogue, prohibited at all times, and anti-doping laboratories publish detection and stability methods for it.

What is the difference between GHRP-6 and ipamorelin?

Same receptor, different selectivity. GHRP-6 releases growth hormone and also ACTH, cortisol and prolactin, and drives hunger strongly; ipamorelin was designed to release growth hormone with little of the rest. This site's ipamorelin-vs-GHRP-6 comparison page lines the two records up.

What is the difference between GHRP-6 and GHRP-2?

GHRP-2 (pralmorelin) is the more potent successor and is approved in Japan as a diagnostic agent; it also raises cortisol and prolactin and stimulates appetite, somewhat less than GHRP-6. No head-to-head trial for any clinical outcome exists.

Can GHRP-6 be taken orally or as a nasal spray?

Both were tested once, in healthy young men: 300 micrograms per kilogram in enteric-coated capsules did nothing to overnight hormones, while 30 micrograms per kilogram intranasally raised growth hormone across the night. Oral dosing in children with short stature did release growth hormone in a 1995 study.

What was the GHRP-6 stroke trial?

COURAGE-2, a Cuban open-label phase 3 trial published in 2026, gave 95 acute stroke patients intravenous EGF 75 micrograms plus GHRP-6 5 mg twice daily for seven days against standard care in 93. Disability at three and six months did not differ in the intention-to-treat analysis.

Which species has GHRP-6 been studied in?

Humans, extensively as an endocrine probe; rats and mice for heart protection, kidney injury, wound healing and appetite; rabbits for scarring; dogs in a Cuban safety study; and fish, where a ghrelin analogue was fed in aquaculture research. Its antagonist, [D-Lys3]-GHRP-6, appears in many more papers and is a different compound.

Sources

Full citations. Every claim above links to one of these by its id.

  1. 1
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  12. 12
Show the remaining 36 sources
  1. 13
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  14. 26
  15. 27
  16. 28
  17. 29
  18. 30
  19. 31
  20. 32
  21. 33
  22. 34
  23. 35
    Diagnosis of adult GH deficiency.
    pmid-17766155 · · peer-reviewed
  24. 36
  25. 37
    Growth hormone secretagogue receptor family members and ligands.
    pmid-11322507 · · peer-reviewed
  26. 38
    Neuroregulation of growth hormone secretion in domestic animals.
    pmid-11311846 · · peer-reviewed
  27. 39
  28. 40
  29. 41
  30. 42
    Growth hormone in obesity.
    pmid-10193871 · · peer-reviewed
  31. 43
    Growth hormone-releasing peptides.
    pmid-9186261 · · peer-reviewed
  32. 44
  33. 45
  34. 46
  35. 47
  36. 48

Reference card

Reference card · generated /compounds/ghrp-6
Compound
GHRP-6, ghrelin mimetics
Evidence tier
Human clinical trial
Indexed publications
738 · 22 RCTs · 41 other clinical trials
Approval
no registered development programme found
Routes reported
intranasal, intravenous, oral, subcutaneous
Reviewed
Adam Mirando, PharmD,

Study figures are as published in each source and are not recommendations. Print or save this card with its date.

Last reviewed and what changed

Newest first. These are the record's own revision dates, and the same dates feed the sitemap.

  1. · Reviewed by Adam Mirando, PharmD, on 2026-09-25.
  2. · Written under the sequencing rule after research/intents/ghrp-6.json: guide (8 sections incl. a twelve-study table), FAQ to 12 plus 5 from the map, dose, weight-normalized, timeline and adverse-event claims from the abstracts, mechanism (ghrelin mimic that found ghrelin), reported-use, regulatory; a cattle study of the antagonist [D-Lys3]-GHRP-6 removed from the evidence table and all claims; misdrafted interactions removed; intent-driven H1 and title.
  3. · Claims drafted extractively from 48 ledger sources by scripts/draft_claims.py: 38 claims, 25 evidence-table rows. Status researched -> draft.
  4. · Claims drafted extractively from 48 ledger sources by scripts/draft_claims.py: 45 claims, 25 evidence-table rows. Status researched -> draft.
  5. · Claims drafted extractively from 48 ledger sources by scripts/draft_claims.py: 48 claims, 25 evidence-table rows. Status researched -> draft.
  6. · Evidence fetched from Europe PMC and ChEMBL by scripts/fetch_evidence.py; claims not yet written.