GHRP-6
Growth Hormone-Releasing Peptide 6, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Checked Oct 28, 2026
The short answer
No human evidence yet for body composition and recovery in healthy adults through a growth hormone boost
Grade D for body composition and recovery in healthy adults: no trial has tested those outcomes.
- Approved?
- Not approved for any use.
- Safety: C, thinly characterized
- In short human studies the measured effects were rises in cortisol and prolactin at the highest IV dose (1.0 mcg/kg); hunger is widely reported but we found no controlled measurement of it for GHRP-6 alone, and there are no long-term human safety data.
The full answer: what it is for, the dose, the units
What people take it for: People take GHRP-6 to raise growth hormone for recovery, muscle and fat loss, or sometimes to stimulate appetite. It is not approved for any use.
Does it work for body composition and recovery in healthy adults through a growth hormone boost? D, no human evidence yet. Result: not tested in humans.
Grade D for body composition and recovery in healthy adults: no trial has tested those outcomes. It does raise growth hormone in controlled human studies (grade B for that lab measurement alone).
No approval for any use.
Highest evidence for any use: A for IV GHRP-6 plus EGF in acute ischemic stroke (two randomized trials, 2024 and 2026; the phase III missed its primary endpoint).
Safety: C, thinly characterized. In short human studies the measured effects were rises in cortisol and prolactin at the highest IV dose (1.0 mcg/kg); hunger is widely reported but we found no controlled measurement of it for GHRP-6 alone, and there are no long-term human safety data.
Do not use if: Active cancer or history of hormone-sensitive malignancies. Insulin resistance or pre-diabetes (GH blunts insulin sensitivity). Pregnancy and breastfeeding (no safety data). Use with caution in anyone with elevated baseline cortisol.
Could it be placebo? Controlled human studies show GHRP-6 beats placebo at raising growth hormone, but no controlled trial tests body composition or recovery, so a placebo effect cannot be ruled out for those.
The dose people use, and the units to draw
No verified dose exists for healthy adults; controlled human studies gave single IV doses of 0.1 to 1.0 mcg/kg, and we found no named non-seller source for a subcutaneous dose.
| Source | Dose | How often and how | Who it was for | Link |
|---|---|---|---|---|
| Bowers et al., J Clin Endocrinol Metab 1990 | 0.1, 0.3 and 1.0 mcg/kg (about 7, 21 and 70 mcg for a 70 kg adult; arithmetic from the per-kg dose) | Single intravenous bolus per test, compared with placebo | 18 normal men | Abstract: peak GH 1.2 (placebo), 7.6, 16.5 and 68.7 ug/L at 0.1, 0.3 and 1.0 mcg/kg; prolactin and cortisol about 2-fold higher only at 1.0 mcg/kg |
| Frieboes et al., Neuroendocrinology 1995 | 50 mcg per bolus, four boluses (200 mcg total) | Repeated intravenous boluses overnight versus placebo | Normal men (number not stated on the PubMed page) | Abstract: 4 x 50 mcg i.v. versus placebo; raised GH, ACTH and cortisol; stage 2 sleep up, slow-wave sleep unchanged |
| Frieboes et al., J Neuroendocrinol 1999 | Oral 300 mcg/kg (enteric-coated capsules); intranasal 30 mcg/kg; sublingual 30 mcg/kg | Single night-time dose versus placebo | Normal young men (number not stated on the PubMed page) | Abstract: oral no change in GH; sublingual trend only; intranasal raised overnight GH significantly, cortisol unchanged |
| Cabrales et al., Eur J Pharm Sci 2013 | 100, 200 and 400 mcg/kg | Single intravenous bolus (pharmacokinetic study, not a GH-response dose) | 9 healthy male volunteers | Abstract: elimination half-life 2.5 +/- 1.1 hours, distribution half-life 7.6 +/- 1.9 minutes |
| Hernandez-Bernal et al., COURAGE-2, J Clin Neurosci 2026 | 5 mg GHRP-6 plus 75 mcg EGF | Intravenous, twice daily for 7 days, combination product, versus standard care (open-label) | 188 adults with acute ischemic stroke (a different use; not a wellness dose) | Abstract: primary endpoint not met; NIHSS 15 or more subgroup (n=27) exploratory |
| Huberman Lab, Peptides: The Science, Uses & Safety with Dr. Abud Bakri (June 2026) | No dose stated for GHRP-6 | Not applicable | Episode discusses growth hormone secretagogues generally (tesamorelin, ipamorelin, MK-677); GHRP-6 is not named in the transcript | Chapter 02:04:01 Growth Hormone Secretagogues, Age Decline, Cancer Risk, Insulin |
Controlled human studies gave single IV doses from 0.1 mcg/kg (Bowers 1990) up to 1.0 mcg/kg for hormone response, with a pharmacokinetic study going to 400 mcg/kg IV (Cabrales 2013); no study gives a subcutaneous wellness dose.
Earlier subcutaneous ranges, schedules and cycle lengths on the site had no named non-seller source and were removed. Checked the Huberman Lab episode with Dr. Abud Bakri (growth hormone secretagogue chapter, GHRP-6 not named) and found no GHRP-6 dose; Examine.com could not be opened, and no Attia source was found for GHRP-6.
Reported by the named source, never prescribed by us.
How many units do I draw?
Use the calculator: units on the syringe equal the dose in mcg divided by the mcg per mL of your mixed vial, times 100 for a U-100 syringe. Open the dose calculator
Why it might work
- GHS-R1a receptor binding in the pituitary and hypothalamusGHRP-6 (His-D-Trp-Ala-Trp-D-Phe-Lys-NH
- PLC/IP3/calcium cascade triggers GH releaseGHS-R1a activation engages phospholipa
- Orexigenic and ACTH/cortisol co-stimulationGHS-R1a activation in the hypothalamic
- GH-driven IGF-1 synthesis and assumed downstream effectsCirculating GH is assumed to reach the
Assumed pathway, not shown in people.
Assumed mechanism (confirmed in humans for GH release, but downstream effects are not proven in humans for most claimed benefits): GHRP-6 binds and activates GHS-R1a (the ghrelin receptor) in pituitary somatotrophs and hypothalamic neurons, triggering GH secretion via PLC/IP3/calcium signaling. This pathway is distinct from and synergistic with the GHRH/cAMP/PKA pathway. GHS-R1a activation also explains the strong orexigenic effect (hunger) and ACTH co-stimulation. Downstream benefits like tissue repair and cardioprotection are hypothesized to occur via GH and IGF-1 elevation plus direct GHS-R1a signaling in peripheral tissues, but this chain has not been demonstrated in human outcome trials.
The trials, claim by claim
The stroke trials tested GHRP-6 together with EGF as an IV hospital treatment, so their letter does not describe the injections people use for recovery or body composition.
- The GH pulse is real and confirmed in humans since 1990, making GHRP-6 one of the better-evidenced gray-market peptides. The hunger that comes with it is not a side effect you can ignore.
- Beyond GH secretion, the claimed benefits like wound healing and cardioprotection are animal data only. No human outcome trial for body composition, recovery, or tissue repair has been completed.
- In the one dose-response study we verified (18 men, IV), cortisol and prolactin rose about 2-fold only at the top dose of 1.0 mcg/kg, while GH rose with each dose step (Bowers 1990, PMID 2108187).
GHRP-6 reliably increases GH secretion in humans
Result: worked
Small human studies confirm an acute GH pulse after IV bolus, dose-dependent from 0.1 to 1.0 mcg/kg (Bowers 1990), and a rise in overnight GH after intranasal dosing (Frieboes 1999). We did not verify a controlled subcutaneous study. No long-duration RCTs on outcomes like body composition or recovery.
Bowers et al. 1990, J Clin Endocrinol Metab (PMID 2108187)Combining GHRP-6 with GHRH produces synergistic GH release greater than either alone
Result: worked
Shown in a controlled human study in 18 normal men (Bowers 1990); randomization is not stated in its abstract. Complementary signaling pathways (PLC/calcium vs cAMP/PKA) explain the synergy mechanistically. Note: PMID 7617137 (Frieboes et al. 1995) is primarily a sleep-EEG and nocturnal secretion study that includes GHRP-6 data; it supports the GH and cortisol co-elevation finding but is not the canonical synergy demonstration paper. Synergy with GHRH was established in the Bowers 1990 and Popovic 1995 literature.
Bowers et al. 1990, J Clin Endocrinol Metab (PMID 2108187)GHRP-6 improves wound healing
Result: not tested in humans
This grade reflects animal data only. PMID 27200188 (Mendoza Mari et al. 2016, Plastic Surgery International) is an animal study in Wistar rats and rabbit ear models, not a human trial. No replicated human wound-healing trial for GHRP-6 exists in the indexed literature. Animal data shows improved granulation, angiogenesis, and anti-fibrotic effects.
PMID 27200188, Plastic Surgery International 2016 (Mendoza Mari et al.), animal study, rats and rabbits onlyGHRP-6 protects the heart from cardiotoxic injury in animal models
Result: not tested in humans
Animal data only. The 2024 Frontiers in Pharmacology study demonstrated protection against doxorubicin-induced cardiotoxicity (not ischemia-reperfusion injury) in rats, via PI3K/Akt, Bcl-2 upregulation, and mitochondrial protection. The injury model is chemotherapy-induced cardiomyopathy, not ischemia-reperfusion. Zero controlled human cardiac trials exist.
Frontiers in Pharmacology 2024, DOI 10.3389/fphar.2024.1402138 (Berlanga-Acosta et al.), animal study, ratsGHRP-6 elevates cortisol and prolactin as a side effect
Result: worked
Confirmed in placebo-controlled human studies. In Bowers 1990 (18 men, IV) prolactin and cortisol rose about 2-fold only at the 1.0 mcg/kg dose, and in Frieboes 1995 (repeated 50 mcg IV boluses overnight) ACTH and cortisol rose versus placebo.
Frieboes et al. 1995, Neuroendocrinology (PMID 7617137)IV GHRP-6 plus EGF did not improve disability at 6 months over standard care in an open-label phase III stroke trial (n=188); a post hoc severe-stroke subgroup (n=27) looked better.
Result: did not work
One open-label RCT of a two-drug combination in a different indication; the primary endpoint was missed and the subgroup result is exploratory. No bearing on subcutaneous wellness use.
COURAGE-2: EGF plus GHRP-6 in acute ischemic stroke, phase III (J Clin Neurosci 2026, PMID 42462342)Risks and the label warnings
Adverse events
Intense hunger within 15-30 minutes of injection is nearly universal and is the most commonly reported reason for discontinuation. Mild water retention, transient flushing, and tingling have been reported. Elevated cortisol (via ACTH co-stimulation) is dose-dependent and real. Elevated prolactin at higher doses. No serious adverse events attributed to GHRP-6 in published human studies, but sample sizes are small and follow-up duration is short.
Contraindications
Active cancer or history of hormone-sensitive malignancies. Insulin resistance or pre-diabetes (GH blunts insulin sensitivity). Pregnancy and breastfeeding (no safety data). Use with caution in anyone with elevated baseline cortisol.
Theoretical concerns
Chronic GH elevation may impair glucose metabolism and insulin sensitivity. Persistent cortisol elevation would be counterproductive for recovery and body composition. Unknown long-term effects on pituitary axis regulation. Theoretical tumor-promotion risk with elevated IGF-1 applies to all GH secretagogues.
What nobody knows yet
No long-duration human trials. Purity and actual peptide content of gray-market research-chemical supply is unverified. Receptor desensitization kinetics over weeks-to-months of use are not well characterized in humans. Interaction with exogenous testosterone or GLP-1 agonists is unknown. No human wound-healing or cardiac outcome trials have been completed.
What else could explain the result
Almost universally stacked with CJC-1295 or modified GRF(1-29) in the wellness community, making it impossible to isolate GHRP-6 contribution from community reports. Many users are also on TRT, which independently improves body composition and recovery. GLP-1 agonists (semaglutide, tirzepatide) directly suppress appetite and could mask or counteract GHRP-6's orexigenic effect. Sleep quality improvements often attributed to GHRP-6 may reflect the natural GH pulse that accompanies deeper sleep rather than a drug effect.
Is the vial what it says?
Cross-checked against the cited sources below. The grade reflects the absence of formal human safety and efficacy data. The founding human study is Bowers 1990 (PMID 2108187). The wound-healing evidence is animal-only (rats and rabbits, Plastic Surgery International), not a human trial. The cardioprotection work used a doxorubicin-induced cardiomyopathy model. PMID 7617137 is a sleep-EEG study, not a dedicated synergy paper.
Half-life and storage
Half-life: Bi-exponential: distribution half-life approximately 7-8 minutes, elimination half-life approximately 2-2.5 hours after IV administration. Subcutaneous GH-stimulating effect peaks within 15-30 minutes and returns to baseline within 2-3 hours.
Once mixed: Moderate. Reconstitute with bacteriostatic water. Stable refrigerated for approximately 30 days post-reconstitution. Sensitive to heat and repeated freeze-thaw cycles. Avoid vigorous shaking.
What I noticed, and what people report
What people report
Volume of reports: moderate. A real body of reports, fairly consistent.
High community usage volume, particularly in bodybuilding and performance optimization forums. GHRP-6 has been in gray-market circulation for 20+ years and there are large bodies of anecdotal user logs.
The hunger side effect is reported with near-universal consistency, which adds credibility since it is a pharmacologically expected consequence of GHS-R1a activation. GH pulse effects are directionally consistent with lab data. Body composition and recovery benefits are inconsistent across anecdotal reports.
Lower than volume would suggest. Most community logs do not control for concurrent TRT, other peptides, training changes, or caloric intake. The hunger effect is the only truly credible signal because it is objective, immediate, and pharmacologically explained.
- Anecdote: Intense hunger within 20-30 minutes of injection is the most consistently reported effect, described as distracting and sometimes difficult to manage on a caloric deficit.
- Anecdote: Users on GHRP-6 plus CJC-1295 stacks report improved sleep quality and more vivid dreams, which they attribute to augmented GH pulses during slow-wave sleep.
- Anecdote: Recovery between training sessions is commonly reported as faster, though nearly all reports involve multiple stacked compounds making attribution impossible.
- Anecdote: Water retention and a slightly puffy face are reported within the first 1-2 weeks and often resolve with continued use. Some users discontinue because of this.
Reports are anecdote, not proof.
Can you tell if it is working?
No non-blood readout directly proves benefit; the only honest objective signal is appetite-driven weight (scale + waist), with DEXA to see whether any gain is lean vs fat.
Bloodwork
A lab moves, but it's noisy, indirect, or off-target, treat it as a hint, not proof.
GHRP-6 is a ghrelin/GHS-R1a agonist that triggers acute pulsatile pituitary GH release (well documented in humans). GH is too pulsatile to catch on a single draw, so the only routine proxy is hepatic IGF-1. But GHRP-6 given alone produces only a modest and inconsistent IGF-1 rise (weaker than GHRH analogs like tesamorelin or oral MK-677), and its most reliable effect, appetite stimulation, has no blood correlate. So a lab shifts, but the signal is noisy and does not fully capture what the compound does: partial, not direct.
A rise above the patient's own pre-treatment baseline, ideally settling into the upper half of the age- and sex-adjusted reference range. Expect a modest move on GHRP-6 monotherapy; a flat IGF-1 does NOT rule out that the compound is working, because its most reliable effect (appetite) is not captured here.
GHRP-6 stimulates pulsatile pituitary GH secretion via GHS-R1a; GH raises hepatic IGF-1, the only stable, routinely orderable integrated readout of GH action. It is the honest efficacy proxy, but a weak one for this compound alone.
Draw baseline
before first dose (fasting morning draw to standardize)
Retest
4-8 weeks
Read this before you spend on labs
A baseline-vs-retest IGF-1 rise is the only honest routine-blood way to confirm GHRP-6 is engaging the GH axis, but it is a weak proxy for THIS compound: GHRP-6 alone produces a modest, inconsistent IGF-1 move, and its most consistent effect is appetite/hunger, which has NO blood correlate, so a flat IGF-1 does not mean the drug is inert. Removed IGFBP-3 as a listed marker: it is orderable but noisy and confirmatory-only, and a flat IGFBP-3 is still consistent with response, which means it is not a usable readout. Off-target cortisol/ACTH and prolactin rises are side effects, not efficacy, do not read those as the drug 'working.' Note also that the two cited studies document acute GH (and ACTH/cortisol) release, not chronic IGF-1 elevation from GHRP-6 alone; the IGF-1 link is class-level inference, which is why this is graded partial/plausible rather than direct/established. Keep draw timing identical between baseline and retest, and treat a supraphysiologic IGF-1 overshoot as a safety flag, not a win.
Other ways to track it
Home scale (daily weight, 7-day rolling average) + waist circumference
GHRP-6's single most reliable human effect is intense hunger within 20-30 min of injection (a direct GHS-R1a/ghrelin-mimetic action). If it is pharmacologically active in you, that shows up objectively as rising caloric intake and body weight over the first weeks. Honest caveat: weight up confirms the drug is DOING something, not that it is delivering any anabolic/recovery benefit - the gain can be food, fat, or water rather than muscle.
Appetite stimulation is the near-universally reported human effect and has no blood correlate; body weight is its honest, directly measurable downstream readout. Kept at partial because it proves activity, not efficacy.
DEXA scan - lean mass, fat mass, and visceral adipose tissue (VAT)
DEXA is an accessible, accurate body-composition scan, but human body-comp outcome data for GHRP-6 is animal-only, and the appetite effect means a caloric surplus can inflate both fat and lean. Its real value is disambiguation: telling you whether the weight the scale shows is lean tissue or fat/VAT. It does not prove efficacy on its own and rides entirely on the appetite/weight signal above.
Class-level GH-secretagogue logic points to lean mass, but there is no human GHRP-6 efficacy data; DEXA only partitions appetite-driven weight change into compartments so a bump is not mistaken for benefit. Held at partial.
Bottom line
No non-blood modality directly proves GHRP-6 delivers a beneficial outcome in humans - chronic body-comp, healing, and recovery claims are animal-only. The one reliable human effect is appetite, objectively visible as weight gain (scale + waist), and DEXA can tell you whether that weight is lean or fat/VAT. Both confirm the compound is pharmacologically active far more than they confirm benefit. The wearable sleep channel was removed: GHRP-6's standalone deep-sleep effect is unvalidated in humans and hopelessly confounded by CJC-1295 co-administration, so it fails the human-validation and efficacy tests and offers no objective proof. Paired with only a partial, inconsistent IGF-1 blood signal, the honest verdict is partial: you can objectively watch it act on you, but you cannot cleanly prove it is helping.
Logging baseline vs retest is the whole game. The Truth Tracker is our free log for bloodwork, DEXA, genetics, and wearable data, bring your own numbers.
How to track itHistory
First documented human use: 1990. Bowers CY et al. demonstrated GH-releasing potency and GHRH synergy in healthy male volunteers (J Clin Endocrinol Metab 1990;70(4):975-982, PMID 2108187).
- 1984Cyril Y. Bowers at Tulane University synthesizes GHRP-6, the first synthetic GH secretagogue, during enkephalin analog research. It becomes the founding compound of the entire GHRP family.
- 1990First published human data: Bowers et al. (PMID 2108187) confirm GHRP-6 stimulates GH release in 18 healthy men and acts synergistically with GHRH, establishing the basis for all subsequent clinical interest.
- 1996GHS-R1a receptor (the ghrelin receptor) is cloned, providing a molecular explanation for GHRP-6's mechanism. GHRP-6 research directly enabled Kojima et al.'s 1999 discovery of endogenous ghrelin.
- 2016Cuban research group publishes animal wound-healing study (PMID 27200188, Plastic Surgery International) showing GHRP-6 improves healing in Wistar rats and rabbit ear models. No human wound-healing trial from this group has been published in indexed journals.
- 2026COURAGE-2, an open-label Phase III trial of IV GHRP-6 combined with EGF in acute ischemic stroke (n=188), is published and misses its primary endpoint (PMID 42462342).
All sources
- PubMed: Bowers et al. 1990, founding human GHRP-6 study (PMID 2108187)(18 normal men; confirms dose-dependent GH pulse and GHRH synergy via IV administration.)
- PubMed: GHRP-6 pharmacokinetics in healthy male volunteers (PMID 23099431)(Nine male healthy volunteers. Establishes human PK profile: distribution half-life 7.6 min, elimination half-life 2.5 h after IV administration.)
- PubMed: GHRP-6 stimulates sleep, GH, ACTH and cortisol in normal man (PMID 7617137)(Sleep-EEG study confirming GH pulse and cortisol co-elevation in humans; primarily a nocturnal secretion and sleep study, not a dedicated GHRH-synergy comparison.)
- PubMed: GHRP-6 wound healing, animal study only (PMID 27200188, Plastic Surgery International 2016)(Animal model only (Wistar rats and rabbit ear wounds). No human subjects. Journal is Plastic Surgery International, not Int Wound J. No human wound-healing replication exists in the indexed literature.)
- Frontiers in Pharmacology: Cardioprotection against doxorubicin-induced cardiomyopathy (2024)(Rat model only. Shows PI3K/Akt, Bcl-2, and mitochondrial protection against doxorubicin cardiotoxicity. Injury model is chemotherapy-induced, not ischemia-reperfusion. No human cardiac data.)
- COURAGE-2: EGF plus GHRP-6 in acute ischemic stroke, phase III (J Clin Neurosci 2026, PMID 42462342)(Open-label randomized trial (n=188) of IV GHRP-6 combined with EGF; missed its primary endpoint. A two-drug combination in a different indication, so it does not test the wellness uses.)
- Bowers CY et al. Growth hormone-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone. J Clin Endocrinol Metab 1990;70(4):975-82. PMID 2108187(dose table)
- Frieboes RM et al. Growth hormone-releasing peptide-6 stimulates sleep, growth hormone, ACTH and cortisol release in normal man. Neuroendocrinology 1995;61(5):584-9. PMID 7617137(dose table)
- Frieboes RM et al. 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):473-8. PMID 10336729(dose table)
- Cabrales A 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):40-6. PMID 23099431(dose table)
- Hernandez-Bernal F et al. Phase III open-label, randomized clinical trial of epidermal growth factor and growth hormone releasing hexapeptide in acute ischemic stroke. J Clin Neurosci 2026;152:112195. PMID 42462342(dose table)
- Huberman Lab, episode page and transcript, hubermanlab.com/episode/peptides-the-science-uses-and-safety-abud-bakri(dose table)
Not medical advice. Grades reflect the evidence as of the date above and will change as data arrives. Reports from users are anecdote, not proof. Talk to a licensed clinician before you act on anything here.