GHRP-2
Growth Hormone Releasing Peptide-2, Pralmorelin, KP-102, GHRP-2 Acetate
Checked Oct 28, 2026
The short answer
Human-trial signal for raising growth hormone and IGF-I levels in adults
Grade B for raising growth hormone, result mixed: it raises GH in every human study, but five days of daily injections did not raise IGF-I, while a continuous 30-day infusion did.
- Approved?
- Approved for: diagnosis of growth hormone secretion insufficiency, single intravenous test dose (Japan PMDA, 2004).
- Safety: C, thinly characterized
- Cortisol, ACTH and prolactin rise with each dose and appetite increases, and there are no long-term human safety data in healthy adults.
The full answer: what it is for, the dose, the units
What people take it for: People take it to raise growth hormone, hoping for better recovery, leaner body composition and sleep. In Japan it is an approved one-time injection used to test for growth hormone deficiency, not a treatment.
Does it work for raising growth hormone and IGF-I levels in adults? B, human-trial signal. Result: mixed.
Grade B for raising growth hormone, result mixed: it raises GH in every human study, but five days of daily injections did not raise IGF-I, while a continuous 30-day infusion did. No human trial tests muscle, fat loss or sleep in healthy adults.
Approved for: diagnosis of growth hormone secretion insufficiency, single intravenous test dose (Japan PMDA, 2004). That does not carry over to daily injections for muscle, fat loss, recovery or anti-aging, and it is not FDA-approved for any use. GHRP Kaken 100 (pralmorelin hydrochloride) package insert, PMDA; approval date Oct 22, 2004 per the PMDA re-examination report
Safety: C, thinly characterized. Cortisol, ACTH and prolactin rise with each dose and appetite increases, and there are no long-term human safety data in healthy adults.
Do not use if: Active cancer or family history of GH-responsive tumors. Diabetes or pre-diabetes (GH raises blood glucose acutely). Pregnancy or breastfeeding. History of pituitary adenoma.
Could it be placebo? Raised GH is measured in blood and cannot be placebo, but no controlled trial tests muscle, fat loss or sleep in healthy adults, so a placebo effect cannot be ruled out for those goals.
The dose people use, and the units to draw
Human studies gave 1 to 2 mcg/kg as one intravenous dose, 100 mcg once daily under the skin for 5 days, or 1 mcg/kg per hour by continuous infusion; the Japanese test dose is 100 mcg intravenously, and no verified self-use dose exists.
| Source | Dose | How often and how | Who it was for | Link |
|---|---|---|---|---|
| Kaken Pharmaceutical, GHRP Kaken 100 package insert (Japan PMDA) | 100 mcg (adults 18 and over); 2 mcg/kg for ages 4 to under 18, capped at 100 mcg above 50 kg | Single dose, slow intravenous injection, fasting, dissolved in 10 mL saline just before use; diagnostic test only | People being tested for growth hormone secretion insufficiency; not a treatment dose | 用法・用量 (Dosage and administration) |
| Arvat et al., Peptides 1997 | 1 mcg/kg and 2 mcg/kg | Single intravenous bolus; compared with GHRH 1 mcg/kg, TRH 400 mcg and hCRH 2 mcg/kg | 6 healthy young adults (22 to 27 years) at both doses; 6 healthy elderly (66 to 73 years) tested at 2 mcg/kg. Similar GH rise from GHRP-2 and hexarelin, higher than GHRH; ACTH and cortisol rose to levels like hCRH | Abstract |
| Nijland et al., Eur J Endocrinol 1998 | 100 mcgUse this dose | Once daily subcutaneous injection for 5 days | 9 healthy young men. Peak GH fell from about 83 to 51 mcg/L between day 1 and day 5 (response attenuation) and IGF-I did not rise | Abstract |
| Mericq et al., J Clin Endocrinol Metab 1998 | 0.3, 1.0 and 3.0 mcg/kg per day | Subcutaneous, one dose level per 2-month period (8 months in all); a fourth period used 3 mcg/kg with GHRH 3 mcg/kg | 6 prepubertal children with growth hormone deficiency. Overnight GH rose in a dose-dependent way, IGF-I and IGFBP-3 did not rise, growth was faster on treatment than before or after | Abstract |
| Laferrere et al., J Clin Endocrinol Metab 2005 | 1 mcg/kg per hour | Continuous subcutaneous infusion for 270 minutes, versus saline | 7 lean healthy men; food intake at a buffet was 35.9% higher with GHRP-2 than with saline | Abstract |
| Bowers et al., J Clin Endocrinol Metab 2004 | 1 mcg/kg per hour | Continuous subcutaneous infusion for 30 days (also 24-hour infusions, alone and with GHRH) | 17 healthy older men and women in the 30-day part; pulsatile GH secretion rose more than 1.8-fold on days 14 and 30 and IGF-I held a plateau | Abstract |
| Van den Berghe et al., Clin Endocrinol 2002 | 1 mcg/kg per hour | Continuous infusion for 5 days; GHRP-2-alone arm, with other arms adding TRH and pulsatile GnRH | 33 men with prolonged critical illness in a four-arm randomized trial (GHRP-2 alone n=9); GHRP-2 alone reactivated GH secretion and normalized IGF-I | Abstract |
| Huberman Lab, Benefits & Risks of Peptide Therapeutics (Apr 1, 2024) | No dose stated for GHRP-2 | Named in a list with GHRP-3 and GHRP-6 as growth hormone releasers; GHRP-3 is described as raising prolactin and cortisol | General audience | Chapter 00:53:44, Ipamorelin, Hexarelin, GHRP-3, MK-677; Risks & Timing (transcript has no inline timestamps) |
Human studies ranged from 0.3 mcg/kg per day under the skin in children (Mericq 1998) to 2 mcg/kg as one intravenous dose (Arvat 1997), with 100 mcg once daily under the skin for 5 days in healthy men (Nijland 1998) and 1 mcg/kg per hour by continuous infusion for up to 30 days (Bowers 2004); the Japanese test dose is 100 mcg intravenously in adults.
The earlier ranges, the stack with CJC-1295, the titration and the on-off cycle had no named non-seller source and are removed. The Huberman Lab April 2024 episode names GHRP-2 without a dose and the Huberman Lab Koniver episode does not mention it. No Dr. Abud Bakri, Attia or Examine statement giving a GHRP-2 dose was found (the Bakri transcript and Examine pages could not be opened).
Reported by the named source, never prescribed by us.
How many units do I draw?
Use the calculator: concentration in mg per mL is vial mg divided by water mL, and units on a U-100 syringe are dose mg divided by concentration, times 100. Open the dose calculator
Why it might work
- Subcutaneous or intranasal administrationGHRP-2 (a synthetic hexapeptide
- GHS-R1a agonism plus hypothalamic somatostatin suppressionGHRP-2 activates the ghrelin / GHS-R1a
- Non-selective pituitary stimulation and cortisol/ACTH co-releaseUnlike the more selective ipamorelin
- Pulsatile GH rise and hepatic IGF-1 inductionThe combined GH pulse drives hepatic I
- Assumed peripheral effectsElevated GH and IGF-1 are assumed to s
Assumed pathway, not shown in people.
ASSUMED (based on receptor pharmacology confirmed in human cells and clinical GH secretion data, not direct mechanistic proof in vivo). GHRP-2 binds the ghrelin receptor (GHSR-1a) in pituitary somatotrophs, triggering calcium influx and protein kinase C activation, which stimulates GH exocytosis. Simultaneously activates hypothalamic GH-releasing pathways and suppresses somatostatin (the GH brake). Also activates ghrelin receptors in the hypothalamus to stimulate appetite via NPY/AgRP neurons. The cortisol/ACTH elevation reflects additional binding at corticotrophs.
The trials, claim by claim
- Reliably spikes GH in humans, confirmed in controlled studies and a Japanese diagnostic approval, but whether that pulse does anything useful for body composition in healthy adults is an open question.
- The cortisol and prolactin co-release are real and documented, not anecdote; that is the key reason ipamorelin exists as a cleaner alternative.
- Almost no one runs it alone. It is nearly always stacked with a GHRH analog, which makes it impossible to know what GHRP-2 is actually contributing to any outcome you see.
GHRP-2 significantly increases GH secretion in healthy humans
Result: worked
Controlled human studies show dose-dependent IV GH release. The primary citation is a single n=12 (6 young, 6 elderly) IV pharmacodynamic study (Arvat 1997, PMID 9285939). Additional human data comes from a Van den Berghe 2002 critical-illness infusion study (n=33, PMID 12030918) and a continuous-infusion appetite study (n=7, PMID 15699539). Approved in Japan as a diagnostic agent for GH deficiency and still in clinical use there (the 2004 Drugs R&D review described it as awaiting approval with a planned 2004 launch; PMID 15230633; primary Japanese trial data is in the regulatory submission and is not publicly accessible as a standalone English PubMed record). The B grade applies to the GH-secretion mechanism claim only, not to any downstream wellness outcome.
Arvat et al. 1997 (PubMed 9285939) - GH, prolactin, ACTH, cortisol in 12 men (6 young, 6 elderly); IV bolus onlyGHRP-2 increases appetite and food intake
Result: worked
Small RCT in 7 healthy lean men showed 36% increase in caloric intake during subcutaneous GHRP-2 infusion vs saline. Effect attributed to ghrelin receptor agonism in hypothalamus. Well-controlled but very small sample. Note: this study used continuous subcutaneous infusion, not the bolus injection used by community protocols.
Laferrere et al. 2005 (PMC2824650, PMID 15699539) - food intake in 7 healthy men; continuous infusion protocolGHRP-2 improves muscle protein deposition and growth performance
Result: not tested in humans
Animal data only. Study in growth-retarded yaks showed enhanced myofiber diameter and protein synthesis pathway activation. No equivalent controlled trial exists in healthy adult humans.
Zhang et al. 2016 (PMC4760683) - yak muscle deposition study; animal model onlyGHRP-2 has anti-inflammatory effects in tissue
Result: not tested in humans
In vitro human granulosa cell study showed attenuation of PKC-induced inflammation. Not a clinical outcome study. Mechanism is plausible but extrapolating to therapeutic use in vivo is speculative.
Ji et al. 2016 (PMC5000754) - granulosa cell inflammation; in vitro human cell study, not a clinical trialGHRP-2 elevates cortisol and prolactin alongside GH
Result: worked
Consistent finding across human studies. GHRP-2 activates ACTH/cortisol pathways at levels comparable to hCRH and raises prolactin (lower than TRH). Documented in the Arvat 1997 pharmacodynamic study and corroborated by the Van den Berghe 2002 critical illness study. This is a documented side-effect mechanism, not a claimed benefit.
Arvat et al. 1997 (PubMed 9285939) - ACTH/cortisol/prolactin in men; corroborated by Van den Berghe 2002 (PMID 12030918)Risks and the label warnings
Adverse events
Consistently documented in human studies: cortisol and prolactin elevation (both transient, occur at standard doses), increased hunger/appetite, water retention, flushing, and transient drowsiness. The cortisol signal is notably stronger than ipamorelin. Cortisol and prolactin bumps are real signals from multiple controlled studies (Arvat 1997 PMID 9285939; Van den Berghe 2002 PMID 12030918), not anecdote.
Contraindications
Active cancer or family history of GH-responsive tumors. Diabetes or pre-diabetes (GH raises blood glucose acutely). Pregnancy or breastfeeding. History of pituitary adenoma.
Theoretical concerns
Chronic GH elevation carries theoretical risks including insulin resistance, fluid retention, and potential stimulation of latent neoplastic growth (GH is a growth factor). No long-term human safety data exists in healthy adults. Elevated prolactin with chronic use could cause gynecomastia or libido effects.
What nobody knows yet
Long-term effects of repeated pulsatile GH stimulation in healthy adults are completely unstudied. The primary human pharmacodynamic data is from IV bolus and continuous infusion protocols, not the subcutaneous bolus injection used by community protocols. Receptor desensitization kinetics with chronic dosing are not well characterized in humans. Interaction with TRT, GLP-1 agonists, and other peptide stacks has not been studied.
What else could explain the result
Almost universally stacked with GHRH analogs (CJC-1295 with or without DAC, modified GRF 1-29), which dramatically amplifies GH response and makes attribution impossible. Frequently co-administered with TRT, which independently improves body composition. Community users rarely run GHRP-2 alone. GLP-1 base effects (if on tirzepatide/semaglutide) suppress appetite, which directly opposes GHRP-2's orexigenic mechanism.
Is the vial what it says?
Compiled from the cited sources below. Where no completed human trial exists, the grade says so.
Half-life and storage
Half-life: Approximately 15-30 minutes plasma half-life (GH peak at 30-60 min post-subcutaneous injection). GH response returns to baseline within 90-120 minutes. Some sources report longer half-life (up to 2.5 hours in animal models). Short enough that timing relative to meals and training matters meaningfully.
Once mixed: Moderate. Reconstitute with bacteriostatic water. Keep refrigerated after reconstitution (stable approximately 30 days at 2-8C). Avoid repeated freeze-thaw. Exposure to elevated temperatures degrades the peptide.
What I noticed, and what people report
What people report
Volume of reports: moderate. A real body of reports, fairly consistent.
High volume of community use and forum discussion, particularly in bodybuilding and anti-aging communities. One of the most discussed GH secretagogues alongside CJC-1295.
Reports are fairly consistent on the GH-pulse feel (flushing, hunger, heaviness post-injection) but body composition outcomes are inconsistent and heavily confounded by stacking.
Lower than volume suggests. Most reports are from stacked protocols. The GH pulse is real, but attributing specific body changes to GHRP-2 vs co-administered compounds is nearly impossible from community data.
- Anecdote: users consistently report a pronounced hunger spike 30-45 minutes after injection, sometimes described as uncomfortable. The one controlled human food-intake study we found tested the related peptide GHRP-2, not GHRP-6.
- Anecdote: post-injection flushing and a warm/heavy sensation are frequently described, particularly at higher doses. Attributed to the GH pulse and transient cortisol bump.
- Anecdote: some users report improved sleep depth, though this is not separated from the GH-during-sleep effect that occurs naturally or from co-administered CJC-1295.
- Anecdote: long-term users on community forums note plateau effects over weeks, consistent with GH secretagogue receptor desensitization.
Reports are anecdote, not proof.
Can you tell if it is working?
Blood IGF-1 is the only honest efficacy signal for GHRP-2; no non-blood modality (DEXA body comp, wearable sleep) survives as an objective efficacy tracker.
Bloodwork
A routine lab actually tracks whether this is working.
GHRP-2 is a ghrelin/GHS-R1a agonist that stimulates endogenous pituitary GH release; sustained GH elevation drives hepatic IGF-1 production, and IGF-1 is a routine, integrated serum marker of GH action, so an efficacy signal does appear in standard LabCorp/Quest bloodwork.
IGF-1 rises versus the patient's own baseline, shifting toward the upper part of the age/sex reference range. Expect a within-range increase, not the supraphysiologic levels seen with injected rhGH.
GHRP-2 drives pituitary GH secretion via the ghrelin receptor; GH induces hepatic IGF-1, the standard integrated readout of GH action in humans (Bowers 2004 showed a sustained IGF-1 plateau on 30-day continuous GHRP-2).
Small upward move that tracks IGF-1; more stable day-to-day than GH and useful as a corroborating signal rather than a primary one.
IGFBP-3 is GH-dependent and co-regulated with IGF-1; it rose alongside IGF-1 during sustained GHRP-2 exposure (Bowers 2004), so it supports but does not independently prove the IGF-1 result.
Draw baseline
Before first dose; morning venous draw. IGF-1 and IGFBP-3 do not require fasting.
Retest
4-8 weeks on stable, adequate dosing (IGF-1 plateaus within ~2 weeks of consistent exposure).
Read this before you spend on labs
IGF-1 is the honest proof that the GH axis is actually being driven, which is exactly what a secretagogue is supposed to do. Two caveats keep this from being a slam dunk: (1) Delivery matters. Continuous/adequate exposure raises IGF-1 to a plateau (Bowers 2004), but 5 days of low-dose daily SC bolus injections in healthy young men caused tachyphylaxis and did NOT move IGF-1 (PMID 9820615). A flat IGF-1 at 4-8 weeks may mean the dose/schedule isn't sustaining the axis, not that GHRP-2 is inert. (2) GHRP-2 also raises cortisol, ACTH, and prolactin via off-target ghrelin-receptor activity; those are NOT efficacy markers and should not be read as \"it's working.\" IGF-1 also does not measure the appetite, sleep, recovery, or body-composition effects people actually chase, only that GH is being secreted downstream.
- Bowers et al. 2004, JCEM, 30-day continuous SC GHRP-2 sustains GH, IGF-1, IGFBP-3 in older men and women
- Sigalos et al. 2017, Am J Mens Health, GH secretagogue treatment raises serum IGF-1 in hypogonadal men
- Bowers & Granda-Ayala 2001, Endocrine, GH/IGF-1 response to acute and chronic GHRP-2 and GHRH in older adults
- Nijland et al. 1998, Eur J Endocrinol, 5-day daily SC GHRP-2 causes response attenuation and does not stimulate IGF-1 in young men
Bottom line
Blood IGF-1 (handled separately, tier=direct) is the only honest way to confirm GHRP-2 is pharmacologically active, and even that shows modest within-range increases. Beyond blood, nothing survives as an efficacy tracker. DEXA lean/fat mass is mechanistic hope, not human-demonstrated for GHRP-2: the body-composition benefit in healthy adults is Grade D extrapolation, the peptide is almost never run without a GHRH analog (so attribution is impossible), and any real effect would fall below single-scan measurement noise, a channel that can't distinguish signal from noise or from the stack isn't a tracker. Wearable sleep is non-informative to negative: GH is coupled to slow-wave sleep physiologically, but the human GHRP-2 evidence does not support a device-detectable SWS gain, so it cannot verify efficacy. The most reproducible human effect is increased appetite/food intake (~36%, Grade B) plus a cortisol/prolactin rise, none cleanly captured by a consumer device, and none the outcome users are chasing. A CGM would likely show glucose drifting up (GH secretagogues reduce insulin sensitivity), but that is a safety/harm signal, not proof the peptide is 'working,' so it is not an efficacy channel. Net: verify with blood IGF-1; treat everything else as unverifiable for efficacy.
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: 1997. Arvat et al. published a controlled human comparison study (intravenous, dose-response) documenting GH, prolactin, ACTH, and cortisol elevation in 12 healthy men (6 young, 6 elderly). PMID 9285939.
- 1980sGHRP-2 developed by Cyril Bowers and colleagues as part of a series of synthetic GH secretagogues based on enkephalin analogs.
- 1997Arvat et al. publish a controlled human dose-response comparison of GHRP-2 and hexarelin vs GHRH in 12 men (6 young, 6 elderly), establishing that GHRPs elicit stronger GH responses than GHRH alone at equivalent IV doses (PMID 9285939).
- 2002Van den Berghe et al. publish a 5-day randomized study of GHRP-2 alone vs GHRP-2 combined with TRH and GnRH in 33 critically ill men, documenting GH and cortisol elevation and metabolic effects (PMID 12030918).
- 2004Pralmorelin (GHRP-2) approved in Japan by PMDA as a diagnostic agent for GH deficiency testing, marketed by Kaken Pharmaceutical. The pivotal Japanese trial data resides in the regulatory submission; a 2004 Drugs R&D review article (PMID 15230633) summarizes the development history, and described approval as pending at its December 2004 publication. Macimorelin, another GH secretagogue, was later approved by FDA (Dec 2017) as an oral diagnostic, and anamorelin is approved in Japan for cancer cachexia.
- 2010s-presentGHRP-2 becomes popular in research and bodybuilding communities as an unscheduled peptide. No FDA approval for any indication. Sold as research chemical in the US.
All sources
- Arvat et al. 1997 - Effects of GHRP-2 and Hexarelin on GH, prolactin, ACTH and cortisol in man (PubMed 9285939). n=12 (6 young, 6 elderly). IV bolus only.(Core human comparative pharmacodynamic study. Single n=12 IV dose-response. Confirmed GH release plus cortisol/prolactin elevation. Route limitation: IV bolus, not subcutaneous.)
- Laferrere et al. 2005 - GHRP-2 increases food intake in healthy men (PMC2824650, PMID 15699539). n=7, continuous subcutaneous infusion.(Small but controlled crossover study in lean men. 36% caloric intake increase vs saline. Real human appetite signal. Used continuous infusion, not bolus injection.)
- Van den Berghe et al. 2002 - Combined GHRP-2, TRH and GnRH in critically ill men (PubMed 12030918). n=33 critically ill men.(5-day randomized study in critically ill patients, not healthy adults. Corroborates GH and cortisol elevation signal. Not a wellness or body composition study.)
- Drugs R&D 2004 review of pralmorelin development and Japanese approval (PubMed 15230633). Review article, not a primary trial.(Authoritative review summarizing pralmorelin clinical development history and PMDA approval. The underlying Japanese pivotal trial data is in the regulatory submission, not publicly available as a standalone English PubMed record.)
- Zhang et al. 2016 - GHRP-2 and cysteamine in yaks with growth retardation (PMC4760683). Animal model.(Animal model for muscle protein deposition claims. Often cited as if it proves human muscle benefit. It does not.)
- Ji et al. 2016 - GHRP-2 attenuation of inflammation in human ovarian granulosa cells (PMC5000754). In vitro cell study.(In vitro human cell study. Anti-inflammatory mechanism is plausible but this is not a clinical outcome study.)
- PMDA package insert for 注射用GHRP科研100 (pralmorelin hydrochloride), third edition revised July 2025; approval number 21600AMZ00573; dosage text matches the PMDA re-examination report of Feb 5, 2014(dose table)
- Arvat E et al. Peptides 1997;18(6):885-891. PMID 9285939. DOI 10.1016/s0196-9781(97)00016-8(dose table)
- Nijland EA et al. Eur J Endocrinol 1998;139(4):395-401. PMID 9820615. DOI 10.1530/eje.0.1390395(dose table)
- Mericq V et al. J Clin Endocrinol Metab 1998;83(7):2355-2360. PMID 9661608. DOI 10.1210/jc.83.7.2355(dose table)
- Laferrere B et al. J Clin Endocrinol Metab 2005;90(2):611-614. PMID 15699539. DOI 10.1210/jc.2004-1719(dose table)
- Bowers CY et al. J Clin Endocrinol Metab 2004;89(5):2290-2300. PMID 15126555. DOI 10.1210/jc.2003-031799(dose table)
- Van den Berghe G et al. Clin Endocrinol (Oxf) 2002;56(5):655-669. PMID 12030918. DOI 10.1046/j.1365-2265.2002.01255.x(dose table)
- Huberman Lab episode, Apr 1, 2024, transcript lines 'GHRP2, GHRP3, GHRP6' and 'GHRP2, 3, 6, and MK677, all of which can potently increase growth hormone'(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.