GHRP-2 (Pralmorelin)
GHRP-2 (Pralmorelin) scored 4.9 / 10 (⚖️ Neutral) on the BioHarmony scale as a Substance → Peptide → Growth / Repair Peptide.
GHRP-2 (pralmorelin) is a ghrelin-receptor peptide that drives a strong growth-hormone pulse, approved in Japan since 2004 as a diagnostic test. It is a stronger releaser than ipamorelin but less selective, raising cortisol, prolactin, and appetite by about 36 percent per Laferrere 2005, with no human body-composition outcome trials.
What is GHRP-2 (Pralmorelin)?
GHRP-2, also called pralmorelin or KP-102, is a lab-made peptide that tells your pituitary to fire off a strong, fast pulse of your own growth hormone. It does this by binding the ghrelin receptor, the same receptor your gut's hunger hormone uses, which is why it both releases growth hormone and makes you hungry. It is a stronger releaser than ipamorelin, and that strength is the whole pitch. A single dose drives a peak growth-hormone response well above an equal dose of GHRH, per Tiulpakov 1995, and continuous dosing keeps growth hormone and IGF-1 elevated for weeks, per Bowers 2004. It lands at Neutral because that real power comes with real baggage.
Here is the part that sets GHRP-2 apart from almost every other peptide in this space. Japan approved it in 2004, not as a treatment, but as a single-dose diagnostic test for growth-hormone deficiency, per Chihara 2007. That is a genuine regulator-validated credential, more formal footing than ipamorelin or any grey-market growth-hormone peptide can claim. But read that carefully: the approval is for a one-time diagnostic test, not for the daily optimization use people actually want it for. For that use, it is a research chemical in a regulatory grey area, never FDA-approved, and banned in tested sport. The score reflects an honest split: strong, reproducible growth-hormone release and a unique clinical credential on one side, and lower selectivity plus thin outcome data on the other.
It helps to picture where GHRP-2 sits in the growth-hormone-peptide family. There are two ways to nudge your pituitary into releasing more growth hormone. One is to mimic the GHRH signal, which is what peptides like CJC-1295 no-DAC, sermorelin, and tesamorelin do. The other is to mimic ghrelin and hit the secretagogue receptor, which is GHRP-2's lane along with ipamorelin and GHRP-6. GHRP-2 is the hard-hitting member of that second group. It releases more growth hormone per dose than ipamorelin, but it does so less cleanly, and that single tradeoff explains almost everything about how it scores. People rarely run it alone. The standard play is to combine a ghrelin-receptor peptide with a GHRH peptide so the two pathways stack, which is why GHRP-2 and CJC-1295 no-DAC show up together so often in real-world protocols.
Terminology
A handful of terms decide how you read this report, because GHRP-2 sits exactly where strong hormone release meets unproven real-world payoff, and because it gets confused with the GHRH peptides it is usually paired with.
- GHRP: Growth-hormone-releasing peptide. A class that works through the ghrelin receptor, distinct from the GHRH peptides. GHRP-2 is one of the strongest members.
- GHS-R1a: The growth-hormone secretagogue receptor type 1a, better known as the ghrelin receptor. The single target GHRP-2 binds to do its job.
- GHRH: Growth-hormone-releasing hormone. A separate signal, hit by peptides like CJC-1295 no-DAC and sermorelin, that GHRP-2 amplifies and is commonly stacked with.
- Pralmorelin / KP-102: The approved pharmaceutical names for GHRP-2 in Japan, used for the diagnostic test.
- IGF-1: Insulin-like growth factor 1. The downstream signal growth hormone produces, the marker users track, and the pathway behind the cancer concern.
- Selectivity: How cleanly a peptide releases growth hormone without touching other hormones. GHRP-2 is less selective than ipamorelin, raising cortisol and prolactin too.
- Saturation dose: The point where the receptor is fully engaged and more peptide adds side effects, not more growth hormone. For GHRP-2 that is near 100 mcg per dose.
- Diagnostic versus therapeutic: GHRP-2 is approved only as a one-time test, not as a treatment course. The distinction is the heart of its regulatory story.
How do you take GHRP-2 (Pralmorelin)?
Dosing & Protocols
Dosing information is summarized from published research and community reports. This is not a prescribing guide. Consult a healthcare provider before starting any protocol.
View 2 routes and 4 protocols
Routes & Forms
| Route | Form | Clinical Range | Community Range |
|---|---|---|---|
| Subcutaneous injection | Lyophilized powder reconstituted with bacteriostatic water | No approved therapeutic dose (approved diagnostic dose is 100 mcg intravenous, single use) | 100 to 300 mcg per injection, 1 to 3 times daily |
| Intravenous (diagnostic only) | Single-dose pralmorelin solution | 100 mcg, single dose, fasting | Not used off-label by this route |
Protocols
Diagnostic test (approved) Clinical
- Dose
- 100 mcg
- Frequency
- Single dose
- Duration
- One test
The approved Japanese growth-hormone-stimulation test, given intravenously and fasted, with peak growth hormone read at 15 mcg per liter as the deficiency cutoff.
Conservative off-label starter Anecdotal
- Dose
- 100 mcg
- Frequency
- Once daily
- Duration
- 8 to 12 weeks
Pre-sleep and fasted to ride the natural overnight growth-hormone pulse. Not an approved protocol.
Standard off-label with a GHRH peptide Anecdotal
- Dose
- 100 to 200 mcg of each
- Frequency
- 1 to 3 times daily
- Duration
- 8 to 12 weeks, often cycled
The common real-world stack pairs GHRP-2 with CJC-1295 no-DAC or sermorelin, since the two hit different receptors that both raise growth hormone. The short half-life is the reason for multiple daily doses and for choosing a short-acting GHRH partner.
Higher off-label dose Anecdotal
- Dose
- 200 to 300 mcg
- Frequency
- 2 to 3 times daily
- Duration
- 8 to 12 weeks
Pushing past saturation raises the off-target cortisol, prolactin, and hunger more than it raises growth hormone. Most experienced users hold near the saturation dose instead.
How this score is calculated →
What are the benefits of GHRP-2 (Pralmorelin)?
Upside contribution: 1.94
| Dimension | Weight | Score | Visual | Weighted |
|---|---|---|---|---|
| Efficacy | 25% | 3.2 | 0.800 | |
| Breadth | 15% | 3.0 | 0.450 | |
| Evidence | 25% | 2.8 | 0.700 | |
| Speed | 10% | 3.4 | 0.340 | |
| Durability | 10% | 2.0 | 0.200 | |
| Bioindividuality | 15% | 3.0 | 0.450 | |
| Total | 2.940 |
Upside Rationale
The upside is concentrated in raw growth-hormone power and a one-of-a-kind clinical credential, not in proven body-composition results. GHRP-2's genuine asset is a strong, reproducible growth-hormone pulse plus a regulator-validated diagnostic approval that no rival peptide holds. Its ceiling is that the human literature is almost entirely acute and diagnostic, with no adult outcome trial for fat loss, strength, or recovery, per Sigalos 2018. Speed is excellent and evidence is unusually formal for the class, but durability is low because everything fades off-drug. Breadth and bioindividuality score moderately on the growth-hormone axis touching many systems and on a predictable response that varies with age and body fat.
What makes GHRP-2 unusual is the gap between how well it is documented and how little it is proven. The growth-hormone response is one of the best-characterized in the entire peptide world, separating healthy adults from deficient patients at about 84.6 versus 1.36 micrograms per liter. Yet not one adult trial has measured whether that surge changes your body.
Nick Urban, on the diagnostic data in Chihara 2007
Efficacy (3.2/5.0): Efficacy is solid on hormone release and capped by missing outcomes. A single intravenous GHRP-2 bolus produced a peak growth hormone of about 110 mU per liter versus 33 for an equal GHRH dose, with a 90-minute area under the curve roughly 3 times higher, per Tiulpakov 1995. In a head-to-head, it out-released ipamorelin on raw potency, per Raun 1998, and continuous dosing held growth hormone elevated 1.8 to 3 times with IGF-1 on a stable plateau across 30 days in older adults, per Bowers 2004. That is a stronger release than most peptides in the class. The reason it is not higher: every one of those numbers is a hormone biomarker. No adult trial has measured whether that translates into fat loss or muscle, which is the gap tesamorelin's outcome data fills.
Breadth of Benefits (3.0/5.0): Breadth is moderate because the growth-hormone axis plausibly touches many systems while human-proven breadth is narrow. Growth hormone and IGF-1 influence body composition, recovery, sleep, skin, and bone in theory, but for GHRP-2 the proven human reach is diagnostics plus one modest pediatric growth result, where height velocity rose from 3.7 to 6.1 cm per year, per Pihoker 1997. Two extra threads add theoretical breadth: it strongly stimulates appetite, per Laferrere 2005, which is a feature for wasting and a bug for recomposition, and in rodents it suppresses muscle-wasting genes through the ghrelin receptor, per Yamamoto 2008. Real but mostly unproven in people.
Evidence Quality (2.8/5.0): Evidence quality is the most interesting dimension, higher than most grey-market peptides yet still short of a treatment-grade base. The standout is a regulator-validated diagnostic: Japan's 2004 approval rests on a pivotal trial that cleanly separated healthy adults from deficient patients, per Chihara 2007, backed by accuracy data showing 81 percent sensitivity and 95 percent specificity against the reference test, per Kinoshita 2013. That is a real clinical credential. But a 2018 review is blunt that few long-term controlled studies exist for this class, per Sigalos 2018, and there is no adult outcome RCT. So the evidence is formal and reproducible for what growth hormone does acutely, and empty for what GHRP-2 does to body composition over time.
Speed of Onset (3.4/5.0): Speed is a clear strength. The growth-hormone peak lands within 60 minutes of a single dose in essentially all subjects, per Chihara 2007, and with chronic dosing IGF-1 rises within 24 hours and stays up, per Bowers 2001. The acute pharmacology is fast and predictable. Any subjective changes people chase, deeper sleep or appetite shifts, also show within the first days rather than weeks. The reason this is not higher is that the fast biomarker move does not equal a fast outcome, since no outcome has been measured.
Durability (2.0/5.0): Durability is low because the effect is functional and fully drug-dependent. GHRP-2 amplifies your own pulsatile release, so when dosing stops, growth hormone and IGF-1 drift back toward baseline. The short half-life of about 33 minutes means each dose is a discrete pulse, per Pihoker 1998. Chronic dosing held the biomarker plateau without rapid tachyphylaxis over 30 days, per Bowers 2004, which is a small plus over a one-shot stimulant, but that is a maintained-while-dosed state, not a lasting change. Nothing in the literature shows a benefit that persists after a cycle ends.
Bioindividuality Upside (3.0/5.0): Response is predictable enough to plan around, with clear modifiers. Older adults and those with lower baseline growth-hormone output tend to respond more, while younger people with a healthy axis often notice little. Synergy with a GHRH peptide is larger in the young and varies by sex, and the magnitude tracks age, abdominal fat, and IGF-1 status, per Bowers 2004. The diagnostic data also shows a wide, reliable separation between healthy and deficient responders, per Chihara 2007. Those known modifiers lift this above average, but they also mean a meaningful share of healthy younger users will feel little beyond hunger.
What are the risks & downsides of GHRP-2 (Pralmorelin)?
Downside contribution: 2.06 (safety risks weighted extra)
| Dimension | Weight | Score | Visual | Weighted |
|---|---|---|---|---|
| Safety | 30% | 2.8 | 0.840 | |
| Side effects | 15% | 3.0 | 0.450 | |
| Cost | 5% | 2.6 | 0.130 | |
| Effort | 5% | 3.2 | 0.160 | |
| Opportunity | 5% | 3.0 | 0.150 | |
| Dependency | 15% | 2.5 | 0.375 | |
| Reversibility | 25% | 1.8 | 0.450 | |
| Total | 2.555 | |||
| Harm subtotal × 1.4 | 2.961 | |||
| Opportunity subtotal × 1.0 | 0.440 | |||
| Combined downside | 3.401 | |||
| Baseline offset (constant) | −1.340 | |||
| Effective downside penalty | 2.061 |
Downside Rationale
The downside is dominated by lower selectivity and thin outcome data rather than acute danger. The defining penalty against the cleaner peers is GHRP-2's off-target load: it raises cortisol, prolactin, and appetite, the exact burdens ipamorelin was engineered to avoid, per Raun 1998. On top of that, the daily-injection logistics, the recurring cost on an unproven optimization use, and a real opportunity cost against the better-evidenced tesamorelin all add weight. There is no documented intrinsic fatal signal, so safety scores on its real, off-target-driven profile rather than a worst-case floor. Dependency is moderate and reversibility is excellent, since it clears fast. The pattern to keep in mind is that none of these downsides is dramatic on its own, but they stack into a meaningful tax on a use case that has no proven payoff to justify it.
Safety Risk (2.8/5.0): Safety risk is moderate and driven by off-target hormones plus unknowns, not a confirmed catastrophic effect. No intrinsic life-threatening event is documented at clinical doses, and a 30-day infusion kept safety labs normal, per Bowers 2004. The genuine concerns are the cortisol and ACTH rise comparable to natural CRH, per Arvat 1997, the prolactin elevation on chronic use, possible reduced insulin sensitivity, and sustained IGF-1 feeding a theoretical proliferation risk that a 2018 review explicitly flags as an unfilled cancer-data gap, per Sigalos 2018. It scores worse than ipamorelin precisely because of those off-targets, and active cancer is an absolute reason to avoid it. There is no approved chronic-therapeutic safety dataset, so long-term safety stays unproven.
Side Effect Profile (3.0/5.0): Side effects are the decisive penalty against ipamorelin. The clearest and best-quantified is hunger: food intake rose 35.9 percent after dosing in lean healthy men, with every subject eating more, per Laferrere 2005. On top of that, a 1 to 2 mcg per kilogram dose raised cortisol, ACTH, and prolactin in humans, per Arvat 1997. Growth-hormone-class water retention, facial puffiness, and finger tingling round out the profile and are dose-dependent. Ipamorelin avoids the cortisol, prolactin, and appetite entirely, which is the whole reason this dimension scores higher here.
Financial Cost (2.6/5.0): Cost is moderate and recurring. Research-grade GHRP-2 is inexpensive per dose, but daily-to-thrice-daily injections, the near-universal GHRH peptide partner, and IGF-1 testing push a real cycle toward a few hundred dollars a month. It is not expensive per vial; the relevant framing is ongoing spend on a use that no human outcome trial supports.
Time/Effort Burden (3.2/5.0): Effort is meaningful. GHRP-2 requires reconstitution with bacteriostatic water, subcutaneous injection one to three times daily on an empty stomach, careful timing around food and sleep, cold storage, and usually a second peptide drawn into the mix. That is a real daily logistics load next to an oral supplement, and the fasted-timing rules add friction most people underestimate.
Opportunity Cost (3.0/5.0): Opportunity cost is genuine because a better-evidenced option exists for the same goal. Tesamorelin is an FDA-approved GHRH analogue with human outcome trials, and you can read the tesamorelin report for the contrast. The common GHRP-2 stack also overlaps heavily with the CJC-1295 no-DAC report, which carries the same caveats. Money and effort spent on an unproven optimization protocol could go to that approved option or to training, protein, and sleep, which move the same targets with far more certainty.
Dependency/Withdrawal (2.5/5.0): Dependency risk is moderate. GHRP-2 is non-suppressive and produces no withdrawal syndrome, so benefits simply fade when dosing stops rather than crashing, per Bowers 2004. The honest caveat is that any benefit is administration-locked: you keep dosing to keep the effect. There is no documented addiction, but the functional reliance is real.
Reversibility (1.8/5.0): Reversibility is excellent and one of GHRP-2's genuine strengths. The roughly 33-minute half-life means a bad reaction or unwanted side effect clears within hours, per Pihoker 1998, and stopping returns the growth-hormone axis to baseline without a taper or lasting change. Nothing about the molecule produces a permanent effect, so a low-regret stop is always available.
Is GHRP-2 (Pralmorelin) worth it?
GHRP-2 lands at Neutral because it pairs genuine strengths, a strong growth-hormone pulse and a one-of-a-kind diagnostic approval, with genuine weaknesses, lower selectivity and an empty adult-outcome file. If you want raw growth-hormone output and accept the appetite, cortisol, and prolactin off-targets, it does deliver a stronger release than ipamorelin, per Raun 1998. If you want a clean profile or evidence-backed fat loss, it is the wrong pick, and the better-supported path is tesamorelin. For any non-diagnostic use it is a research chemical, so sourcing and verification matter as much as the pharmacology. The two biggest real-world frictions are the hunger spike and the unregulated supply.
✅ Best for: Experienced peptide users who want a stronger growth-hormone pulse than ipamorelin and understand they are trading selectivity for it. Older adults with lower baseline growth-hormone output, who tend to respond more. People who will pair it with a short-acting GHRH peptide to exploit the documented synergy, per Bowers 2004. Anyone who can source verified pharmaceutical-grade material with a certificate of analysis and will monitor IGF-1, glucose, and the cortisol load. Users who already have training, protein, and sleep dialed in and want a closely tracked experiment rather than a proven staple.
❌ Avoid if: You have active or hormone-sensitive cancer, since growth-hormone and IGF-1 signaling can promote proliferation. You are pregnant or breastfeeding, with no safety data. You have uncontrolled diabetes or insulin resistance, because growth hormone opposes insulin. You are prone to high prolactin or cortisol problems, which GHRP-2 directly worsens, per Arvat 1997. You are trying to lose weight and cannot manage the roughly 36 percent appetite surge, per Laferrere 2005. You compete in tested sport, since it is banned at all times under WADA S2. You cannot verify source quality, because grey-market contamination may exceed the intrinsic risk.
The honest trade with GHRP-2 is right there in the numbers. You buy a stronger growth-hormone pulse and the only regulator-validated credential in the whole GHRP class, and you pay for it with a 36 percent jump in hunger and a cortisol rise that ipamorelin simply does not have.
Nick Urban, on the Raun 1998 head-to-head
What is GHRP-2 (Pralmorelin) best for?
The overall BioHarmony score reflects the intervention's primary evidence profile. These subratings are independent assessments per use case.
| Use Case | Score | Summary |
|---|---|---|
| ○ Body Composition / Fat Loss Primary | 4.2 | Body composition scores moderate because the growth-hormone rise behind it is real and reproducible, but no adult human trial measures fat loss or lean mass for GHRP-2. Continuous dosing held growth hormone elevated 1.8 to 3 times and kept IGF-1 at a stable plateau over 30 days in older adults, per Bowers 2004, which is the strongest signal that the axis stays activated. The honest gap is that these are surrogate biomarkers. The only true clinical outcome is a modest pediatric height-velocity gain, per Pihoker 1997, and the appetite spike per Laferrere 2005 actively works against a fat-loss goal. |
| ○ Recovery / Repair Primary | 4.0 | Recovery scores moderate on mechanism rather than proof. GHRP-2 raised growth hormone and sustained IGF-1, the hormones behind tissue repair, per Bowers 2004, and in rodents it directly suppressed the muscle-wasting genes Atrogin-1 and MuRF1 through the ghrelin receptor, per Yamamoto 2008. Both point toward an anti-atrophy and repair role. The cap is that no human study measures recovery, soreness, or healing for GHRP-2, so the score reflects strong supporting physiology with an empty human outcome file, the same pattern that holds across this peptide class. |
Frequently Asked Questions
What does GHRP-2 actually do, and how does it work?
GHRP-2 tells your pituitary to release a sharp pulse of growth hormone by binding the ghrelin receptor, the growth-hormone secretagogue receptor type 1a, per Laferrere 2005. It is not a GHRH peptide and does not use the GHRH receptor. Instead it amplifies your own GHRH signal and partly opposes somatostatin, the brake on growth hormone, per Doi 2004. That dual action is why it is a strong releaser and why it pairs well with a GHRH peptide.
How much GHRP-2 do people use, and what is it stacked with?
The only approved dose is a single 100 mcg intravenous bolus for the diagnostic test, per Chihara 2007. Off-label optimization use commonly cites 100 to 300 mcg subcutaneous, 1 to 3 times daily, fasted, and these are not approved doses. The ghrelin receptor saturates near 100 mcg per dose, so larger amounts mostly add cortisol and hunger. Most users pair it roughly 1:1 with a short-acting GHRH peptide such as CJC-1295 no-DAC, because the two raise growth hormone more together than alone, per Bowers 2004.
What does the human evidence on GHRP-2 actually show?
GHRP-2 has strong acute evidence and almost no outcome evidence. A single dose drives a peak growth-hormone response well above an equal dose of GHRH, per Tiulpakov 1995, and continuous dosing held growth hormone elevated and IGF-1 on a stable plateau over 30 days, per Bowers 2004. But a class review notes few long-term controlled studies exist, per Sigalos 2018. No adult body-composition or strength trial has ever been run, so the practical payoff is inferred from biomarkers.
Why is GHRP-2 approved in Japan, and what is the diagnostic test?
Japan approved pralmorelin as a single-dose diagnostic test for growth-hormone deficiency, the unique credential in this peptide class. In the validation study, a 100 mcg dose produced a peak growth hormone of about 84.6 mcg per liter in healthy adults versus 1.36 in deficient patients, with a 15 mcg per liter cutoff, per Chihara 2007. A later study found 81 percent sensitivity and 95 percent specificity against the insulin tolerance test, per Kinoshita 2013. The approval is diagnostic, not therapeutic.
What are the side effects of GHRP-2?
The signature off-targets are cortisol, prolactin, and hunger. A 1 to 2 mcg per kilogram dose raised prolactin, ACTH, and cortisol in humans, with cortisol-releasing activity comparable to the natural CRH hormone, per Arvat 1997. Food intake rose about 36 percent after dosing in lean men, per Laferrere 2005, since GHRP-2 mimics the hunger hormone ghrelin. Growth-hormone-class water retention, facial puffiness, and finger tingling are also common and dose-dependent.
Is GHRP-2 safe, and what are the long-term risks?
GHRP-2 has no documented intrinsic fatal or catastrophic signal at clinical doses, and a 30-day infusion kept safety labs normal, per Bowers 2004. The real concerns are the off-target cortisol and prolactin load, possible reduced insulin sensitivity, and sustained IGF-1 feeding a theoretical proliferation risk, all flagged in a class review that notes the cancer-data gap, per Sigalos 2018. There is no approved chronic-therapeutic safety dataset, so long-term safety is genuinely unproven.
GHRP-2 versus ipamorelin: which should I choose?
GHRP-2 is the stronger releaser; ipamorelin is the cleaner one. In a head-to-head, GHRP-2 had higher potency but raised ACTH and cortisol, while ipamorelin, the first selective growth-hormone secretagogue, did not raise either above baseline, per Raun 1998. GHRP-2 also drives appetite and prolactin that ipamorelin avoids. If you want raw growth-hormone output, GHRP-2 wins; if you want a clean profile with less hunger and cortisol, see the ipamorelin report. Most users who want stronger output stack GHRP-2 with a GHRH peptide.
Who should avoid GHRP-2, and how fast does it work?
Avoid GHRP-2 with any active or hormone-sensitive cancer, in pregnancy, with uncontrolled diabetes, or where high cortisol or prolactin is harmful, since these are the pathways it pushes. Competitive athletes must avoid it too, as it is banned at all times under WADA category S2. On speed, the growth-hormone peak lands within 60 minutes of a single dose, per Chihara 2007, and IGF-1 rises within 24 hours of chronic dosing, per Bowers 2001.
What could change GHRP-2 (Pralmorelin)'s score?
BioHarmony scores are living assessments. New research, regulatory changes, or personal context can shift the score up or down. These are the most likely scenarios that would change this intervention's rating.
The fastest way up is a real adult outcome trial, and the fastest way down is a confirmed safety signal on the off-targets it already shows. Because the current score rests on strong biomarkers with no body-composition data, even one modest outcome study would move Efficacy and Evidence together more than usual. A clean win for the cleaner peers, or a documented harm from the cortisol and IGF-1 load, would pull it the other way. The diagnostic approval is locked in, so the swing factors are almost entirely on the optimization-use side.
| Scenario | Dimension shifts | New Score |
|---|---|---|
| A human trial shows real body-composition or recovery benefit | Efficacy 3.2 to 4.0, Evidence 2.8 to 3.6 | 5.3 / 10 ⚖️ Neutral |
| A head-to-head confirms the GHRP-2 plus GHRH stack beats either alone in outcomes | Efficacy 3.2 to 3.8, Breadth 3.0 to 3.6 | 5.1 / 10 ⚖️ Neutral |
| Longer human safety data clears the cortisol and IGF-1 concerns | Safety 2.8 to 2.2, Side effects 3.0 to 2.6 | 5.3 / 10 ⚖️ Neutral |
| A credible cancer or metabolic harm signal emerges | Safety 2.8 to 4.0, Evidence 2.8 to 2.4 | 4.3 / 10 ⚠️ Caution |
| Independent testing keeps finding mislabeled or contaminated product | Safety 2.8 to 3.4, Bioindividuality 3.0 to 2.5 | 4.6 / 10 ⚖️ Neutral |
| A trial shows the appetite and cortisol load outweighs the growth-hormone gain | Side effects 3.0 to 3.8, Efficacy 3.2 to 2.6 | 4.6 / 10 ⚖️ Neutral |
Key Evidence Sources
- Raun 1998, Eur J Endocrinol: ipamorelin was the first selective growth-hormone secretagogue; in swine GHRP-2 had higher potency but raised ACTH and cortisol while ipamorelin did not.. 1998 head-to-head study: GHRP-2 potency vs selectivity, cortisol and ACTH off-targets
- Arvat 1997, Peptides: GHRP-2 at 1 to 2 mcg per kilogram raised prolactin, ACTH, and cortisol in humans, with cortisol-releasing activity comparable to CRH.. 1997 human study quantifying prolactin and cortisol elevation; dose-response
- Pihoker 1997, J Endocrinol: intranasal GHRP-2 raised height velocity from 3.7 to 6.1 cm per year in short-stature children over 6 to 24 months, a modest but significant gain.. 1997 pediatric treatment trial, the longest-duration human outcome dataset
- Chihara 2007, Eur J Endocrinol: the pivotal KP-102 diagnostic validation, peak growth hormone 84.6 vs 1.36 mcg per liter, 15 mcg per liter deficiency cutoff.. 2007 diagnostic validation trial underlying the Japanese approval
- Bowers 2004, J Clin Endocrinol Metab: a 30-day subcutaneous infusion in older adults held growth hormone elevated 1.8 to 3 times and IGF-1 on a stable plateau, with normal safety labs.. 2004 chronic-dosing study, strongest sustained biomarker evidence and GHRH synergy
- Sigalos 2018, Sex Med Rev: a review of growth-hormone secretagogues noting few long-term controlled studies, a glucose and insulin-sensitivity concern, and an unfilled cancer-data gap.. 2018 class safety review flagging the evidence and oncology gaps
- Tiulpakov 1995, Clin Endocrinol: an intravenous GHRP-2 bolus produced peak growth hormone about 110 mU per liter versus 33 for an equal GHRH dose, with a 90-minute area under the curve roughly 3 times higher.. 1995 head-to-head trial quantifying GHRP-2 potency over GHRH and synergy
- Pihoker 1998, J Clin Endocrinol Metab: a phase I pharmacokinetic study in children found a GHRP-2 terminal half-life of about 33 minutes.. 1998 pharmacokinetic study establishing the short half-life
- Doi 2004, Arzneimittelforschung: KP-102 pharmacology showed GHRP-2 depends on endogenous GHRH and partly opposes somatostatin, raising ACTH and corticosterone in rats.. 2004 mechanism study: GHRH dependence and somatostatin resistance
- Laferrere 2005, J Clin Endocrinol Metab: subcutaneous GHRP-2 increased ad-libitum food intake by 35.9 percent versus saline in lean healthy men.. 2005 human study quantifying the appetite increase, the clearest off-target effect
- Kinoshita 2013, Endocr J: the GHRP-2 test had 81.3 percent sensitivity and 94.5 percent specificity for severe adult growth-hormone deficiency against the insulin tolerance test.. 2013 diagnostic accuracy study versus the reference test
- Bowers 2001, Endocrine: in growth-hormone-deficient-pattern older adults, 10 mcg per kilogram gave about twice the response of 1 mcg per kilogram, and chronic dosing raised IGF-1 within 24 hours.. 2001 acute and chronic dose-response study
- Yamamoto 2008, Life Sci: GHRP-2 suppressed the muscle-wasting genes Atrogin-1 and MuRF1 through the ghrelin receptor in rat muscle, independent of IGF-1.. 2008 preclinical anti-atrophy mechanism study, rodent and cell culture only
- WADA 2026 Prohibited List: growth-hormone-releasing peptides are prohibited at all times under category S2.. 2026 anti-doping status under the S2 peptide-hormone category
What does the evidence say about GHRP-2 (Pralmorelin)?
Evidence on this intervention is summarized across three complementary streams: contemporary clinical research, pre-RCT-era pharmacology and observational use, and the traditional medical systems that documented it first. Convergence across streams signals higher confidence; divergence is surfaced honestly.
Modern Clinical Research
Confidence: Medium
Citations: Chihara 2007, Bowers 2004, Raun 1998, Laferrere 2005, Sigalos 2018
Pre-RCT-Era Pharmacology and Use
Confidence: Limited
Citations: Raun 1998
What to Track If You Try This
These are the data points that matter most while running a 30-day Experiment with this intervention.
How to read this section
- Pre
- Test or score before starting the protocol. Anchors a baseline.
- During
- Track while running the protocol so you can see if anything is changing.
- Post
- Re-test after a full cycle to confirm the change held.
- Up
- The marker should rise. For most positive outcomes, that is a good sign.
- Down
- The marker should fall. For most positive outcomes, that is a good sign.
- Stable
- The marker should hold steady. Big swings in either direction are a yellow flag.
- Watch
- Direction depends on dose, timing, and your baseline. Pay close attention to the trend.
- N/A
- No expected direction. The entry is there to anchor a baseline reading.
- Primary
- The Pulse dimension most likely to shift. Track this first.
- Secondary
- Also relevant, but a smaller or less consistent shift. Track if Primary is unclear.
Bloodwork to Order
Open These Markers In Your Dashboard
- IGF 1 Pre | Expected Watch During | Expected Up
- Fasting Glucose During | Expected Watch
- Cortisol During | Expected Watch
Pulse Dimensions to Watch
- Body During | Expected Watch | Primary
- Sleep During | Expected Up | Secondary
- Energy During | Expected Watch | Tertiary
Subjective Signals (Daily Voice Card)
- Hunger or appetite surge within an hour of injection Scale 1-5 | During | Expected Watch
- Water retention, facial puffiness, or hand and finger tingling Scale 1-5 | During | Expected Watch
Red Flags: Stop and Consult
- Rising fasting glucose or HbA1c: stop and consult a clinician, especially with diabetes or prediabetes.
- New or worsening numbness or tingling, a possible fluid-related nerve compression: reduce dose or stop.
- Any active or suspected cancer: do not use, since growth-hormone and IGF-1 stimulation is contraindicated.
- Signs of high prolactin such as low libido or menstrual changes on chronic use: stop and reassess.
Other interventions for Body Composition
See all ratings →📊 How BioHarmony scoring works
BioHarmony translates a weighted expected-value calculation into a reader-facing 0–10 score. Tier bands: Skip 0–3.6, Caution 3.7–4.7, Neutral 4.8–5.7, Worth Trying 5.8–6.9, Strong Recommend 7.0–7.9, Top-tier 8.0+.
Harm-type downsides (safety risk, side effects, reversibility, dependency) carry a 1.4× precautionary multiplier. Harm weighs more than benefit. Opportunity-type downsides (financial cost, time/effort, opportunity cost) are subtracted at face value.
Use case subratings are independent assessments of how well the intervention addresses specific health goals. They are not components of the overall score. Each subrating reflects the scorer's judgment based on use-case-specific evidence, safety, and effect sizes.
Every dimension is evaluated on a 1–5 scale, and the baseline (1) is subtracted before weighting. A perfect intervention with zero downsides contributes zero penalty rather than a residual floor, so top-tier scores are actually reachable.
EV = Upside − Downside
EV = 1.940 − 2.061 = -0.121
Formula v0.5 maps EV = 0 to score 5.0. Above neutral, 1 EV point equals 1 score point. Below neutral, 1 EV point equals about 0.71 score points, so EV = −7 reaches 0.0 while EV = +5 reaches 10.0. Both sides use the full 5-point half-scale.
Score = 5 + (-0.121 / 7) × 5 = 4.9 / 10
