GHRP-2

GHRP-2 (pralmorelin, KP-102) is a small synthetic peptide, six amino acids long, that acts on the ghrelin receptor to trigger a pulse of growth hormone (GH) from the pituitary gland ¹⁶. It belongs to the growth hormone-releasing peptide (GHRP) family first developed in the 1980s, and it is more potent than the family's original member, GHRP-6 ²³. It is also the only GHRP to reach regulatory approval, licensed in Japan as an intravenous diagnostic agent for GH stimulation testing ¹³.

That approval reflects where the strongest evidence sits. Japanese endocrinologists use a 100 microgram intravenous bolus of GHRP-2 to measure GH reserve in healthy people and to classify deficiency, screen the adrenal axis, and evaluate pituitary tumors ⁶. In healthy adolescents, the same dose produces median GH peaks near 90 ng/mL, compared with roughly 3 ng/mL in organic growth hormone deficiency ⁴.

Beyond diagnosis, GHRP-2 reproduces several effects of ghrelin, the body's natural hunger and growth-hormone signal. It acutely increases food intake in healthy men ²⁹, reactivates pulsatile GH secretion during prolonged critical illness ²², and improves tendon-bone healing in a rat rotator cuff model ². Those tissue and performance angles are the reason it circulates in research and community settings, but no human trials have tested GHRP-2 for muscle gain, fat loss, or injury recovery, so those claims currently rest on animal data and GH-axis inference ¹.

Growth hormone is not released as a steady drip. The pituitary releases it in pulses, and one of the switches that triggers a pulse is the ghrelin receptor (GHS-R1a). GHRP-2 binds and activates that receptor, the same one the natural hormone ghrelin uses, which sends the signal to release a burst of GH ¹⁶.

That path is separate from the one used by growth hormone-releasing hormone (GHRH), which is why the two classes are often combined. In human pituitary cells, GHRP-2 drives GH release mainly through the protein kinase C (PKC) and calcium pathway, while GHRH works through the cyclic AMP (cAMP) pathway ²⁶. The effect also survives when the GHRH receptor is broken: mice with a nonfunctional GHRH receptor still release GH in response to GHRP-2, showing the peptide has its own route through GHS-R1a ¹⁴.

GHRP-2 does not only touch growth hormone. It also prompts the pituitary to release ACTH, which raises cortisol, through a mechanism distinct from CRH ¹⁰. And because it mimics ghrelin, it stimulates hunger ²⁹. In prolonged critical illness, a continuous intravenous infusion reactivated the suppressed GH rhythm and normalized IGF-1 and its binding proteins over five days ²².

One practical wrinkle is response fade. Five consecutive days of subcutaneous dosing in healthy young men caused the GH response to shrink with each day, with no rise in IGF-1 ²⁵. That finding is why research and community protocols favor intermittent pulses rather than constant daily saturation (community protocol).

GHRP-2's documented effects range from well-established human findings to animal-only hints. The table below separates what human studies show from what remains preclinical.

Effect	Setting	Strength of evidence
Robust GH pulse release	Healthy adults and adolescents, 100 µg IV	Strong (human) 3
Increased food intake	Healthy men and obese subjects	Strong (human) 29
ACTH and cortisol release	Human diagnostic testing	Strong (human) 6
Reactivation of GH axis in critical illness	5-day infusion	Moderate (one RCT) 22
Weight gain in anorexia nervosa	1-year intranasal case	Low (single case) 12
Tendon-bone healing, fewer M1 macrophages	Rat rotator cuff model	Preclinical 2
Reduced muscle proteolysis after burn	Rats	Preclinical 17
Anti-inflammatory effects	Rat arthritis model, cell studies	Preclinical 9
Muscle gain, fat loss, recomposition	No trial data	No direct evidence 1

The GH release data are the backbone of the clinical literature. A 100 microgram intravenous bolus produces a mean peak GH of about 25 ng/mL in healthy adults, and markedly higher median peaks of roughly 89-90 ng/mL in healthy adolescents ³. Elderly people respond less strongly, and a peak below roughly 8 ng/mL helped distinguish normal GH reserve from deficiency in that group ⁵.

The appetite effect is the most reproducible non-diagnostic human finding, consistent with GHRP-2 acting like ghrelin at its receptor ²⁹. Healing, muscle preservation, and anti-inflammatory claims are supported only by animal and cell work so far, and the performance-use literature itself notes the absence of human efficacy trials ¹.

Three distinct dosing patterns appear in the GHRP-2 literature: a single diagnostic bolus, a clinical infusion, and the pulsed subcutaneous schedule used in community research.

Diagnostic and clinical patterns

Approved diagnostic testing in Japan uses a single 100 microgram intravenous bolus, with GH sampled over the following 30-60 minutes ⁴. A small randomized trial in prolonged critical illness used a continuous 1 µg/kg/hour infusion for five days, which reactivated pulsatile GH and normalized IGF-1 ²². A one-year daily intranasal course in a patient with severe anorexia nervosa is the longest human exposure on record ¹².

Community research pattern

The most common non-diagnostic pattern is subcutaneous: roughly 1 µg per kg of body weight per injection, which lands at about 100-300 micrograms for most adults, taken two to three times daily while fasted (community protocol). The timeline above shows this schedule with its built-in off days, typically 5 days on and 2 days off within 8-12 week cycles. Fasted dosing matters because food and insulin blunt the GH response to a secretagogue, and multiple small pulses preserve the acute spike better than one large daily dose (community protocol) ²⁵.

The reason for that structure is tachyphylaxis. Five consecutive days of daily subcutaneous dosing in healthy young men progressively dulled the GH response and never raised IGF-1 ²⁵. Scheduled days off let GHS-R1a sensitivity recover between exposure blocks (community protocol).

Rats and cattle have received far larger weight-based doses in preclinical work, for example 100 µg/kg/day subcutaneously in arthritic rats, which does not translate into a human schedule ²¹.

GHRP-2 is supplied as a lyophilized (freeze-dried) powder in injection-grade vials for research handling, matching the intravenous formulation used diagnostically in Japan ¹³. The standard diluent is bacteriostatic water, which contains a small amount of benzyl alcohol; sterile saline is an alternative (community protocol).

Preparation is gentle. Run the diluent slowly down the inside of the vial wall, then swirl to dissolve the powder. Do not shake, since violent mixing can damage the peptide. Unopened lyophilized powder keeps long-term at -20°C and for weeks to months at refrigerator temperature (2-8°C), protected from light and moisture (practitioner consensus). Once reconstituted, the solution belongs in the refrigerator at 2-8°C and is typically used within 14-30 days; repeated freeze-thaw cycles should be avoided (practitioner consensus). Wipe the vial stopper with alcohol before each draw, and discard any solution that turns cloudy or contains particles (community protocol).

The interactive calculator below handles the concentration and dose-volume math. One supply-chain note from the literature: seized research vials have contained authentic GHRP-2 ⁴¹, a structurally modified glycine analogue of GHRP-2 has also been identified in an injection vial ¹³, and a nutritional supplement tablet was found to contain about 50 µg of the peptide ²⁸. In the published studies, unregulated products are authenticated by mass spectrometry ¹³.

The formal interaction literature is thin, but several clinically relevant patterns are documented.

Recombinant human GH. A 100 microgram intravenous dose of GHRP-2 raises both the pituitary-made and recombinant 22 kDa GH isoforms, leaving the ratio used by anti-doping immunoassays unchanged, which can mask recombinant GH use during the detection window ¹⁵. Endogenous GH negative feedback also dulls secretagogue output during exogenous GH exposure (mechanistic).

Glucocorticoids. GH responses to GHRP-2 survive prednisone therapy, unlike GHRH-driven secretion ⁴⁰. On the other side, GHRP-2 itself raises ACTH and cortisol ⁶, so combining it with corticosteroid bursts adds to total cortisol exposure.

Somatostatin analogues. Somatostatin directly blunts GHRP-2-induced GH release in pituitary cell models, so drugs like octreotide functionally oppose the peptide ³⁴.

TRH and GnRH. In the critical-illness trial, adding TRH and pulsatile GnRH to a GHRP-2 infusion normalized thyroid hormones and raised LH and testosterone by 312%, while also preventing the white blood cell and lactate rise seen with GHRP-2 alone ²².

Insulin and sulfonylureas. The class profile includes dysglycemia ¹, and a cachectic patient's symptomatic hypoglycemia resolved during a year of intranasal GHRP-2 ¹², so glucose dynamics can shift in both directions.

Other GHRPs and peptide stacks. Combining GHRP-2 with GHRP-6, hexarelin, or ipamorelin means several agonists competing for the same receptor, with summed cortisol and prolactin exposure and no clear added benefit. The documented synergy is with GHRH analogues such as modified GRF 1-29, which act through the complementary cAMP pathway ²⁶.

Tachyphylaxis, meaning a fading response to the same dose, is a documented feature of GHRP-2 rather than a rumor. Healthy young men receiving daily subcutaneous injections for five consecutive days showed a progressively smaller GH response with no rise in IGF-1 ²⁵. Short cycles and scheduled days off are the community answer, built around that observation (community protocol).

The common research pattern is 8-12 weeks on followed by 2-4 weeks off, with 5 days on and 2 days off inside the on-phase, and multiple small fasted pulses rather than one big daily dose (community protocol). Intermittent pulsing preserves the acute GH spike, which is the compound's defining output, while off periods let the ghrelin receptor recover sensitivity and let prolactin and cortisol normalize between blocks (mechanistic).

There is a limit to how much higher doses can buy. Pituitary capacity, not the dose, caps the response: mice with depleted somatotroph reserve release only a small GH pulse even with GHRP-2 on board ¹⁴. Practitioner consensus holds that beyond about 300 micrograms per injection, added prolactin and cortisol exposure outweighs added GH output (practitioner consensus).

Signals that a break serves the protocol include a missing post-dose hunger surge, fluid retention, joint aches, nipple sensitivity, fragmented sleep, or a rising fasting glucose, all of which map onto the peptide's documented endocrine profile ¹. A responsive 100 microgram bolus is the usual check before restarting after a washout (practitioner consensus).

The rational stacks for GHRP-2 follow one principle: pair it with something that opens a different door to growth hormone.

GHRH analogues (CJC-1295 without DAC, sermorelin, tesamorelin). GHRP-2 and GHRH act through separate receptor pathways, PKC/calcium for the former and cAMP for the latter in human pituitary cells ²⁶. The combination is additive in pituitary cell work and in cattle ³⁴, and the standard community pairing is 100 micrograms of GHRP-2 with 100 micrograms of modified GRF 1-29, repeated fasted two to three times daily (community protocol).

Healing peptides (BPC-157, TB-500). GHRP-2 improved tendon-bone healing, bone density, and biomechanical strength in a rat rotator cuff model ², so it commonly appears in post-injury stacks with connective-tissue peptides, although no direct interaction data exist (community protocol).

GnRH analogues (triptorelin and related). In the critical-illness trial, pulsatile GnRH alongside GHRP-2 reactivated LH and testosterone and blocked the white cell and lactate rise seen with GHRP-2 alone ²². That axis-restoration rationale underpins recovery stacks that include a GnRH pulse (community protocol).

Combinations with no documented upside include other ghrelin-receptor agonists (GHRP-6, hexarelin, ipamorelin), which compete for the same receptor and sum cortisol and prolactin exposure; recombinant GH, which feeds back to suppress endogenous release and muddies anti-doping interpretation ¹⁵; and IGF-1 analogues, which feed back against the GH axis (mechanistic).

Because daily GHRP-2 attenuates its own response ²⁵, most stacks cycle the secretagogue rather than expanding the stack with more GHS-R1a agonists (community protocol).

GHRP-2 (pralmorelin) holds one clinical approval anywhere: Japan, for intravenous diagnostic use in growth hormone stimulation testing ¹³. No FDA approval exists in the United States for any indication, and no approval exists anywhere for performance, body-composition, or anti-aging use ¹. In the US it circulates as an unregulated research peptide, it is not scheduled under the Controlled Substances Act, and compounding pharmacies cannot legally prepare it from bulk API since it is not an approved drug or listed bulk substance.

In sport, GHRP-2 is prohibited at all times under the WADA Prohibited List, in the S2 category for peptide hormones and growth factors ¹. Detection is operational, not theoretical: after a single 100 microgram intravenous dose, unchanged GHRP-2 and its AA-3 metabolite were found in every volunteer's urine ¹⁵, and after intranasal dosing, parent peptide and metabolites remained detectable for up to 47 hours ¹¹. Dried blood spot methods ⁴⁴ and aptamer-based enrichment followed by mass spectrometry ⁴⁶ extend detection to blood and improve sensitivity, and real-world urine positives in athletes have been confirmed ⁴⁵.

The peptide also carries a masking hazard. Because GHRP-2 raises both pituitary and 22 kDa (recombinant-pattern) GH isoforms without changing their ratio, it can hide recombinant GH use on the isoform immunoassay while the peptide itself remains detectable ¹⁵.

Supply-chain findings complete the picture: GHRP-2 has been found in an over-the-counter nutritional supplement tablet ²⁸, in seized unlabeled vials quantified by NMR and mass spectrometry ⁴¹, and in a modified glycine analogue form apparently built to evade targeted screening ¹³.

The most consistent human effect of GHRP-2 is also its most common side effect: hunger. Clinical studies show acute increases in food intake in healthy and obese adults ²⁹, which is on-target ghrelin-receptor signaling rather than an idiosyncratic reaction.

Endocrine shifts travel with it. GHRP-2 reliably releases ACTH and cortisol at diagnostic doses ⁶, raises prolactin in synchronization with GH and TSH during infusion ³⁶, and the class-wide adverse profile in reviews includes fluid retention, joint and muscle aches, appetite changes, dysglycemia, and injection-site reactions ¹. One cautionary case: a patient with Cushing's disease, whose pituitary tumor expressed the ghrelin receptor, showed an exaggerated 38-fold ACTH surge after a 100 microgram dose ¹⁸.

Desensitization is the dose-frequency issue. Five consecutive days of daily subcutaneous dosing in healthy young men dulled the GH response with no rise in IGF-1 ²⁵, which is why schedules in community research are built around days off.

The documented contraindications are structural. Because GHRP-2 can drive GH release directly from acromegalic tumor cells in culture ²⁶ and spike ACTH from corticotroph tumors ¹⁸, active pituitary adenomas are a hard stop. Active malignancy is a precaution because the GH-IGF-1 axis carries mitogenic concerns for this class ¹, and pregnancy and breastfeeding have zero human data.

Practical monitoring in the literature centers on glucose, the adrenal axis, prolactin, and IGF-1. A flat IGF-1 weeks into a cycle suggests the GH response has faded ²⁵, and morning cortisol plus ACTH should be checked if fatigue or cushingoid features appear ¹⁰. For older adults the GHRP-2 test is considered relatively safe among provocative endocrine tests, so age alone is not a barrier in diagnostic use ⁵.