> Research Use Only Disclaimer: GHRP-2 (Pralmorelin) is a research peptide not approved by the FDA for human use in the United States. While it holds regulatory approval in Japan (as Pralmorelin) for diagnostic GH stimulation testing, it is not approved for therapeutic use in the US, EU, or most other jurisdictions. All dosing information, protocols, and data presented in this article are sourced from peer-reviewed scientific literature and are provided strictly for educational and research purposes. This article does not constitute medical advice. Do not administer GHRP-2 or any research peptide to humans outside of an approved clinical or research context.
What Is GHRP-2?
GHRP-2 (Growth Hormone Releasing Peptide-2), also known by its clinical name Pralmorelin and research designation KP-102, is a synthetic hexapeptide growth hormone secretagogue (GHS). It was developed in the late 1980s and became one of the most studied members of the GHRP class, progressing through human clinical trials and ultimately receiving regulatory approval in Japan for diagnostic growth hormone stimulation testing.
Its amino acid sequence — His-D-Trp-Ala-Trp-D-Phe-Lys-NH₂ — was designed to mimic the GH-releasing activity of ghrelin while maintaining stability against enzymatic degradation. Unlike native ghrelin, GHRP-2 does not require octanoylation for activity, making it more practical for research applications.
GHRP-2's Clinical Distinction: The Japanese Approval
GHRP-2 (Pralmorelin) is unique among synthetic GHRPs in that it received regulatory approval in Japan (2001) as a diagnostic agent for evaluating pituitary GH secretory capacity. This regulatory history provides a substantial clinical pharmacokinetic dataset that most research peptides lack — making it one of the best-characterized synthetic GHRPs from a human dosing standpoint.
The approved diagnostic dose in Japan is a single IV injection of 100 mcg administered to the subject after an overnight fast. The resulting GH peak at 15–30 minutes post-injection is then interpreted against reference ranges for GH deficiency diagnosis.
This clinical precedent directly informs the subcutaneous research dosing ranges used in contemporary GHRP-2 studies.
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GHRP-2 Mechanism of Action: GHS-R1a Agonism
GHRP-2 exerts its primary effects through potent agonism at the growth hormone secretagogue receptor type 1a (GHS-R1a), the receptor for endogenous ghrelin. This activation triggers:
1. Hypothalamic GHRH release: GHS-R1a stimulation in the hypothalamic arcuate nucleus causes release of endogenous GHRH (growth hormone-releasing hormone), amplifying the pituitary signal
2. Direct pituitary stimulation: GHRP-2 simultaneously acts directly on pituitary somatotroph cells, triggering GH release via calcium-dependent signaling and phospholipase C activation
3. Somatostatin suppression: GHRP-2 inhibits hypothalamic somatostatin release, further amplifying the GH pulse by reducing the primary brake on GH secretion
This dual hypothalamic-pituitary mechanism is why combining GHRP-2 with a GHRH analog (CJC-1295, Sermorelin, Tesamorelin) produces synergistic — not merely additive — GH release in research settings.
Ghrelin Mimetic Activity and Appetite Effects
As a ghrelin receptor agonist, GHRP-2 partially mimics ghrelin's broader physiological role beyond GH secretion. Research in healthy volunteers and GH-deficient patients has documented modest appetite-stimulating effects with GHRP-2 administration — though significantly less pronounced than GHRP-6, which produces strong orexigenic (hunger-inducing) effects.
Studies by Laferrere et al. (2005) found that GHRP-2 at 1 mcg/kg IV produced statistically significant increases in subjective hunger ratings in fasted subjects, with a peak at approximately 30 minutes post-injection. This ghrelin-mediated appetite effect is relevant for research designs studying the ghrelin axis and its role in energy homeostasis, but is considerably milder than what is observed with GHRP-6 or native ghrelin.
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GHRP-2 Dosing Ranges: Evidence from the Literature
Standard Research Dose Range
The clinical literature on GHRP-2 (Pralmorelin) provides unusually clear dose-response data compared to most research peptides. Published subcutaneous and intravenous studies cluster around the following ranges:
| Dose Category | Dose Range | Typical GH Peak (AUC) |
|---|---|---|
| Low / Conservative | 50–100 mcg per injection | ~15–25 ng/mL (IV reference) |
| Standard Research | 100–200 mcg per injection | ~25–50 ng/mL |
| High / Receptor Saturation | 200–300 mcg per injection | ~40–60 ng/mL (diminishing return above 200 mcg) |
Key dose-response finding: Research by Popovic et al. (1995) and Arvat et al. (1997) demonstrated that GHRP-2 GH release approaches saturation at approximately 2 mcg/kg (roughly 150–170 mcg for a 75 kg subject). Beyond this threshold, additional dose increments produce progressively smaller GH gains while increasing cortisol and prolactin co-release. This pharmacodynamic ceiling reinforces the use of 100–200 mcg as the practical research range.
Weight-Based Reference Calculations
For researchers calibrating doses against body weight data from the clinical literature:
| Body Weight | Low Dose (1 mcg/kg) | Standard (1.5 mcg/kg) | High Dose (2 mcg/kg) |
|---|---|---|---|
| 60 kg (132 lb) | 60 mcg | 90 mcg | 120 mcg |
| 70 kg (154 lb) | 70 mcg | 105 mcg | 140 mcg |
| 80 kg (176 lb) | 80 mcg | 120 mcg | 160 mcg |
| 90 kg (198 lb) | 90 mcg | 135 mcg | 180 mcg |
| 100 kg (220 lb) | 100 mcg | 150 mcg | 200 mcg |
The most common dose cited in published studies is 100 mcg, which aligns with the approved diagnostic dose (IV) and provides a strong GH pulse without disproportionate cortisol/prolactin elevation.
Frequency Protocols Used in Research
| Protocol Type | Frequency | Research Application |
|---|---|---|
| Single bolus | Once | Diagnostic GH stimulation testing, receptor pharmacology |
| Short-cycle | 1–2× daily × 7–14 days | GH pulse characterization, desensitization kinetics |
| Sustained (with breaks) | Once daily × 5 days on / 2 days off | Sustained GH secretion studies |
| Combination stack | Once daily with GHRH analog | GHRH/GHRP synergy research |
Desensitization note: Unlike Hexarelin, GHRP-2 demonstrates moderate rather than rapid receptor desensitization. Research protocols extending beyond 2–4 weeks typically incorporate 2-day rest intervals per week to maintain receptor sensitivity. Studies by Huhn et al. (1993) in GH-deficient children found that GH responses remained meaningful for up to 6 months with a pulsatile dosing approach.
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Timing Considerations for GH Pulse Optimization
Timing of GHRP-2 administration significantly affects GH pulse amplitude. Research observations:
Fasted State vs. Fed State
Fasted administration (recommended in most research protocols):
- •Somatostatin tone is lower in the fasted state
- •GH pulse amplitude is typically 40–60% higher compared to post-meal administration
- •Most published studies use an overnight fast or minimum 3-hour post-meal window
Post-meal administration:
- •Elevated blood glucose and free fatty acids increase somatostatin tone
- •GH pulse amplitude is substantially attenuated
- •Insulin peaks post-meal further blunt GH release
- •Generally avoided in research protocols seeking maximal GH pulse characterization
Pre-Sleep Administration
GH physiology produces the largest endogenous GH pulse in the first hours of slow-wave sleep. Administering GHRP-2 approximately 30–60 minutes before sleep onset is a common research timing approach, designed to amplify the endogenous nocturnal GH pulse rather than produce an independent daytime pulse. This timing is supported by research from Ghigo et al. (1994) showing synergistic effects when GHRP-2 is co-administered during the early sleep phase.
GHRH Co-Administration Timing
When used in combination protocols with GHRH analogs (CJC-1295, Sermorelin):
- •Both compounds are typically co-administered simultaneously (same injection or within 5 minutes)
- •The GHRH analog primes the pituitary while GHRP-2 simultaneously suppresses somatostatin and directly stimulates somatotrophs
- •This combination consistently produces 2–4× the GH AUC of either compound alone in published studies
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Reconstitution Protocol for Research Use
> For research purposes only. The following reconstitution information is provided for laboratory researchers handling lyophilized GHRP-2 peptide. See also: Peptide Reconstitution Calculator.
Materials Required
- •Lyophilized GHRP-2 powder (verified purity ≥98% by HPLC)
- •Bacteriostatic water (0.9% benzyl alcohol in sterile water) — preferred for multi-dose vials
- •Sterile water for injection — for single-use or same-day use
- •Insulin syringe (0.3 mL capacity, 29–31 gauge needle recommended)
- •Alcohol swabs (70% isopropyl)
- •Cold storage (2–8°C refrigerator for reconstituted solution)
Reconstitution Calculator: Common Vial Sizes
2 mg (2,000 mcg) vial:
| Bacteriostatic Water Added | Resulting Concentration | Volume per 100 mcg dose |
|---|---|---|
| 1.0 mL | 2,000 mcg/mL | 0.05 mL (5 IU on insulin syringe) |
| 2.0 mL | 1,000 mcg/mL | 0.10 mL (10 IU) |
| 4.0 mL | 500 mcg/mL | 0.20 mL (20 IU) |
5 mg (5,000 mcg) vial:
| Bacteriostatic Water Added | Resulting Concentration | Volume per 100 mcg dose |
|---|---|---|
| 2.5 mL | 2,000 mcg/mL | 0.05 mL (5 IU) |
| 5.0 mL | 1,000 mcg/mL | 0.10 mL (10 IU) |
| 10.0 mL | 500 mcg/mL | 0.20 mL (20 IU) |
Step-by-Step Reconstitution
1. Allow both the GHRP-2 vial and bacteriostatic water vial to reach room temperature
2. Wipe rubber stoppers on both vials with alcohol swabs; allow to dry completely (30 seconds)
3. Draw the calculated volume of bacteriostatic water into the insulin syringe
4. Insert the syringe into the GHRP-2 vial and inject the water slowly along the inner glass wall — do not inject directly onto the lyophilized powder cake, as this can cause peptide degradation
5. Gently swirl the vial — do not shake, vortex, or agitate forcefully
6. Allow to fully dissolve; solution should appear clear and colorless (1–2 minutes)
7. Label the vial immediately: compound name, concentration (mcg/mL), reconstitution date
8. Store reconstituted solution at 2–8°C
Stability and Storage
| Form | Storage Conditions | Typical Stability |
|---|---|---|
| Lyophilized powder | Room temperature, sealed | 12–24 months |
| Lyophilized powder (long-term) | -20°C freezer | 24–36 months |
| Reconstituted with BAC water | 2–8°C refrigerator | 28–30 days |
| Reconstituted with sterile water | 2–8°C refrigerator | Use within 24–72 hours |
Critical: Avoid repeated freeze-thaw cycles of reconstituted GHRP-2. If preparing for multiple uses, reconstitute with bacteriostatic water rather than sterile water to maintain antimicrobial stability over the multi-day research period.
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Cortisol and Prolactin Considerations in Research Design
One pharmacologically important distinction between GHRP-2 and more selective secretagogues (particularly Ipamorelin) is GHRP-2's documented co-stimulation of cortisol and prolactin release in addition to GH.
Magnitude of Effect
Data from Arvat et al. (1997) and other groups consistently show:
- •Cortisol: Intravenous GHRP-2 at 1 mcg/kg elevates cortisol by approximately 30–60% above baseline in healthy adults, peaking at 30–45 minutes post-injection and returning to baseline by 60–90 minutes
- •Prolactin: A similar transient prolactin elevation of 20–40% above baseline is observed, with the same kinetic profile
- •ACTH co-release: A modest ACTH elevation accompanies the cortisol rise, suggesting the effect is partially mediated through the hypothalamic-pituitary-adrenal axis
Implications for Research Design
For studies specifically examining GH-mediated endpoints:
- •If cortisol or prolactin are confounders in your research design, consider Ipamorelin instead — it is highly selective for GH release with no documented cortisol or prolactin co-stimulation
- •For studies of the full ghrelin-axis signaling cascade (where cortisol/prolactin co-stimulation is a relevant readout), GHRP-2 provides a more complete receptor-engagement model than Ipamorelin
For comparative research designs, GHRP-2's moderate cortisol/prolactin response places it between Ipamorelin (none) and Hexarelin (high) on the selectivity spectrum.
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GHRP-2 vs. Other GHRPs: Comparison for Research Selection
When selecting among GHRPs for a research protocol, the following comparison provides a structured decision framework. See also: GHRPs Compared: Full Research Guide and Ipamorelin vs GHRP-2 Comparison.
| Property | GHRP-2 (Pralmorelin) | Ipamorelin | GHRP-6 | Hexarelin |
|---|---|---|---|---|
| GH Pulse Potency | ★★★★☆ High | ★★☆☆☆ Moderate | ★★★☆☆ Moderate | ★★★★★ Highest |
| Cortisol/Prolactin | Moderate | None | Moderate | High |
| Appetite Stimulation | Mild | None | Strong (hunger) | Moderate |
| Desensitization Risk | Moderate | Low | Moderate | High (rapid) |
| Clinical Approval | Yes (Japan, diagnostic) | No | No | No |
| Research Literature Depth | Very extensive | Extensive | Extensive | Moderate |
| Selectivity Profile | Moderate | High | Moderate | Low |
| Typical Research Dose | 100–200 mcg | 200–300 mcg | 100–200 mcg | 75–150 mcg |
Choosing GHRP-2 vs. Alternatives
Choose GHRP-2 when:
- •Strong GH pulse amplitude is needed with a well-characterized pharmacokinetic profile
- •Research benefits from the existing clinical pharmacokinetic dataset (Pralmorelin dosing data)
- •Moderate ghrelin-axis engagement (including appetite signaling) is relevant to the study
- •A balance between potency (vs Ipamorelin) and selectivity (vs Hexarelin) fits the protocol
Choose Ipamorelin instead when:
- •Maximum receptor selectivity is required (GH-only readout, no cortisol/prolactin confounding)
- •Chronic administration across weeks/months is planned (lower desensitization risk)
- •Appetite/orexigenic signaling must be excluded from the research design
Choose Hexarelin instead when:
- •Maximal acute GH stimulation is the research objective and selectivity is less critical
- •Cardiac/cardioprotective research is involved (CD36 receptor pathway)
- •Short-term pulse-amplitude studies where desensitization is less relevant
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GHRP-2 in Combination Research Protocols
GHRP-2's mechanism of action — simultaneous somatostatin suppression, hypothalamic GHRH release, and direct pituitary stimulation — makes it particularly well-suited for combination with GHRH analogs.
Synergistic GHRH/GHRP-2 Combinations
Published research demonstrates that GHRP-2 combined with CJC-1295, Sermorelin, or Tesamorelin consistently produces 2–4× the GH area under the curve compared to either compound alone. The mechanism is complementary signal convergence:
- •GHRH analog (CJC-1295, Sermorelin): Directly stimulates pituitary GHRH receptors, priming somatotroph cells for peak GH release
- •GHRP-2: Simultaneously suppresses somatostatin (removing the brake) and provides additional GHSR-1a-mediated stimulation
This synergy is well-documented in both healthy adults and GH-deficient patients (Bowers et al., 1990; Müller et al., 1999) and forms the pharmacological basis for most multi-compound GH secretagogue research designs.
For combination research protocols, GHRP-2 doses are often reduced to 50–100 mcg (vs 100–200 mcg as monotherapy) given the substantially amplified GH response when combined with a GHRH analog.
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Summary: GHRP-2 Dosage Quick Reference
| Parameter | Research Range |
|---|---|
| Standard dose | 100–200 mcg per injection |
| Low/conservative dose | 50–100 mcg |
| High dose (saturation studies) | 200–300 mcg |
| Administration route | Subcutaneous injection |
| Reconstitution solvent | Bacteriostatic water (preferred) |
| Typical reconstitution concentration | 500–1,000 mcg/mL |
| Optimal timing | Fasted state; 30–60 min pre-sleep for nocturnal studies |
| Frequency (standard protocols) | 1–3× daily with cycle breaks |
| Storage (reconstituted, BAC water) | 2–8°C, up to 30 days |
| Key selectivity consideration | Moderate cortisol/prolactin co-release; mild appetite effect |
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Related Research Resources
- •GHRP-2 Complete Research Profile
- •GHRPs Compared: GHRP-2 vs GHRP-6 vs Ipamorelin vs Hexarelin
- •Ipamorelin vs GHRP-2: Side-by-Side Comparison
- •Peptide Reconstitution Calculator
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> Research Use Only. GHRP-2 (Pralmorelin) is not approved by the FDA for therapeutic use. All information in this guide is derived from peer-reviewed scientific literature and is intended for qualified researchers studying peptide pharmacology under appropriate institutional oversight. This content does not constitute medical advice, and this compound should not be administered to humans outside of a properly approved research context.