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GHRP-2

Not FDA approved KP-102 · Pralmorelin · Growth Hormone-Releasing Peptide 2

Not approved by the FDA for general clinical use. Pralmorelin (GHRP-2) was clinically investigated for GH deficiency diagnosis but did not receive approval for routine therapeutic use in the US. Research peptide only.

What is GHRP-2?

GHRP-2 (Growth Hormone-Releasing Peptide 2), also known by its generic name pralmorelin, is a synthetic hexapeptide that acts as a growth hormone secretagogue. It was developed in the 1980s in Cyril Bowers’ laboratory as part of a series of peptides designed to mimic the effect of ghrelin — the “hunger hormone” — on the anterior pituitary.

Unlike GHRH analogs such as CJC-1295, which act directly on GHRH receptors, GHRP-2 exerts its effect primarily through the GHS-R1a receptor (Growth Hormone Secretagogue Receptor 1a), the endogenous receptor for ghrelin. This complementary mechanism of action is why the GHRP-2 + CJC-1295 combination generates such marked synergy: both molecules act on distinct but convergent pathways for GH release.

GHRP-2 is differentiated from its close relative GHRP-6 primarily in its side effect profile. While GHRP-6 produces a pronounced increase in appetite (an effect directly mediated by ghrelin receptor stimulation), GHRP-2 has a more moderate ghrelinergic effect, making it the preferred option when GH stimulation is desired without the exacerbated hunger component. In terms of potency for GH release, both are comparable, though some studies report GHRP-6 may generate slightly higher peaks at equivalent doses.

Mechanism of Action

GHRP-2 acts through multiple convergent mechanisms:

1. Direct agonism at GHS-R1a (ghrelin receptor): GHRP-2 binding to GHS-R1a receptors on somatotroph cells of the anterior pituitary activates phospholipase C, elevates diacylglycerol (DAG) and inositol triphosphate (IP3), and triggers intracellular calcium influx that initiates GH granule exocytosis.

2. Stimulation of endogenous GHRH: Beyond its direct pituitary action, GHRP-2 acts on hypothalamic neurons to promote endogenous GHRH release. This dual mechanism — hypothalamic + pituitary — is the primary reason for the synergy observed when combined with exogenous GHRH analogs.

3. Somatostatin inhibition: GHRP-2 can partially suppress somatostatin (SRIF), the primary inhibitor of GH secretion. By reducing somatostatinergic tone, the threshold for GH release decreases and the resulting pulses have greater amplitude.

The most relevant downstream effects documented in research include:

  • GH elevation: Short-duration but high-amplitude peaks, occurring 1-3 hours after injection.
  • IGF-1 elevation: Sustained increase in insulin-like growth factor 1, a key mediator of GH’s anabolic and reparative effects.
  • Anti-inflammatory effects: Preclinical studies have identified anti-inflammatory properties independent of GH elevation, possibly mediated by GHS-R1a receptors in peripheral tissues.
  • Body composition improvement: Lean mass gain and visceral fat reduction in extended research models.

Reported Protocol

Standard reconstitution: 5 mg vial + 2.5 mL bacteriostatic water = 2 mg/mL (2000 mcg/mL). Each 0.1 mL contains 200 mcg.

WeeksReported DoseFrequency
1–2100 mcg1–2×/day SC, fasted
3–4200 mcg1–3×/day SC, fasted
5–12300 mcg1–3×/day SC, fasted

Higher-frequency research protocols (3×/day) report injections at three specific times: upon waking, pre-workout, and at bedtime. In all cases, the fasted condition (minimum 2 hours without carbohydrate or protein intake) is considered critical to maximize the GH response.

Optimal reported stack: GHRP-2 + CJC-1295 No DAC (or Sermorelin). The commonly used ratio is 1:1 in micrograms, injected simultaneously. This combination exploits the GHRH+GHRP synergy, where the combined effect significantly exceeds the action of either compound alone.

Reported Side Effects

  • Increased appetite: Present due to the ghrelinergic mechanism, though significantly lower than with GHRP-6. This is a key differentiator when choosing between the two peptides.
  • Mild water retention: Related to GH and IGF-1 elevation; more pronounced in the first weeks of use.
  • Mildly elevated cortisol: GHRP-2 can moderately stimulate the hypothalamic-pituitary-adrenal axis, with cortisol increases observed in some studies. At standard doses (≤300 mcg/dose) this effect is generally modest.
  • Post-injection drowsiness: Particularly notable with the nighttime dose, which may be desirable as it can enhance deep sleep and the nocturnal GH surge.
  • Numbness or paresthesias: In extremities at high doses or with prolonged use, related to IGF-1 elevation.
  • Lipohypertrophy: With repeated use at the same injection site.

Storage

  • Lyophilized (powder): Store at -20°C, protected from light. Stable until indicated expiration date.
  • Reconstituted: Store at 2-8°C. Stable for up to 30 days (greater stability than reconstituted CJC-1295 No DAC).
  • Do not freeze the reconstituted solution.
  • Use insulin syringe (0.3-1 mL) for precise dosing.
  • Rotate injection sites between abdomen, thigh, and deltoid.

This content is for educational purposes only. Not medical advice. Always consult a healthcare professional before starting any research protocol.

Reported protocol (research reference)

Vial sizes 5 mg
Reported dose Research protocols report: escalation from 100 mcg (weeks 1-2) to 300 mcg (weeks 5-12), subcutaneous 1-3 times daily in a fasted state. Reconstitution: 5 mg + 2.5 mL bacteriostatic water = 2 mg/mL.
Half-life 15-30 minutes. Very short, pulsatile half-life — injection timing and fasted state are critical.
FDA status Not FDA approved
This information is for educational and research reference only. It is not medical advice. We do not sell, prescribe, or recommend any treatment. Dosages cited come from research literature and are not an indication for human use. Always consult a licensed healthcare provider.