Peptide class
Synthetic peptides that bind the ghrelin receptor (GHS-R1a) on pituitary somatotrophs, stimulating pulsatile growth hormone secretion independent of the GHRH pathway.
| Compound | Mechanism | Primary reported use | Profile |
|---|---|---|---|
| Ipamorelin | Selective ghrelin receptor agonist; minimal cortisol/prolactin impact | GH pulse stimulation, body composition, sleep quality | View profile |
| GHRP-2 | Potent ghrelin receptor agonist; elevates cortisol and prolactin | GH secretagogue research | Coming soon |
| GHRP-6 | Ghrelin receptor agonist with pronounced appetite stimulation | GH secretagogue research, appetite research | Coming soon |
| Hexarelin | Most potent GHRP; significant desensitisation on repeated use | Research on GH secretion ceiling and desensitisation | Coming soon |
GHRPs are synthetic mimetics of ghrelin, an endogenous peptide hormone produced primarily by the stomach that acts on the GHS-R1a receptor in the pituitary and hypothalamus. GHS-R1a activation stimulates growth hormone secretion through a distinct pathway from GHRH — these two pathways are complementary and can be co-activated for synergistic GH pulse amplitude. GHRPs do not suppress somatostatin (the GH-inhibitory hormone) in the way GHRH analogues do, but are less sensitive to somatostatin gating than GHRH analogues.
GHRPs differ substantially in their off-target receptor activity. Ipamorelin is noted in research for its selectivity: at research doses it stimulates GH without meaningfully raising cortisol, prolactin, or ACTH — a profile that older GHRPs like GHRP-2 and GHRP-6 do not share. GHRP-6 also stimulates appetite strongly via ghrelin receptor activity in hypothalamic feeding centres, which may be a research variable of interest or an unwanted effect depending on context. Hexarelin is the most potent but also the most prone to receptor desensitisation with repeated use.
Because GHRPs and GHRH analogues act on different receptors, they are commonly co-administered to produce synergistic GH pulses. Ipamorelin combined with CJC-1295 (a long-acting GHRH analogue) is one of the most commonly reported research stacks in GH axis biology, and the pharmacological rationale for the combination is well-established.
GHRPs were developed in the 1980s–90s as tools for investigating the GH secretagogue pathway; the ghrelin receptor was identified in 1996. Early human research showed robust GH-stimulating effects with all class members.
Ipamorelin emerged as the selectivity-optimised representative and has the most favourable research profile for GH-axis studies without hypothalamic-pituitary-adrenal (HPA) axis confounding. Research has investigated GHRPs for their potential role in body composition, recovery, sleep quality (via GH-mediated slow-wave sleep effects), and anti-aging. The GHRH-GHRP combination paradigm has been explored in ageing populations where endogenous GH secretion is reduced.
Ipamorelin
The most selective GHRP available as a research compound; produces a clean GH pulse without meaningful cortisol or prolactin elevation at research doses. Commonly reported doses range from 100 to 300 mcg per dose, administered once to three times daily via subcutaneous injection. Frequently combined with CJC-1295 or Sermorelin for synergistic effect.
GHRP-2
A potent ghrelin receptor agonist with greater cortisol and prolactin elevation than Ipamorelin; useful in research where ACTH axis stimulation is a variable of interest. Research has investigated it for its potential role in GH secretion studies and catabolic conditions.
GHRP-6
Shares the ghrelin receptor mechanism but additionally stimulates appetite markedly via hypothalamic feeding pathways; this may be researched as either a benefit or a confounding variable depending on study design. Historically the most studied GHRP in early research literature.
Hexarelin
The most potent GHRP in terms of GH pulse amplitude, but also the most subject to rapid receptor desensitisation with repeated administration; often used in research specifically designed to study the ceiling effects and tachyphylaxis of the GHS-R1a system.