Every peptide in this category acts on growth hormone release, but they do so through two entirely separate receptors: GHRH analogs act at the GHRH receptor on somatotrophs, and GHRPs act at the ghrelin receptor GHS-R1a. Sorting the catalogue by that division — rather than by marketing category — makes the whole landscape legible in about two minutes.
The two families
| Peptide | Family | Receptor | Molecular weight | Structural note |
|---|---|---|---|---|
| Sermorelin | GHRH analog | GHRH receptor | 3,357.93 Da | The native GHRH(1-29) amide — the minimal active fragment |
| CJC-1295 (no DAC) | GHRH analog | GHRH receptor | 3,367.93 Da | GHRH(1-29) with four substitutions for protease resistance |
| CJC-1295 with DAC | GHRH analog | GHRH receptor | 3,647.28 Da | Same backbone plus a reactive linker for albumin conjugation |
| Tesamorelin | GHRH analog | GHRH receptor | 5,135.86 Da | Full-length GHRH(1-44) with an N-terminal acyl modification |
| Ipamorelin | GHRP / GHS | GHS-R1a (ghrelin receptor) | 711.85 Da | Pentapeptide, Aib-His-D-2-Nal-D-Phe-Lys-NH2 |
| GHRP-2 | GHRP / GHS | GHS-R1a | 817.97 Da | Synthetic hexarelin-family hexapeptide |
| GHRP-6 | GHRP / GHS | GHS-R1a | 873.01 Da | His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 |
| Hexarelin | GHRP / GHS | GHS-R1a, also CD36 | 887.04 Da | 2-methyl-Trp substituted hexapeptide |
The molecular weights alone tell the story: the GHRH analogs cluster at 3.3–5.1 kDa because they are fragments of a 44-residue hormone, while the GHRPs sit under 900 Da because they are short synthetic sequences with unnatural residues, unrelated to ghrelin's own structure despite acting at ghrelin's receptor.
What each family does to the axis
GHRH receptor agonism acts on the amplitude of the natural pulse: it drives somatotroph output but cannot override the somatostatin brake that shapes when release occurs. A GHRH analog therefore works within existing pulsatile architecture rather than replacing it.
GHS-R1a agonism does something different. Ghrelin receptor activation both stimulates somatotroph release directly and attenuates somatostatin tone, which is why GHRPs are described as affecting pulse frequency as well as magnitude. That mechanistic non-overlap is the entire published basis for studying the two families together: work going back to the classic secretagogue literature reported greater growth hormone release from a GHRH analog plus a GHRP combination than from either alone.
Selectivity is what separates the GHRPs
All four ghrelin receptor agonists in the catalogue hit the same receptor; they differ in what else they do.
- Ipamorelin is the selective one. It is reported to stimulate growth hormone release with minimal effect on cortisol and prolactin, which is why it appears in most combination research designs where a clean readout matters.
- GHRP-2 is more potent at the receptor but is reported to produce more collateral endocrine activity.
- GHRP-6 is notable for pronounced appetite-related signalling, consistent with ghrelin's orexigenic role — useful if that is the research question, confounding if it is not.
- Hexarelin is the most potent of the group and also binds CD36, giving it a cardiovascular research literature the others lack. It is also the one most associated with receptor desensitisation on repeated exposure.
The selectivity trade-off is worked through in ipamorelin vs GHRP-2.
Half-life is the other axis
Duration of receptor engagement varies by roughly three orders of magnitude across this catalogue, and it is engineered rather than incidental. Native GHRH is cleared within minutes because dipeptidyl peptidase-4 cleaves its N-terminus; sermorelin, being the unmodified fragment, inherits that vulnerability. The four substitutions in the CJC-1295 backbone block that cleavage and extend circulation into the range of hours. The DAC conjugate goes further still by tethering the peptide to serum albumin, converting a short-lived signal into a sustained one measured in days. Tesamorelin takes a third approach, using an N-terminal acyl group on the full 44-residue sequence.
The research consequence is that these molecules answer different questions. A short-acting analog probes an acute, pulsatile response; a long-acting conjugate probes sustained receptor occupancy, which is a different physiological situation and not simply a more convenient version of the same one. The GHRPs, all small and rapidly cleared, sit firmly at the acute end regardless of which one is chosen.
The CJC-1295 naming problem
This is the most persistent confusion in the category and it is worth stating plainly. The name CJC-1295 was originally applied to a GHRH(1-29) analog bearing a drug affinity complex — a maleimidopropionyl linker that forms a covalent bond with albumin in circulation, extending the half-life dramatically. In common research-supply usage, "CJC-1295" without qualification now usually means the tetra-substituted GHRH(1-29) analog without that linker, also called Mod GRF (1-29).
The two are different molecules with different pharmacokinetics: 3,367.93 Da without DAC and 3,647.28 Da with it, a 279 Da difference that is trivially visible on a mass spectrum. The four substitutions shared by both — at positions 2, 8, 15 and 27 — exist to resist dipeptidyl peptidase cleavage and to reduce chemical degradation of the backbone. The head-to-head is in CJC-1295 vs CJC-1295 with DAC.
Regulatory status differs sharply across the family
These peptides are not in the same legal position as each other, which surprises people who treat the category as uniform. Sermorelin was approved as a medicine and later withdrawn from the market for commercial rather than safety reasons. Tesamorelin is an approved prescription medicine in a specific indication and appears in our catalogue only as a prescription reference listing. CJC-1295 in either form, ipamorelin, and the GHRPs have never been approved anywhere, and following FDA review of bulk substances several of them are not eligible for pharmacy compounding in the United States. Research-grade material across the whole family is supplied for laboratory use only.
Choosing reference standards
If the research question concerns GHRH receptor pharmacology, the choice is between a native fragment (sermorelin, closest to endogenous), a protease-resistant analog (CJC-1295 no DAC, longer-lived without albumin conjugation), and a long-acting conjugate (CJC-1295 with DAC). If it concerns ghrelin receptor pharmacology, the choice is essentially about selectivity, with ipamorelin as the clean probe and the others as deliberately less selective tools.
Fixed-ratio co-formulations exist for combination designs — CJC-1295 (no DAC) + ipamorelin is the most-used pairing — with the same blend-versus-separate-vial trade-off that applies everywhere: a blend fixes the ratio, separate vials preserve the ability to vary one arm. The family is catalogued at GHRPs and secretagogues.
One arithmetic note for anyone comparing across families: 5 mg of ipamorelin is about 7.02 µmol while 5 mg of tesamorelin is about 0.97 µmol — a seven-fold molar difference for the same label mass. Molar terms, always.