They are not alternatives — they act on different receptors. CJC-1295 is a GHRH analogue that signals the pituitary to release growth hormone. Ipamorelin is a ghrelin receptor agonist that both signals release and eases somatostatin, the brake. That is why the two are so often studied as a pair rather than compared.
| CJC-1295 no DAC from $80 | Ipamorelin from $55 | |
|---|---|---|
| Class | GHRH analogue | Ghrelin receptor agonist |
| Receptor | GHRH receptor | GHS-R1a |
| Length | 29 amino acids | 5 amino acids |
| Half-life | About 30 minutes (no DAC) | Short |
| Effect on somatostatin | None reported | Reduces tone |
| Selectivity | GHRH receptor | Minimal cortisol and prolactin |
| Strengths stocked | 10MG | 5MG, 10MG |
Growth hormone release is controlled by two opposing signals: GHRH promotes it and somatostatin restrains it. A GHRH analogue presses the accelerator. A ghrelin receptor agonist presses the accelerator by a different route and eases the brake at the same time.
Published endocrinology describes synergy between the classes, which is the basis for the combined vial. What ipamorelin adds over the older GHRP compounds is selectivity: comparable growth hormone release without the marked cortisol, prolactin and appetite effects of GHRP-6.
Bowers and colleagues documented synergy between GHRH and growth hormone-releasing peptides as far back as 1990. Acting through separate receptors means the combined response is reported as larger than either alone, which is the mechanistic argument behind the CJC / IPA vial we stock.
Research on that specific commercial pairing is thin. The class-level pharmacology is well documented; a blend is not a trial.
CJC-1295 originally referred to the version carrying a drug affinity complex, which binds albumin and extends the half-life to days. The DAC-free version — modified GRF(1-29) — clears in around half an hour, and produces a pulse rather than sustained elevation. They share a name and are pharmacologically different compounds, so identity confirmation is worth more here than almost anywhere else in the range.
Growth hormone release from the pituitary is governed by an accelerator and a brake. GHRH from the hypothalamus promotes release; somatostatin restrains it. The natural output is pulsatile because those two signals alternate rather than sit constant, and pulsatility matters: sustained elevation downregulates receptors and is associated with the adverse-effect profile of exogenous growth hormone.
CJC-1295 acts on the accelerator. It is GHRH(1-29) — the receptor-binding portion of the 44-residue hormone, which retains full activity — with four substitutions that resist enzymatic breakdown, chiefly DPP-4 cleavage at the N-terminus.
Ipamorelin acts elsewhere. It binds GHS-R1a, the ghrelin receptor, which both prompts release and reduces somatostatin tone. Pressing the accelerator while easing the brake is the mechanistic argument for using the two together, and it is why the question is rarely "which one".
The growth hormone-releasing peptides came out of Cyril Bowers' work in the 1980s and 90s, before the ghrelin receptor had been identified — their activity implied a receptor nobody had found, which is how the field got to ghrelin in 1999. GHRP-6 and GHRP-2 came from that line.
Both carry collateral effects. GHRP-6 stimulates appetite markedly, which is unsurprising given it activates the receptor ghrelin uses. Both raise cortisol and prolactin alongside growth hormone. In a study where those hormones matter, that is a confound rather than a side effect.
Ipamorelin was developed at Novo Nordisk specifically to remove it, and the original 1998 paper describes it as the first selective growth hormone secretagogue: comparable release without the marked ACTH, cortisol, prolactin and appetite response. That selectivity is the entire reason it, rather than GHRP-6, is the usual partner for a GHRH analogue.
CJC-1295 originally described the version carrying a drug affinity complex — a maleimide linker that binds albumin and extends the half-life to days. Early clinical work on that version reported sustained elevation of growth hormone and IGF-1, which is the data most often cited for "CJC-1295" generally.
The DAC-free version, modified GRF(1-29), clears in around half an hour. It produces a pulse and leaves the somatostatin brake and IGF-1 feedback intact, which is precisely why pulsatility research prefers it. The two share a name and are different pharmacological propositions; the published data on one does not describe the other.
Commercially this is the most confused label in the range. The two differ by the linker, which changes the mass, so mass spectrometry settles which is in the vial. A supplier who cannot say which they are selling is telling you something.
The class-level pharmacology is genuinely well documented: synergy between GHRH and growth hormone-releasing peptides was reported by Bowers and colleagues in 1990, and combined administration is used clinically to test pituitary growth hormone reserve. Ipamorelin has its own later literature including rodent bone-density models and a clinical programme in postoperative ileus, which did not lead to approval.
What does not exist is a trial of the specific commercial blend. The reasoning for pairing them is mechanism and class data, not a study of the vial. Stating it the other way round — as though the combination had been tested — is the common overstatement in this corner of the market.
Neither compound is registered in Australia. Both fall under WADA S2, which covers growth hormone secretagogues including GHRH analogues and ghrelin receptor agonists, prohibited at all times and specifically screened for by anti-doping laboratories.
We stock CJC-1295 no DAC at 10MG, ipamorelin at 5MG and 10MG, and the pair pre-blended at 5+5MG and 10+10MG. The blend is labelled by its parts because with a combination the per-compound amount is the number that means something.
Growth hormone release is regulated by IGF-1 feedback: growth hormone prompts hepatic IGF-1 production, and IGF-1 in turn restrains further release. Because both compounds act on the pituitary rather than replacing growth hormone, that loop stays intact — which is the pharmacological distinction between a secretagogue and exogenous growth hormone, and the reason the two are not interchangeable in a study design.
It also caps what a secretagogue can do. The pituitary can only release what it holds, so the ceiling is the gland's own capacity, not the amount administered. That is why the combined GHRH-plus-secretagogue test is used clinically to measure pituitary reserve: it is a probe of the gland, not a bypass of it.
Both are supplied lyophilised and both are stable for long periods dry and cold. Reconstituted with bacteriostatic water and refrigerated, the practical window is weeks — the benzyl alcohol inhibits bacterial growth, which sterile water does not.
Peptides of this length are sensitive to agitation: directing the diluent down the side of the vial and swirling rather than shaking avoids the foaming that indicates denatured peptide. It is a small handling detail that costs nothing and preserves what you paid for.
We make CJC-1295 no DAC at 10MG, ipamorelin at 5MG and 10MG, and the blend at 5+5MG and 10+10MG, in Blacktown, NSW, at ≥99% HPLC purity with 0 ppm heavy metals. All are supplied for in-vitro and laboratory research only, to buyers aged 18 and over.
No. Both act on the pituitary, so IGF-1 feedback stays intact and the ceiling is the gland's own capacity rather than the amount administered.
They act on different arms of the same system — GHRH receptor and ghrelin receptor — and class-level synergy between the two has been documented since 1990.
Yes. Both fall under WADA S2, prohibited at all times, and anti-doping laboratories screen specifically for growth hormone secretagogues.
The original characterisation reports it does not, which is the selectivity that distinguishes it from the earlier GHRPs.
Growth hormone is normally released in pulses. Sustained elevation downregulates receptors and is associated with the adverse-effect profile of exogenous growth hormone, which is why short-acting secretagogues are preferred in pulsatility research.
The 1998 characterisation described it as the first selective growth hormone secretagogue: release comparable to GHRP-6 without the marked cortisol, prolactin and appetite response.
No. Synergy between the GHRH and GHS classes is documented, including work from 1990, but the specific commercial blend has not been trialled.
By mass. The DAC version carries a maleimide linker that changes the molecular weight, so mass spectrometry distinguishes it from modified GRF(1-29).
CJC-1295 is a GHRH analogue acting on the GHRH receptor. Ipamorelin is a ghrelin receptor agonist acting on GHS-R1a, which also reduces somatostatin tone.
They act on separate receptors, and published endocrinology reports synergy between the two classes. We stock the pair pre-blended.
No drug affinity complex. With DAC the half-life extends to days; without it, around thirty minutes, producing a pulse rather than sustained elevation.
Ipamorelin is selective: published comparisons report similar growth hormone release without the marked cortisol, prolactin and appetite effects.
This comparison summarises published research for educational purposes. It is not medical advice. OzPeptides products are sold for research and laboratory use only, not for human consumption. 18+ only.