CJC-1295 vs Ipamorelin

How they differ structurally

The CJC-1295 we stock is the version without the drug affinity complex, usually written CJC-1295 no DAC or Mod GRF 1-29. It’s CAS 863288-34-0 and it’s a 29-amino-acid peptide based on the first 29 residues of growth-hormone-releasing hormone, GHRH, which is the part of the native hormone that carries its receptor-binding activity. Four residues in that sequence are substituted relative to native GHRH(1-29) to resist enzymatic cleavage and improve stability, which is what the Mod in Mod GRF stands for. There’s a separate molecule, CJC-1295 with DAC, that adds a reactive linker designed to bind serum albumin, and much of the human literature under the CJC-1295 name concerns that version. Ours is the no-DAC form, and it comes to you in the same vial as ipamorelin in the CJC-1295 / Ipamorelin combination, 10mg total. The learn page for the combined vial covers the DAC distinction in more depth.

Ipamorelin, CAS 170851-70-4, is a pentapeptide, five residues long, and shares no sequence with GHRH at all. It was designed in the 1990s as a synthetic growth-hormone secretagogue, a class of small peptides and non-peptides that act at the ghrelin receptor, and it contains unnatural residues including D-amino acids and a naphthylalanine, which is typical of that class and gives the short chain its stability. We stock it on its own at 10mg, and the ipamorelin learn page goes through the design history.

So the structural comparison is 29 mostly natural residues built from a hypothalamic hormone versus five heavily engineered residues built from scratch.

Receptor and mechanism differences

This is where the two are cleanly different, and it’s the reason they’re so often paired. GHRH, and by extension CJC-1295 no DAC, acts at the GHRH receptor on somatotroph cells in the anterior pituitary. That receptor is G-protein coupled and signals through cyclic AMP, and its activation is the primary physiological driver of growth hormone synthesis and pulsatile release. A GHRH analogue, in published pituitary cell and animal models, raises growth hormone output through this direct pituitary route.

Ipamorelin acts at a different receptor entirely: the growth hormone secretagogue receptor, also called the ghrelin receptor, whose natural ligand is the stomach hormone ghrelin. That receptor is present in the pituitary and the hypothalamus, and its activation in models raises growth hormone release through a route that’s partly direct on somatotrophs and partly through the hypothalamus. The original characterization paper on ipamorelin reported that it stimulated growth hormone release in animal and cell models without a matching rise in cortisol or prolactin, which is why it’s described as a selective secretagogue; earlier compounds in the class, such as GHRP-6, were less selective in that respect.

Because the two receptors sit on overlapping cell populations and signal through partly separate pathways, the published rationale for combining a GHRH analogue with a secretagogue is that they act synergistically in models rather than additively. That’s the mechanistic idea behind the combined vial. It’s also why, if you’re studying either receptor in isolation, you’d want the individual compounds rather than the blend, and why a study that uses only the blend can’t attribute an effect to either receptor alone.

What the literature compares

The GHRH(1-29) analogue literature is old and reasonably deep, because the native 1-29 fragment was characterised in the 1980s and various stabilised versions followed. Much of it is pituitary cell culture and rodent work on growth hormone release and on the pulsatility of that release. The specific human data under the CJC-1295 name mostly concern the DAC version, including a 2006 study in healthy adults that reported prolonged growth hormone and IGF-1 elevation with that albumin-binding form. Those results don’t transfer directly to the no-DAC molecule, whose action in circulation is much shorter, and you should keep the two apart when you read.

Ipamorelin’s core literature is the 1998 characterization paper from Novo Nordisk, which established its selectivity profile in rat pituitary cells and in vivo, plus a smaller number of later studies in rodent models including some on gastrointestinal motility. There was also a short clinical program for a post-operative ileus indication that didn’t proceed. The published record is thinner than for the GHRH analogues, and selectivity data from other labs is limited.

Direct comparisons of a GHRH analogue against a secretagogue in the same model exist, mainly from the 1990s when the secretagogue class was being characterised, and they generally report that combining the two classes gives a larger growth hormone response than either alone. Studies using CJC-1295 no DAC and ipamorelin specifically, as opposed to other members of each class, are scarce, and the literature is thin here.

Handling differences in the lab

Both are handled the same way. Each arrives as a lyophilized powder in a sealed vial, and sealed vials should be kept at -20C and protected from light. Reconstitute with bacteriostatic water run gently down the inside of the vial, and swirl rather than shake until the solution is clear. Keep everything sterile, label the vial with the contents and the date, hold reconstituted material at 2-8C, use it within 28 days, and avoid freeze-thaw.

There are two practical points worth knowing. First, the combined vial contains two peptides of very different length and chemistry, and any analytical work you do on it, such as an HPLC check of your own stock, will show two main peaks rather than one. That’s expected. Second, CJC-1295 no DAC is the longer and more hydrophobic of the two and is the one more likely to adsorb to surfaces or aggregate if handled roughly, so treat the combined vial with the same care you’d give a 29-mer on its own. Ipamorelin on its own is a small, stable pentapeptide and is about as forgiving as a peptide gets.

If your design needs the two compounds as independent variables, order the ipamorelin vial separately and pair it with a standalone GHRH analogue; the combined vial fixes the ratio, which suits a pilot but not a factorial study.

Which to order for which research question

If your question is about the GHRH receptor, cyclic AMP signalling in somatotrophs, or the direct pituitary arm of growth hormone regulation, you want a GHRH analogue on its own, and you’d read the GHRH(1-29) literature for your assay conditions. The combined vial isn’t the right reagent for that question because you can’t separate the two contributions.

If your question is about the ghrelin receptor, secretagogue selectivity, or the hypothalamic arm, ipamorelin on its own is the compound, and the 1998 paper is the place to start.

If your question is about the interaction between the two pathways, which is the question most people ordering the combination have in mind, then the combined vial is a reasonable starting point for a pilot, and a proper study would add each compound alone as a control. Whichever route you go, every lot is tested for HPLC purity, mass spectrometry identity and bacterial endotoxin, by a named third-party lab, with the lot COA on the product page, and the certificate library is at /coas/. Purity is >99%, and vials are vialed, finished, tested and shipped in the USA, with orders processing within 1 business day.