CJC-1295 (No DAC) and Ipamorelin: GHRH Analog and Ghrelin Mimetic Research

Growth hormone secretion is one of the most tightly choreographed processes in endocrinology — pulsatile, rhythmic, and governed by two opposing hypothalamic signals. Two research compounds map directly onto that control system: CJC-1295 (No DAC), a stabilized analog of growth-hormone-releasing hormone (GHRH), and Ipamorelin, a selective mimetic of ghrelin acting at the growth hormone secretagogue receptor. Because they engage two different receptors converging on the same pituitary cells, the pair has become the most studied — and most searched — combination in growth-hormone-axis research.

This article covers both compounds: what they are, the receptor biology under investigation, why researchers study them together, and the practical laboratory considerations. As with everything in our Research Library, this is educational material about research-use-only compounds — nothing here describes or supports human use.

The GH Axis in Brief

The hypothalamus releases GHRH, which stimulates pituitary somatotrophs to secrete growth hormone; somatostatin provides the opposing brake. A third input, the stomach-derived hormone ghrelin, amplifies GH release through its own receptor (GHS-R1a). GH pulses then drive hepatic IGF-1 production, which feeds back to close the loop. Nearly all research on these compounds is, at bottom, research on manipulating specific nodes of this circuit in experimental models.

CJC-1295 (No DAC): a Stabilized GHRH Analog

Native GHRH(1-29) — the minimal fully active fragment of GHRH — has a serum half-life measured in minutes, degraded rapidly by the enzyme DPP-IV. That instability makes the native peptide difficult to study in vivo. CJC-1295 (No DAC), also called modified GRF(1-29) or tetrasubstituted GRF(1-29), addresses this with four amino acid substitutions that confer resistance to enzymatic cleavage while preserving GHRH-receptor activity.

The “No DAC” designation matters and is a persistent source of confusion in the literature: the original CJC-1295 developed by ConjuChem carried a Drug Affinity Complex (DAC) — a reactive group that covalently binds serum albumin, extending half-life to roughly a week. Research by Teichman and colleagues (2006) on the DAC version reported sustained elevations of GH and IGF-1 lasting days after single administration in early human studies. The No DAC version studied and supplied for research lacks that albumin-binding group: it retains the stabilizing substitutions but clears far faster, producing a GH pulse rather than a sustained elevation. Researchers care about the distinction because pulsatility itself is physiologically meaningful — sustained non-pulsatile GH signaling behaves differently from pulsed signaling in experimental models.

Ipamorelin: a Selective Ghrelin Mimetic

Ipamorelin is a pentapeptide developed by Novo Nordisk in the 1990s as a growth hormone secretagogue. Its defining research property, established in the foundational characterization by Raun and colleagues (1998), is selectivity: in animal models it stimulated GH release with potency comparable to GHRP-6 while showing no significant effect on ACTH or cortisol at GH-releasing doses — the off-target signals that complicate research with earlier secretagogues like GHRP-2 and GHRP-6. That clean receptor profile is why Ipamorelin became the default ghrelin-mimetic tool compound in GH-axis research.

Mechanistically, Ipamorelin activates GHS-R1a on somatotrophs and hypothalamic neurons — the same receptor targeted by ghrelin, whose discovery by Kojima and colleagues in 1999 explained what the synthetic secretagogues had been binding all along. The broader history of GH-releasing peptides as a class — from the early enkephalin-derived compounds through modern selective secretagogues — is reviewed by Bowers (1998).

Why the Combination Is Studied

The research rationale for pairing a GHRH analog with a ghrelin mimetic is receptor complementarity:

  • Different receptors, same target cell. GHRH-R signaling (via cAMP) and GHS-R1a signaling (via phospholipase C/IP3) engage distinct intracellular pathways in somatotrophs, and studies of combined administration have reported synergistic — not merely additive — GH release.
  • Ghrelin mimetics also work upstream, amplifying hypothalamic GHRH output and functionally opposing somatostatin, which reinforces the same pulse the GHRH analog initiates.
  • Preserved pulsatility. Because the No DAC analog and Ipamorelin are both short-acting, combined models retain the pulsatile secretion pattern that defines physiological GH signaling — a design consideration central to how researchers interpret downstream IGF-1 and metabolic readouts.

This mechanism pairing is why the compounds are supplied together as an Ipamorelin/CJC-1295 (No DAC) blend alongside the standalone CJC-1295 No DAC 10mg.

Reading the Literature Critically

  • Nomenclature noise. “CJC-1295” in the literature sometimes means the DAC version, sometimes mod GRF(1-29); findings on one don’t automatically apply to the other. Half-life, pulsatility, and study design differ fundamentally between them. Any citation should be checked for which molecule was actually studied.
  • Human data is thin and old. The Teichman human work concerns the DAC version; controlled human data on the No DAC analog and on Ipamorelin is limited (Ipamorelin’s clinical development, including a postoperative-ileus program, was discontinued). The bulk of the combination literature is animal and mechanistic work.
  • Axis complexity. GH readouts are exquisitely sensitive to sampling timing, feedback state, and model choice. Apparent contradictions in the literature frequently trace to pulsatile sampling design rather than the compounds themselves.

Laboratory Considerations

Verification. Both compounds are supplied lyophilized and third-party tested for identity and ≥99% purity, with batch reports published in our COA Library before purchase — see how to read a Certificate of Analysis for a walkthrough. Sequence verification matters doubly here given the mod-GRF substitutions that define the No DAC analog.

Storage and reconstitution. Store lyophilized material at −20°C protected from light; reconstitute with bacteriostatic water or sterile solvents per protocol. Full guidance in our storage and handling best practices.

Related compounds. Both sit in our Growth & Longevity research category alongside Tesamorelin, a distinct stabilized GHRH analog with its own substantial clinical literature.

Summary

CJC-1295 (No DAC) and Ipamorelin map onto the two stimulatory inputs of the GH axis — a DPP-IV-resistant GHRH analog and a selective ghrelin-receptor agonist — and the research case for the pair rests on receptor complementarity and preserved pulsatility. The literature rewards careful reading: the DAC/No DAC distinction and the pulse-sensitive nature of GH measurement are where sloppy sourcing produces wrong conclusions. For laboratories studying GH-axis signaling, verified sequence identity is the precondition for interpreting any of it.

Browse CJC-1295 No DAC 10mg, the Ipamorelin/CJC-1295 blend — each with published batch COAs — or explore the full catalog of third-party tested research peptides.


Research Use Only. All compounds referenced are intended solely for laboratory research and development purposes. Not for human or veterinary use. This article is educational material and does not describe, encourage, or support any use in humans or animals.

References

  1. Raun K, et al. Ipamorelin, the first selective growth hormone secretagogue. European Journal of Endocrinology, 1998.
  2. Teichman SL, et al. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. Journal of Clinical Endocrinology & Metabolism, 2006.
  3. Kojima M, et al. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature, 1999.
  4. Bowers CY. Growth hormone-releasing peptide (GHRP). Cell and Molecular Life Sciences, 1998.
  5. Sackmann-Sala L, et al. Activation of the GH/IGF-1 axis by CJC-1295, a long-acting GHRH analog, results in serum protein profile changes in normal adult subjects. Growth Hormone & IGF Research, 2009.
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