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Free U.S. shipping on orders over $150CJC-1295 No DAC (GHRH analog) and GHRP-6 (ghrelin receptor agonist) stimulate endogenous GH via complementary cAMP and Ca²⁺ signaling pathways.
Preclinical and clinical GHRH+GHS studies demonstrate synergistic GH release compared to either alone, supporting dual-pathway activation of the somatotroph axis in research settings.
CJC-1295 No DAC is a modified analog of growth hormone–releasing hormone designed to stimulate endogenous growth hormone (GH) secretion by activating GHRH receptor (GHRH-R) on anterior pituitary somatotrophs. This “No DAC” version does not contain the albumin-binding component, resulting in a shorter half-life and a more physiologic, pulse-like stimulation of GH release.
CJC-1295 No DAC activates the adenylyl cyclase–cAMP–protein kinase A (PKA) pathway following GHRH-R binding.
This signaling cascade promotes transcription and secretion of GH, which then increases circulating insulin-like growth factor-1 (IGF-1) through hepatic stimulation [1].
By amplifying endogenous pulsatile GH release rather than replacing GH directly, CJC-1295 without DAC preserves feedback regulation via somatostatin and IGF-1.
GHRP-6 (growth hormone–releasing peptide-6) is a synthetic hexapeptide classified as a growth hormone secretagogue (GHS).
It stimulates endogenous GH release by binding to the growth hormone secretagogue receptor (GHS-R1a), the same receptor activated by the endogenous hormone ghrelin. GHRP-6 specifically stimulates hunger more than GHRP-2, which may be more beneficial for weight gain.
Unlike GHRH analogs, GHRP-6 activates a distinct signaling pathway. After binding to GHS-R1a, it stimulates the phospholipase C (PLC)–inositol triphosphate (IP3)–calcium pathway, increasing intracellular calcium and GH secretion from anterior pituitary somatotrophs [2].
This mechanism is independent of the cAMP pathway used by GHRH.
CJC-1295 No DAC (a GHRH analog) and GHRP-6 (a ghrelin/GHS receptor agonist) can be paired because they stimulate endogenous growth hormone (GH) release through distinct, convergent control pathways:
This dual-pathway stimulation can increase GH pulse amplitude and responsiveness without relying on a single upstream signal.
A key mechanistic finding supporting “synergy” is that ghrelin/GHS receptor activation can potentiate GHRH-driven signaling.
In a cell study expressing cloned GHRH and GHS receptors, ghrelin/GHS compounds alone did not increase cAMP, but co-activation of GHS and GHRH receptors produced a cAMP response approximately 2x higher than GHRH alone, suggesting receptor-level cross-talk [3].
Complementary pituitary cell work also describes cross-talk between PKC-linked signaling and the cAMP/PKA axis during GRF/GHRP stimulation.
One pathway supplies the canonical “drive” signal, while the other increases secretory gain and somatotroph excitability.
Direct, peer-reviewed clinical studies explicitly testing CJC-1295 No DAC with GHRP-6 together are currently lacking.
While published studies typically evaluate GHRH + GHRP-6 (rather than CJC-1295 specifically), the physiology is directly relevant because CJC-1295 is a GHRH-receptor agonist. Therefore, these published results may be extrapolated to explain the benefits of CJC-1295 combined with GHRP-6.
Human endocrine studies have repeatedly shown that co-administration of GHRH and GHRP-6 elicits larger GH responses than either secretagogue alone [4].
A clinical study evaluated growth hormone (GH) responses to GHRP-6 (90 μg IV), GHRH (100 μg IV), and combined GHRP-6 + GHRH in 21 patients with non–insulin-dependent diabetes mellitus (NIDDM). Patients were divided into three groups:
Each participant received all three stimulation tests on separate occasions.
Results showed that:
The impaired response to GHRH in overweight diabetics can be partially overridden by GHRP-6, consistent with dual-pathway mechanisms.
The study provides clinical evidence for synergistic GH stimulation when GHRP-6 and GHRH are co-administered.
A balanced 1:1 mass ratio (5 mg + 5 mg) can be described conceptually as aiming to equally engage both upstream control systems, GHRH-R (cAMP/PKA) and GHS-R1a (Ca²⁺-linked signaling), to maximize complementary pathway activation rather than over-weighting a single mechanism.
Beyond that general logic, optimal ratios are not established in publicly available combination studies and should be treated as empirical parameters.
References:
1 Teichman, S. L., Neale, A., Lawrence, B., Gagnon, C., Castaigne, J.-P. and Frohman, L. A. (2006) 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. J. Clin. Endocrinol. Metab. 91, 799–805
2 Oliveira, J. H. A., Vieira, J. G. H., Abucham, J. and Lengyel, A. M. J. (2003) GHRP-6 is able to stimulate cortisol and ACTH release in patients with Cushing’s disease: comparison with DDAVP. J. Endocrinol. Invest., Springer Science and Business Media LLC 26, 230–235
3 Cunha, S. R. and Mayo, K. E. (2002) Ghrelin and growth hormone (GH) secretagogues potentiate GH-releasing hormone (GHRH)-induced cyclic adenosine 3’,5'-monophosphate production in cells expressing transfected GHRH and GH secretagogue receptors. Endocrinology, The Endocrine Society 143, 4570–4582
4 Micić, D., Macut, D., Popović, V., Kendereski, A., Sumarac-Dumanović, M., Zorić, S., et al. (1999) Growth hormone (GH) response to GH-releasing peptide-6 and GH-releasing hormone in normal-weight and overweight patients with non-insulin-dependent diabetes mellitus. Metabolism, Elsevier BV 48, 525–530
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). CJC1295 (No DAC) + GHRP-6 is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
Every lot undergoes our 6-panel testing protocol: identification by ESI-MS, purification by RP-HPLC, conformity, sterility screening, quantification of net peptide content, and LAL endotoxin screening. Full analytical data is published in the Certificate of Analysis for each lot.
Lyophilized peptides should be stored at -20°C or below for long-term stability. Once reconstituted, peptides should be stored at 2–8°C and used within a reasonable timeframe depending on the specific compound. Avoid repeated freeze-thaw cycles. Always store in a dry environment away from direct light.
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No. All compounds sold by Genesis Peptides are strictly for in vitro and preclinical laboratory research purposes only. They are not approved for human consumption, therapeutic use, or diagnostic purposes. By purchasing, you confirm the products will be used solely for legitimate research applications.
A Certificate of Analysis (COA) is a document issued by our analytical laboratory that reports the results of all quality control tests performed on a specific lot of product. Each COA includes HPLC chromatograms, mass spectra, endotoxin results, and quantification data where applicable. COAs are available in our COA Library for every lot we have shipped.
Yes. We offer volume pricing for universities, research institutions, and laboratories with recurring needs. Discounts begin at 100+ units and scale with volume. Contact our team for a custom quote tailored to your research requirements.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.
Snapshot CJC-1295 No DAC (GHRH analog) and ipamorelin (GHS-R1a agonist) stimulate endogenous GH through complementary cAMP and Ca²⁺ signaling pathways. Clinical and mechanistic studies of GHRH+GHS-R1a agonists co-administration demonstrate amplified pulsatile GH release compared to either pathway alone, supporting dual-axis activation of the somatotroph system. What Is CJC-1295 Without DAC? CJC-1295 without DAC is a synthetic analog of growth hormone–releasing hormone (GHRH amino acid 1–29 or Mod GHF1-29 ). This CJC-1295 is designed to stimulate endogenous growth hormone (GH) secretion through activation of the GHRH receptor (GHRH-R) on anterior pituitary somatotrophs. Without the Drug Affinity Complex (DAC), it does not bind albumin, resulting in a shorter half-life and more physiologic, pulse-like GH stimulation. Mechanistically, it activates the adenylyl cyclase–cAMP–protein kinase A (PKA) signaling cascade, promoting GH release and downstream increases in circulating insulin-like growth factor-1 (IGF-1) [1]. Because it works upstream at the hypothalamic–pituitary axis, CJC-1295 without DAC preserves endogenous inhibitory feedback regulation via somatostatin and IGF-1. What Is Ipamorelin? Ipamorelin is a selective growth hormone secretagogue (GHS) that binds to the ghrelin receptor (GHS-R1a) on anterior pituitary somatotrophs [2]. It stimulates endogenous GH release primarily through activation of the phospholipase C (PLC)–IP3–calcium signaling pathway, increasing intracellular calcium and promoting pulsatile GH secretion [3]. Unlike earlier GHS compounds and ghrelin itself, ipamorelin is relatively selective for GH release, with minimal stimulation of ACTH, cortisol, or hunger compared to less selective secretagogues [2]. By acting through a pathway distinct from GHRH analogs, ipamorelin is frequently studied in combination paradigms evaluating complementary stimulation of the somatotroph axis. Synergy CJC-1295 without DAC and ipamorelin stimulate endogenous growth hormone (GH) release through distinct but convergent regulatory pathways within the HPA axis. Their combined use is based on dual activation of GHRH and ghrelin receptor systems via: GHRH receptor > adenylyl cyclase–cAMP–PKA (CJC-1295) GHS-R1a > phospholipase C (PLC)–IP3–Ca²⁺(Ipamorelin) Because these pathways operate independently, their combined activation should increase both the magnitude and efficiency of GH pulsatility. Although published studies typically evaluate GHRH combined with GHRP compounds (such as GHRP-6 or ghrelin) rather than ipamorelin specifically, the mechanistic framework likely applies to ipamorelin due to its selective GHS-R1a agonism. Cell-based studies demonstrate that co-activation of GHRH and GHS receptors can produce approximately twofold greater cAMP signaling compared to GHRH alone, suggesting receptor-level cross-talk and amplification of somatotroph responsiveness [4]. A clinical study evaluated whether ghrelin, the endogenous ligand for the GHS receptor, interacts synergistically with growth hormone–releasing hormone (GHRH) to stimulate GH secretion [5]. 8 male adults were administered ghrelin (0.08, 0.2, and 1.0 μg/kg) intravenously alone or combined with 1.0 μg/kg GHRH. Results showed that combined administration with GHRH: Produced significantly greater GH responses than either peptide alone (p < 0.05)[a] GH response exceeded the sum of the individual responses, demonstrating true supra-additive synergy (p < 0.050 No synergistic interaction with ACTH or prolactin secretion This study demonstrates that co-administration of ghrelin and GHRH produces true synergistic GH release in humans, exceeding additive stimulation from either agent alone. The findings support the concept that dual activation of the GHRH receptor and GHS receptor enhances pituitary somatotroph responsiveness. In some metabolic conditions (e.g., obesity-associated blunting of GHRH response), GHS agonists partially restored GH responsiveness [6]. Ipamorelin Pairing Ipamorelin is highlighted in research contexts due to its relative selectivity for GH release, with minimal stimulation of ACTH and cortisol compared to earlier GHRP compounds. This selective profile may allow more targeted evaluation of somatotroph activation without broader pituitary axis activation. When paired with a short-acting GHRH analog such as CJC-1295 without DAC, the goal is typically to: Preserve physiologic pulsatility Enhance GH pulse amplitude Maintain endogenous feedback regulation The absence of the DAC component in CJC-1295 results in a shorter half-life, aligning more closely with natural episodic GH dynamics rather than prolonged elevation. Dose and Ratio Considerations Balanced ratios such as 2 mg + 2 mg or 5 mg + 5 mg can be conceptually described as targeting simultaneous engagement of: The GHRH-R/cAMP axis (transcriptional and secretory priming) The GHS-R1a/Ca²⁺ axis (secretory amplification) Proportional dosing may theoretically promote coordinated receptor activation. However, precise optimization of dose ratios has not been definitively established in controlled combination trials and remains an empirical parameter in research settings. References: 1 Sackmann-Sala, L., Ding, J., Frohman, L. A. and Kopchick, J. J. (2009) 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 Horm. IGF Res., Elsevier BV 19, 471–477 2 Raun, K., Hansen, B. S., Johansen, N. L., Thøgersen, H., Madsen, K., Ankersen, M., et al. (1998) Ipamorelin, the first selective growth hormone secretagogue. Eur. J. Endocrinol., Oxford University Press (OUP) 139, 552–561 3 Mear, Y., Enjalbert, A. and Thirion, S. (2013) GHS-R1a constitutive activity and its physiological relevance. Front. Neurosci., Frontiers Media SA 7, 87 4 Cunha, S. R. and Mayo, K. E. (2002) Ghrelin and growth hormone (GH) secretagogues potentiate GH-releasing hormone (GHRH)-induced cyclic adenosine 3’,5'-monophosphate production in cells expressing transfected GHRH and GH secretagogue receptors. Endocrinology, The Endocrine Society 143, 4570–4582 5 Hataya, Y., Akamizu, T., Takaya, K., Kanamoto, N., Ariyasu, H., Saijo, M., et al. (2001) A low dose of ghrelin stimulates growth hormone (GH) release synergistically with GH-releasing hormone in humans. J. Clin. Endocrinol. Metab., The Endocrine Society 86, 4552 6 Popovic, V., Damjanovic, S., Micic, D., Djurovic, M., Dieguez, C. and Casanueva, F. F. (1995) Blocked growth hormone-releasing peptide (GHRP-6)-induced GH secretion and absence of the synergic action of GHRP-6 plus GH-releasing hormone in patients with hypothalamopituitary disconnection: evidence that GHRP-6 main action is exerted at the hypothalamic level. J. Clin. Endocrinol. Metab., The Endocrine Society 80, 942–947
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