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Free U.S. shipping on orders over $150CJC-1295 (no DAC) + GHRP-2 leverages complementary growth hormone (GH) axis stimulations through distinct receptor mechanisms. These peptides can engage two distinct upstream regulatory pathways that influence endogenous GH release. Combined, they can provide a model for evaluating dual-pathway stimulation of pituitary activity, pulsatile hormone dynamics, and downstream metabolic signalling.
CJC--1295 without DAC (also called Mod GHF1-29) is a synthetic and chemically modified form of growth hormone–releasing hormone (GHRH) without containing the drug affinity complex (DAC) [1]. This dramatically shortens the peptide's half-life, thus more closely mimicking the natural pulsatile endogenous GHRH secretion. It produces a brief rise in growth hormone (GH) and insulin growth factor-1 that clears quickly from circulation rather than prolonged stimulation. In contrast, when CJC-1295 with DAC binds to albumin, it can persist for multiple days, thereby sustaining GHRH receptor stimulation [1].
CJC-1295 without DAC is structurally derived from GRF(1-29), the biologically active component of GHRH [2, 3]. Unlike sermorelin, which has natural amino acids, CJC-1295 without DAC has stabilizing substitutions, including D-amino modifications at position 2. As a result, this version of CJC-1295 resists dipeptidyl peptidase-4 degradation and has prolonged activity while preserving receptor affinity [2, 3]. This is thought to shorten exposure time, reduce the risk of receptor desensitization, and avoid chronically elevated baseline GH. Because it acts and clears quickly, it can be timed around sleep when GH naturally peaks and paired strategically with a GHRP that offers easier dosing adjustments.
Growth Hormone Releasing Peptide-2 (GHRP-2) is a synthetic ghrelin receptor agonist peptide [4]. It mimics the action of the gut-derived hormone ghrelin, which influences hunger [4]. Ghrelin naturally binds to the growth hormone secretagogue receptor GHS-R1a. GHS-R1a is found in both the pituitary gland and the hypothalamus [4]. GHRP-2 was developed as a research compound to stimulate growth hormone secretion through this ghrelin pathway [4].
Both GHRP-2 and CJC-1295 stimulate GH secretion through two distinct, yet complementary, receptor pathways [1, 4].
GHRP-2 activates ghrelin receptor GHS-R1a, engaging calcium-mediated signalling that promotes acute GH release [5]. When GHRP-2 binds to GHS-R1a in the pituitary, GHRP-2 stimulates growth hormone release in a pulsatile manner [6]. Whereas, in the hypothalamus, GHRP-2’s binding to GHS-R1a activates appetite pathways [6]. Unlike CJC-1295 or other GHRH analogs, GHRP-2 activates a different intracellular pathway involving Gq/11 signalling, calcium influx, and amplification of GH secretion [7]. This allows GHRP-2 to work synergistically with GHRH analogs.
In contrast, CJC-1295 acts at the GHRH receptor to enhance cAMP-mediated GH synthesis and secretion [2].
Combined, this dual-pathway stimulation is hypothesized to support both the amplitude and duration of GH secretion, potentially preserving physiologic pulsatility while extending the overall GH exposure window. Both GHS-R1a and GHRH analog converge on pituitary somatotroph activation. GHRP-2 predominantly drives PKC/Ca2+-linked signalling that amplifies secretory output, whereas GHRH receptor signalling is cAMP/PKA-mediated, supporting GH synthesis and release.
In vitro studies show that combined GHRH and CHRP-2 increase GH release and transcriptional signaling more than either alone, suggesting dual-pathway synergistic effects [8].
in vivo and clinical evidence also confirm that the combination of GHRH and GHRP-2 produces stronger growth hormone responses [9, 10]. Human studies using GHRH(1-29) in combination with GHRP-2 show greater GH increases than with single-peptide administration [9]. In hypogonadal men, GHRP-2 administration alone can induce up to 47-fold GH increase, and up to 54-fold increase when combined with GHRH [11]. Animal studies show similar results, with combined stimulation leading to significantly amplified GH release [10].
The combined formula, using similar potencies, is geared toward balancing receptor engagement. Because both peptides act on different but complementary pathways, using equivalent doses may provide proportional activation of both the GHRH receptor and the ghrelin receptor.
References:
1 Ionescu, M. and Frohman, L. A. (2006) Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. J. Clin. Endocrinol. Metab., The Endocrine Society 91, 4792–4797
2 Jetté, L., Léger, R., Thibaudeau, K., Benquet, C., Robitaille, M., Pellerin, I., et al. (2005) Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog. Endocrinology, The Endocrine Society 146, 3052–3058
3 Scarborough, R., Gulyas, J., Schally, A. V. and Reeves, J. J. (1988) Analogs of growth hormone-releasing hormone induce release of growth hormone in the bovine. J. Anim. Sci., Oxford University Press (OUP) 66, 1386–1392
4 Laferrère, B., Abraham, C., Russell, C. D. and Bowers, C. Y. (2005) Growth hormone releasing peptide-2 (GHRP-2), like ghrelin, increases food intake in healthy men. J. Clin. Endocrinol. Metab., The Endocrine Society 90, 611–614
5 Ghigo, E., Arvat, E., Muccioli, G. and Camanni, F. (1997) Growth hormone-releasing peptides. Eur. J. Endocrinol., Oxford University Press (OUP) 136, 445–460
6 Bowers, C. Y., Momany, F. A., Reynolds, G. A. and Hong, A. (1984) On the in vitro and in vivo activity of a new synthetic hexapeptide that acts on the pituitary to specifically release growth hormone. Endocrinology, The Endocrine Society 114, 1537–1545
7 Gondo, R. G., Aguiar-Oliveira, M. H., Hayashida, C. Y., Toledo, S. P., Abelin, N., Levine, M. A., et al. (2001) Growth hormone-releasing peptide-2 stimulates GH secretion in GH-deficient patients with mutated GH-releasing hormone receptor. J. Clin. Endocrinol. Metab., The Endocrine Society 86, 3279–3283
8 Yan, M., Hernandez, M., Xu, R. and Chen, C. (2004) Effect of GHRH and GHRP-2 treatment in vitro on GH secretion and levels of GH, pituitary transcription factor-1, GHRH-receptor, GH-secretagogue-receptor and somatostatin receptor mRNAs in ovine pituitary cells. Eur. J. Endocrinol., Oxford University Press (OUP) 150, 235–242
9 Bowers, C. Y. and Granda-Ayala, R. (1996) GHRP-2, GHRH and SRIF interrelationships during chronic administration of GHRP-2 to humans. J. Pediatr. Endocrinol. Metab., J Pediatr Endocrinol Metab 9 Suppl 3, 261–270
10 Argente, J., García-Segura, L. M., Pozo, J. and Chowen, J. A. (1996) Growth hormone-releasing peptides: clinical and basic aspects. Horm. Res., S. Karger AG 46, 155–159
11 Sinha, D. K., Balasubramanian, A., Tatem, A. J., Rivera-Mirabal, J., Yu, J., Kovac, J., et al. (2020) Beyond the androgen receptor: the role of growth hormone secretagogues in the modern management of body composition in hypogonadal males. Transl. Androl. Urol., AME Publishing Company 9, S149–S159
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). CJC1295 (No DAC) + GHRP-2 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.
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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 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 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 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. Synergy 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: CJC-1295 without DAC works via GHRH receptor–adenylyl cyclase–cAMP signaling. GHRP-6 activates GHS-R1a and triggers a PLC/IP3/Ca²⁺-linked secretory pathway. 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. Evidence in the Literature 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: Group A: Normal weight Group B: Overweight Group C: 8 normal-weight healthy controls Each participant received all three stimulation tests on separate occasions. Results showed that: There was no significant difference in GH when given just GHRP-6 in all 3 groups. Overweight individuals had a significant impairment in GH levels when given GHRH alone compared to control and normal weight individuals (p < 0.05). GH was synergistically and significantly increased when participants received the combined GHRP-6 and GHRH (p < 0.05). 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. Comments on Dosage 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
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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