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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.
GHRP-6, also written GHRP6 or growth hormone-releasing peptide-6, is described as a growth hormone secretagogue hexapeptide. A review lists GHRP-6 among growth hormone secretagogues (GHS), which it names among the agents most commonly encountered in clinical practice and online self-administration protocols. In one study, GHRP6 was co-administered with epidermal growth factor (EGF), and the authors describe this combination as a promising neuroprotective candidate.
No, the facts do not describe GHRP-6 as a steroid. One source describes GHRP-6 as a growth hormone secretagogue hexapeptide. A review names GHRP-6 as a growth hormone secretagogue (GHS) among the agents most commonly encountered in clinical practice and online self-administration protocols. Neither fact mentions steroid structure, so this answer rests only on how the compound is named and classified.
In animal studies, D-Lys-3-GHRP-6 is a ghrelin receptor antagonist, and the authors used it to test the role of ghrelin. [D-Lys3]-GHRP-6 is described as a growth hormone secretagogue receptor (GHSR) antagonist. In animal work, molecular docking and a pharmacological experiment with [D-Lys3]-GHRP-6 (D-Lys3) were used to verify the Ghrelin/GHSR pathway. In one rat study of traumatic brain injury, [D-Lys3]-GHRP-6 was injected intraperitoneally after the rats woke up.
In the randomized open-label human acute stroke trial, GHRP6 was tested as part of a combined EGF+GHRP6 therapy given twice daily for 7 days to 95 patients, while 93 patients received standard care. In that trial, severe adverse events occurred in 48 of 188 patients, and none were considered treatment-related. These findings are about the combined EGF+GHRP6 therapy in that trial, not about GHRP6 given alone.
In a clinical trial in humans, GHRP6 combined with EGF showed no differences from standard care in the intention-to-treat population for modified Rankin Scale, Barthel index, or survival. In a human clinical trial, patients in the middle cerebral artery territory treated with EGF+GHRP6 had greater infarct volume reduction at 30 days. The COURAGE-2 study missed its primary endpoint but suggested potential benefit of EGF+GHRP6 in moderate-to-severe stroke in humans, and its authors said this warranted further studies targeting that subpopulation.
In a rat model of acute ischemic stroke, EGF combined with GHRP6 modulated 40 proteins at 3 hours and 223 proteins at 24 hours after treatment in the ischemic penumbra. In these rats, anti-apoptotic and mitochondrial proteins were modulated in the ischemic penumbra after EGF plus GHRP6 treatment. At 24 hours after treatment in rats, proteins linked to reactive oxygen species detoxification, heat shock factor 1 activation, and negative regulation of cellular hypoxia response were significantly modulated by GHRP6 combined with EGF.
In human oocytes cultured in vitro, GHRP-6 showed potential in promoting nuclear maturation by significantly inducing the appearance of the first polar body (PB1) within 24 hours. In the same in vitro study, GHRP-6 did not show statistically significant improvements in cytoplasmic maturation in metaphase 2 (MII) oocytes during that timeframe. Real-time PCR in human oocytes cultured in vitro found that, despite the early PB1 appearance at 24 hours, GHRP-6 did not elevate the expression of the CENP-E or LINGO2 genes. In the in vitro maturation procedure, the optimal GHRP-6 concentration was determined to be 75 ng/ml, resulting in a maturation rate of 70% on the first day and 80% on the second day.
In animal studies, GHRP-6 hydrogel treatment was found to have beneficial therapeutic effects on acute kidney injury (AKI) by targeting metabolic reprogramming. In the same animal studies, GHRP-6 hydrogel treatment enhanced the survival of tubular epithelial cells in the ischemic microenvironment by activating the mTOR-P70 pathway.
In a mouse study, GHRP-6 was examined for its ability to attenuate pulmonary damage caused by intratracheal LPS or zymosan combined with platelet activating factor. In the acute lung injury scenario in mice, GHRP-6 reduced neutrophilic alveolitis, attenuated lung compliance failure, and contributed to improved alveolar-capillary permeability. In the chronic scenario in mice, GHRP-6 preserved lung parenchymal integrity and accounted for meager collagen accumulation.
In broiler chickens, co-injection of the (D-Lys-3)-GHRP-6 form of GHRP6 with LEAP2 was reported to significantly decrease LEAP2-induced hypophagia (P<0.05). The same paper also reports that this co-injection significantly increased the hypophagic effect of LEAP2 in broiler chickens (P<0.05), a result that conflicts with the decrease reported in the same results section. The authors concluded that LEAP2-induced hypophagia is mediated via ghrelin and CB1 and CB2 receptors in neonatal chickens, a conclusion drawn in part from the (D-Lys-3)-GHRP-6 co-injection experiment.
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.