Researchers have tested the interaction of CJC-1295 with GHRP-6 to see if it would yield a higher release of growth-hormone (GH) than either compound used alone. The expectation is a synergistic stimulation that will increase GH production and release, thereby aiding in the repair of minor muscle and ligament damage.
GHRP-6 is the synthetic laboratory analogue of the ghrelin pathway consisting of six-amino acids. It’s believed to increase GH by stimulating the growth-hormone secretagogue receptor (GHS-R1a) in the pituitary and hypothalamus. GHRP-6, although active at the ghrelin receptor, is not sequence-homologous with ghrelin; it’s structurally an opioid analogue of MET-enkephalin- but no opioid action is reported by researchers. It’s classed with other growth-hormone secretagogues (GHSs).
CJC-1295-also referred to as tetra-substituted GRF (1-29)-is a synthetic analog of growth hormone -releasing hormone (GHRH) which, allegedly, induces release oh GH. It is nearly identical to the first 29 amino acids of natural GHRH, the sequence that will be bound by the GHRH receptor, but substitutes four positions (2, 8, 15, and 27). Those substitutions are intended to make it more resistant to cleavage by dipeptidyl peptidase-4 such that the peptide has time to act.
CJC-1295 GHRP-6 Blend (10mg) Research
CJC1295 + GHRP-6 Blend and Growth Hormone Levels
Stud 1 (placebo or CJC-1295, 20-40 years).
Twenty to forty-year-old men were divided into two groups: a placebo group and a group that was administered CJC-1295. Blood was drawn before and after dosing. In comparison to placebo, the peptide group experienced a roughly 7.5-fold increase in growth hormone (GH). Incremental increases were seen and were sustained a week later.
Study 2 (dose escalation, 20-60 years).
In the second trial, 20- to 60-year-olds received increasing doses of CJC-1295 or placebo. Serial blood draws on follow-up provided dose response-GH was elevated up to tenfold. As Madalina Ionescu and colleagues outline, prolonged stimulation of GHRH pathways may increase trough GH and consequently elevate IGF-1, the major anabolic intermediary of GH. Long -acting GHRH preparations have promise for individuals whose pituitary remains able to secrete GH.
Study 3 (GHRP-6 + arginine, ages 6-11).
Children 6-11 received GHRP-6 either alone or with arginine. Following treatment, GH increased significantly in both to certain level, indicating that the peptide stimulated GH weather was co-administered with arginine.
CJC-1295 & GHEP-6 Combination and Hypothyroidism
Reduced production of growth hormone (GH) is a sign of hypothyroidism. During a 1997 clinical trial, hypothyroid subjects were injected with either GHRP-6, GHRH, or both in combination (the combination similar in concept to the combination of CJC-1295 and GHRP-6). The combination resulted in higher GH levels significantly than either of the individual peptides.
What is the cause of this increase? GHRP-6 has been postulated to reverse the effect of somatostatin, a natural suppressor of GH release, as GHRH induces the pituitary to release GH. Both, when used together, seemed to act synergistically. When F.R. Pimentel-Filho and colleagues reported GHRH plus GHRP-6 caused significantly greater GH response, with resultant involvement of somatostatin. Their findings further suggested that thyroid hormones can modulate GHRH- and GHRP-6 induced GH release by different mechanisms, and they urged further investigations to explain how it is done.
CJC-1295 and GHRP-6 Peptide Mix and Cellular Healing
In studies involving animals in which researchers created injury and multi-organ failure, either GHRP-6 alone or GHRP-6 with epidermal growth factor (EGF) was given to test subjects. Results of the studies indicated the peptide did something to cells in the gut’s epithelium, such as speeding up cell migration to about three times the normal rate. Treatment also seemed to minimize detrimental effects of organ failure by as much as 50-85%.
GHRP-6 might also enjoy the company of the CD36 receptor, expressed on most cell types-muscle and fat cells, and immune cells, too. CD36 is associated with fat metabolism (uptake and metabolism), immune signaling, inflammation, and angiogenesis (formation of new blood vessels). Through activity in these pathways-particularly inflammation and angiogenesis-GHRP-6 might be involved in tissue repair across organs.
CJC-1295 and GHRP-6 Peptide Mixture and Diabetic Gastrointestinal Activity
Diabetes can disrupt the gut, delaying gastric emptying and food passage through the small and large intestines. Researchers tried growth-hormone-releasing peptides like GHRP-6 when diabetes were artificially induced in mice in laboratory experiments. Gastric emptying was accelerated and intestinal transit enhanced with the presence of the peptide. Astonishingly, colonic transit remained unchanged in these experiments.
CJC-1295 and GHRP-6 Peptide Blend and Heart Rate
Initial animal research implies a heart advantage with GHRH-class medications like CJC-1295. The medications were found to stabilize heart rate and enhance function in mice following a heart attack in experiments. Researchers with Andrew V. Schally reported evidence of healing cardiac tissue and enhanced pumping capacity. Within models, GHRH agonists were associated with enhanced ejection fraction and reduced infarcts in rats, reduced scar tissue in swine, and reduced cardiac hypertrophy in mice-factors that indicate a possible role in recovery of infarct.
CJC-1295 & GHRP-6 Peptide Blend and Neuroprotection
GHRP-6 has also been studied for its neuroprotective and tissue-repairing potential. In a single mouse study to examine the brain’s TGF-1 system-the traditional downstream GH pathway of GH action-one week of GHRP-6 exposure increased IGF-1 mRNA in the hypothalamus, cerebellum, and hippocampus but not in the cerebral cortex. Such a profile indicates GH and GHRP-6 can promote IGF-1 signaling in specific brin areas.
The same experiment assessed other sections of the pathway. IGFBP-2 (an IGF-binding protein) and IGF-1 receptor expression remained unaltered, but where IGF-1 was increased, there was evidence of Akt and Bad phosphorylation-a marker that cell-survival pathway was being activated. MAPK and GSK-3β remained unaltered.
Apoptosis markers biased in favor of survival in those areas where AGF-1 was higher: the anti-apoptotic protein Bcl-2 rose, but not the pro-apoptotic Bax. Lastly, IGFBP-5, under normal conditions associated with neuron survival, rose predominantly in the hypothalamus, suggesting a potential neuroendocrine function there.
