Ipamorelin is a pentapeptide, meaning that it is composed of five amino acids, that mimics the body’s natural GH release.  Ipamorelin is a growth hormone releasing peptide (GHRP) and analogue of the hormone Ghrelin. It induces GH release and increases the number of somatarophs(cells responsible for GH release) in a GH pulse by suppressing somatostatin.
I have not used IGF-1 but I have used a stack of Ipamorelin and CJC 1295 no DAC. I did not do any lab tests before, during or after but definitely noticed increased fat loss and better sleep. I was not trying to increase muscle so there was no change to speak of for me. But you are not recommending their use even without IGF-1, is that correct? I do not compete in anything so WADA is not a concern.
"I have been on elitesarms products since start of this year. Have tried the mk2866, lgd4033, rad140, sr9009 and the gw. Absolutely amazing results ofcourse with a combination of a strict diet, cardio and exercise regime I manage to drop 12kg and stay under 12% Body fat and also increase my lean muscle mass and overall strength and endurance. The directions and website is extremely user friendly and simple to order. The best thing about it is they deliver so quickly and efficiently with no problems! Absolutely helpful with any enquiries and prompt. Highly recommend and wouldn't go anywhere else for sarms products." Anonymous
On this page: 1. Scheduling proposals referred to the October 2012 meeting of the Advisory Committee on Chemicals Scheduling (ACCS#6) | 2. Scheduling proposals referred to the October 2012 meeting of the Advisory Committee on Medicines Scheduling (ACMS#7) | 3. Scheduling proposals referred to the October 2012 joint meeting of the Advisory Committee on Chemicals Scheduling and Advisory Committee on Medicines Scheduling (ACCS-ACMS#4)

GHRP was first envisioned to be an analog of GHRH but, from comparison of the activity of GHRH and GHRPs between 1982 and1984, it was hypothesized to reflect the activity of a new hormone regulator of GH secretion, yet to be isolated and identified. Intravenous bolus GHRP releases more GH than GHRH in humans, but the reverse occurs in vitro. GHRPs are pleiotropic peptides with major effects on GH, nutrition, and metabolism, especially as an additional hormone in combination with GHRH as a new regulator of pulsatile GH secretion. The first indication of pleiotropism was an increase of food intake by GHRP. A major reason for the prolonged initial interest in the GHRPs has been its similar, yet different and complementary, action with GHRH on GH regulation and secretion.
Since CD36 is implicated in angiogenesis regulation, special attention was addressed to the population of neovessels as to their general morphology. By routine staining, we ascertained that GHRP-6 treatment did not reduce the number of vessels, which also exhibited normal structure, organization, and distribution. Furthermore, CD31 expression was detected in all these vascular structures suggesting mature angiogenesis. Conclusively, GHRP-6 administration did not hinder wound angiogenesis in any respect (Figure 3(a)), as compared to placebo-treated wounds (Figure 3(b)). These histological findings support the scoring on the ECM maturation and the quantification of inflammatory cells across the wounds (Table 2).

It is important to understand that GHRP-6 doses on its own provides considerable HGH release from the pituitary gland, but is nowhere near as effective as the potential HGH release resultant from GHRP-6 combined with a GHRH such as Mod GRF 1-29 (CJC-1295 without DAC). Studies have demonstrated that the combination of GHRP-6 and a GHRH analogue such as Mod GRF 1-29 will generate a 77% increase in HGH output compared to GHRP-6 administration alone[8]. Other studies have gone so far as to explicitly state that GHRP-6 requires GHRH in order to stimulate maximal HGH stimulation as evidenced by the fact that in test subjects, the inclusion of a GHRH can increase HGH output by an additional 81 – 95%[9].

Growth hormone releasing peptide (GHRP) 2 is a type of peptide therapeutic that mimics the effects of ghrelin, the “hunger hormone”. Ghrelin is a hormone that helps regulate appetite as well as energy distribution and rate of use, or metabolism. In the 1980’s, ghrelin was discovered to be the body’s natural ligand (or binding molecule) of the GHRP receptor in the anterior pituitary. This was a significant discovery, as it highlighted the role of ghrelin in hGH secretion and growth regulation. Modern biotechnology has used this knowledge to develop peptides that can be administered to mimic ghrelin’s hGH stimulation, but in a more targeted fashion. GHRP 2 is one such peptide, stimulating hGH secretion by 7-15 times, increasing appetite and meal initiation, while also decreasing fat mass and cholesterol. GHRP 2 is ideal for patients who are hypercatabolic, due to critical illness, cancer, AIDS, etc. It should be noted that GHRP 2 can also increase levels of prolactin, aldosterone, and cortisol.
SARMs stimulate androgen receptors specifically in muscle and bone cells, hence assisting with muscle and bone growth, while having little effect on the other cells in the body (unlike regular steroids). They have a special affinity for certain tissues like muscle and bone, but not for others, like the prostate, liver, and brain. This means more rapid muscle and bone growth without unwanted growth in other parts of your body.
Serum ghrelin levels vary as a function of energy balance. Ghrelin levels are increased in anorexia and decreased in obesity.78 Thus, it is possible that ghrelin may be an important player in food intake behavior and perhaps in chronic over- and under-nutrition as well.9 Because of its dual effects, ghrelin may be a critical hormonal signal of nutritional status to the somatotropic axis, playing a role in integrating energy balance with the growth process.10
In March 1972, the Drugs and Poisons Schedule Subcommittee (DPSSC) decided to include vitamin D in Schedule 4 when the recommended daily dosage on the label exceeds 10 micrograms. This recommendation was based on a recommendation by the Nutrition Committee of the National Health & Medical Research Council that the attention of pharmaceutical firms be drawn to the dangers of vitamin A overdose.
CJC 1295 has shown some amazing results as a growth hormone releasing hormone (GHRH) analog. Not only has CJC 1295 shown potential to increase growth hormone and IGF-I secretion and effects, but it has been able to do so in very large amounts. CJC 1295 Stimulates Growth Hormone Secretion, and will keep a steady increase of HGH and IGF-1 with no increase in prolactin, leading to fat loss, and increased protein synthesis thereby promoting growth.

Dose-wise, studies have shown that the body will release a decent amount of natural GH with a dose of only 100mcg (termed the SATURATION DOSE) injected subcutaneously or intramuscularly. Higher doses can be used up to 300-500mcg in a single shot but double the dose does not mean double the GH; the amount of release is not directly proportional and the ratio of release diminishes as the dose climbs. I personally find 250mcg to be my sweet spot and doesn’t cost too much to run a short cycle at that dose.
MGF stands for mechano growth factor—a peptide derived from insulin-like growth factor-1 (IGF-1), which plays a large role in childhood development and continues to have anabolic effects throughout adulthood. MGF has the ability to encourage repair and growth of wasted tissue through the activation of muscle stem cells, thereby increasing the synthesis of proteins necessary for tissue growth. This peptide is ideal of anyone suffering from muscle loss, either due to old age or a particular condition (i.e., HIV, cancer, etc.)
Years ago, our group examined the cytoprotective effects exerted by the GHRP-6 preventive administration in the hepatic tissue subjected to I/R, as in other distal organs from the ischemic site (ie, lungs, kidneys, and small intestine). Histological and biochemical results allowed us to conclude that the pharmacological preconditioning induced by the GHRP-6 treatment attenuated I/R liver damage. Besides respiratory distress syndrome like pulmonary changes, intestinal transmural infarct and acute tubular necrosis in kidneys were significantly reduced. These results indicated for the first time a systemic cytoprotective effect for the GHRP-6, suggesting its potential efficacy to control the inflammatory response associated with acute I/R and shock, which eventually originated multiple organs damage (MOD). Cytoprotection induced by GHRP-6 treatment was also related to the attenuation in the generation of ROS and preservation of the antioxidant defense reserves. Histological analysis as the assessment of myeloperoxidase activity evidenced a clear anti-inflammatory GHRP-6-induced effect in the liver and remote organs. Moreover, the molecular mechanism mediating the action of GHRP-6 peptide was shown to involve the phosphatidylinositol 3-kinase/RAC-alpha serine/threonine-protein kinase (PI-3K/AKT1) pathway, as the induction of the hypoxia-inducible factor-1 alpha (HIF-1α) all committed in cellular survival.51 Subsequently, Granado et al52 examined the potential anti-inflammatory impact of GHRP-2 in lipopolysaccharide (LPS)-challenged rats. GHRP-2 administration attenuated the effects of LPS on the elevation of circulating levels of transaminases, nitrites/nitrates, and tumor necrosis factor-alpha (TNF-α), via direct interaction with liver nonparenchymal cells. Globally, the exogenous administration of these two synthetic GHRPs appeared to exert a potent hepatoprotective role by attenuating the inflammatory response orchestrated by liver-resident macrophages. Another line of evidences document the benefits of 15-daily injections of GHRP-2 (100 μg/kg) in arthritic rats, so that the treatment ameliorated the external symptoms of arthritis and decreased the circulating levels of interleukin 6 (IL-6) as the nitrite/nitrate release from peritoneal macrophages in vitro. This experiment extrapolated the counter-inflammatory properties of GHRP-2 to a nonepithelial organ and suggested again a direct interaction with ghrelin receptor of immune cells.53 Similarly, effects have been attributed to ghrelin by inhibiting the inflammatory response via AKT1-activated pathway with a concomitant reduction of myeloperoxidase activity, the rate of apoptosis, and oxidative stress.54 All these data suggest that GHRPs exert a mutually inclusive beneficial effect by directly protecting parenchymal organs epithelial cells, and simultaneously by modulating the magnitude of the inflammatory response by direct interaction with the effector immune cells. Supporting the protective effect of GHRP-6 on epithelial organs, a recent study has excellently described and dissected the mechanistic bases on how GHRP-6 prevented gastric mucosal damage induced by water immersion restraint (WRS) and other forms of stress. The data indicated that the protective effect of GHRP-6 on WRS-induced gastric mucosal injury is somehow mediated by peripherally suppressing the vagal efferent effect on the stomach, including gastric acid secretion. Although more studies are clearly demanded, the present findings open the possibility to use GHRP-6 in preventing Curling ulcers.55
Since GHRP-6 influences natural GH release, rules for its administration are similar to those when administering GH itself, i.e. do not have the dose within a 2 hour window after a meal, and/or wait 30 minutes till eating after dosing, due to any endogenous insulin release from the meal possibly stunting the release of natural GH and its uptake by the relevant cells.
Boasting similar structure as CJC-1295, sermorelin is commonly used for anti-aging purposes. But it is also considered useful for muscle building. It accounts for 29 amino acids of the 44 that make up growth hormone releasing hormones. This peptide is very potent for improving HGH levels, as shown in studies. It was observed that the 1-29 amino acid chain is mainly responsible for the ability of GHRH to stimulate release of growth hormone by the pituitary. However, sermorelin has very short half-life of about 10 minutes or less.
In June 2005, the NDPSC decided to reschedule pantoprazole from Schedule 4 to Schedule 3 when in oral preparations containing 20 mg or less of pantoprazole for the relief of heartburn and other symptoms of gastro-oesophageal reflux disease (GORD), in packs containing not more than 14 days' supply. This decision was based on the available efficacy and safety data which supported a Schedule 3 entry.
The interim decision was to include in Schedule 4 and in Appendix D Item 5 Growth Hormone Releasing Hormones (GHRHs), Growth Hormone Secretagogues (GHSs), Growth Hormone Releasing Peptides (GHRPs) as well as new individual substance entries for CJC-1295, ipamorelin, pralmorelin (Growth Hormone Releasing Peptide-2), Growth Hormone Releasing Peptide-6, hexarelin and AOD-9604.
An intact hypothalamic-pituitary axis is required to achieve the maximal effect of GHSs on GH release. GHRH and somatostatin both influence the action of GHSs, augmenting and diminishing the magnitude of the GH pulse, respectively. When GHRH is administered in combination with GHSs, the effect is synergistic, the magnitude of the GH pulse being greater than that obtained from the sum of the two agents administered separately. GHS stimulation of GH secretion requires the presence of GHRH. In members of a family with a homozygous inactivating mutation of the GHRH receptor, hexarelin was ineffective in stimulating GH release. In addition, children who are GH-deficient as a result of pituitary stalk transsection are unresponsive to GHSs. Thus, somatotroph exposure to GHRH is necessary for GHSs to exert their action.
TO-2 hamster model of DCM was characterized by progressive LV dilation, LV wall thinning, LV systolic dysfunction, and reduced life span; both GHRP-2 and GHRP-6 ameliorated all the dysfunctional ventricular parameters and reduced the progression of the DCM.34 We also examined the potential impact of GHRP-6 in a rat model of DCM/heart failure induced by doxorubicin (DX). The concurrent administration of GHRP-6 was undertaken with the purpose to study the potential prophylactic impact before the cardiac function demise. As part of the prolonged treatment with DX, the concurrent administration of GHRP-6 completely prevented failure of cardiac function, which was evaluated as the percentage of ejection fraction by echocardiography (Figure 2, prevention). This effect significantly increased the survival of animals. Similar results were obtained in the therapeutic administration schedule, with functional recovery of cardiac muscle to physiological levels (Figure 2, regression), also attenuating systemic damages and, consequently, decreasing the mortality rates of rats. In the experimental model of DX-induced cardiac and systemic damage, GHRP-6 additionally attenuated various extracardiac damages observed in the renal tubular and bronchoalveolar epithelial structures as in the hepatic parenchyma.35
The key to your exercise recovery rests firmly on how well you behave between the sheets. No, not like that, sleep is a time when your muscles repair and a big catalyst for this is the recovery power lies in your hormones, namely GH. Research in the journal Neuroendocrinology found GHRP6 supplementation improves the quality, but not duration, of your sleep. And better sleep is a formidable gladiator in your armoury if you want to make your muscles more maximus, plus it can improve your ability to heal from injury, but it’s not all gravy. Some users do report feeling painfully ravenous, preventing them from getting quality kip. If this is the case then have a big feast after a dose, then hit the hay. Good cop for anyone looking to build, bad cop for anyone looking to lean up.