Ipamorelin is a man-made peptide that is part of the growth hormone family. Rated as one of the safest in the peptide industry, it has strong growth hormone releasing properties. From this, it is a huge winner with athletes and bodybuilders. This is because it builds muscle and keeps weight down quickly. It works by sending signals to the pituitary gland at the base of the brain and adjusts and controls various body functions through the endocrine system. It binds certain receptors inside cells. This allows cells to respond and change, encouraging growth and regulation of hormones. Ipamorelin can help with:
Conclusions: Subcutaneous administration of CJC 1295 resulted in sustained, dose-dependent increases in GH and IGF-I levels in healthy adults and was safe and relatively well tolerated, particularly at doses of 30 or 60 ug/ kg. There was evidence of a cumulative effect after multiple doses. These data support the potential utility of CJC 1295 as a therapeutic agent.
Hypertrophic scarring is a form of abnormal, exuberant healing, locally aggressive, and recurrent cutaneous fibroproliferative condition, characterized by excessive extracellular matrix (ECM) accumulation during the cutaneous healing process. Including keloids and hypertrophic scars (HTS), these aberrant processes lead to esthetically disfiguring scars, patients’ psychological stress, and functional impairment [1]. The cellular and molecular mechanisms underlying the formation of these raised dermal scars are poorly understood. Recent whole genome profiling and proteomic studies have led to the identification of regulatory elements with different expression profiles in HTS and keloid tissues [2]. The limited understanding of the pathophysiology of these processes has led to investigating a broad spectrum of potential antihypertrophic scarring candidates [3].
As an athlete, you can also increase your dosage cycle for a period of 12 to 16 weeks at a time, to maximize your gains. Do so gradually if you opt to go this route. Make sure you increase your daily dosage (1 to 2 doses per day, etc.) gradually. Start off with lower dosage levels as well, and see how it interacts with your body. You don’t want to experience withdrawal, nor do you want to experience negative side effects when using Ipamorelin for longer dosage cycles. So, make sure you monitor your progress, see how you feel as you go, and make notes if/when you do experience negative side effects, so you can balance down to the proper dosage levels.
Despite all these pharmacological advantages and that GHRPs exhibit a broad safety profile, their clinical development has been erratic and irregular. This has been a deterrence factor for their definitive positioning within cardiology and intensive care medicine for years. In the meantime, novel drugs and therapeutic strategies are demanded to protect organs and tissues exposed to ischemia and other lethal insults in the clinical practice.
The other submission commented on the consideration to place AOD-9604 in Appendix D. The submission supported listing in Schedule 4, but raised concerns that listing the substance in Appendix D would limit any future development work, including clinical trials that are currently being conducted on the substance. The submitter notes that there are currently 5 clinical trials notified to the TGA using this substance , with these approved clinical trials going ahead on the basis that the substance is safe for human use. Inclusion in Appendix D may place unnecessary burden on those conducting these clinical trials.
Mostly, these peptides are sold as lyophilized powder in 2mg containers. Bacteriostatic water should be mixed with the powder in order to reconstitute it. To make the dosage of 100mcg per injection, 2ml bacteriostatic water should be mixed into 2mg of lyophilized powder. This reconstituted mixture should be then injected inside the muscles or under the skin. The mixture should be kept under refrigeration at all times otherwise it will degenerate and will not be effective anymore.
In more recent years, these data were further substantiated using again the TO-2 hamster DCM biomodel in which GHRP-2 reduced the progression of LV remodeling, dysfunction, and the ensued myocardial fibrosis by an antioxidant mechanism.36 The abovementioned myocardial fibrotic process amelioration reveals an additional potential use for GHRP in an unmet medical need. Chronic treatment with hexarelin in spontaneously hypertensive rats, in addition to decreasing ventricular hypertrophy, diastolic dysfunction, and high blood pressure, significantly reduced cardiac fibrosis by decreasing interstitial and perivascular myocardial collagen deposition and myocardial hydroxyproline content. Mechanistically, hexarelin treatment increased matrix metalloproteinase (MMP)-2 and MMP-9 activities and decreased myocardial mRNA expression of tissue inhibitor of metalloproteinase (TIMP)-1.37
With a blend of peptide and GH supplements, Ipamorelin can greatly help you in your weight loss endeavours. Using it with IGF-1 which is a natural growth hormone, can help you achieve even greater results. With lower dosage, you won’t increase muscle mass, your body will naturally decrease body fat levels, and you will begin to metabolize food faster, meaning you burn more calories in less time, for greater weight loss results.
The increase in GH secretion due to IPAMORELIN (and other GHRP) leads to an increase in IGF-1 (thought to be the anabolic mechanism of GH).  As we get older GH and subsequently IGF-1 decrease substantially.  This decline is thought to be one of the major causes of the ageing process.  By increasing these levels again there is increased collagen synthesis, promotion of lean muscle mass, bone strength, improved healing capability, improved sleep cycle, increased energy, repair and regeneration of internal organs, strengthening of joints/cartilage/connective tissue, and anti ageing effects on the skin. 
Just as the name suggests, GHRH helps to stimulate secretion of growth hormone. The duration of secretion induced will depend on the specific type of peptide that you use. An important thing to note here is that these substances are effective only to a limit. Exceeding the saturation dose, which may vary between individuals, will not improve the amount of HGH that is secreted. Below are a few peptides that fall in the GHRH group.
If GHRP-6 is powerful for growth hormone release, this peptide is even stronger, albeit slightly so. GHRP-2 is used for similar purposes as the other compound. But it does not fire up appetite as the other peptide is known to do. This may make it more ideal for people interested in improving lean muscle mass. Furthermore, it does not desensitize when taken in low doses without observing breaks as required for other peptides.
For example, there are Growth Hormone Releasing Peptides (GHRP’s with names such as ipamorelin and hexarein) which allow for a slow and steady growth hormone release that produces a pulse which mimics natural growth hormone release times and Growth Hormone Releasing Hormones (GHRH’s such as Mod-GRF) for an even stronger natural release of growth hormone and greater presence of growth hormone precursors known as GH “frags” or fragments.

CJC-1295 and Mod GRF 1-29 are administered in micrograms (mcg) rather than milligrams (mg) – the unit of administration of other steroids and performance-enhancing drugs. It has also been found that a 100mcg dose is enough to fully saturate the receptors in the anterior pituitary. This is called the saturation dose. After a dose of 100mcg has been administered, the subsequent dosages will achieve only half the effect.

In 1982, the natural hormone "Growth Hormone Releasing Hormone" (GHRH) was identified after a prolonged search. Soon, researchers discovered that those GH-Releasing Peptides (specifically GHRP-6 & GHRP-2) followed a mode of action which bound them to and was mediated through receptors different from those for GHRH. Furthermore, researches discovered that these GH-Releasing Peptides acted synergistically with the natural hormone Growth Hormone Releasing Hormone (GHRH), which is related to Sermorelin, in both laboratory animals and humans to produce large releases of Growth Hormone. In the 1980s, the first highly potent GH-Releasing peptide, GHRP-6, was developed. Due to a strong GH release response from the the peptide, it became the first member of a class called Growth Hormone secretagogues. GHRP-6 is a hexapeptide composed of 6 amino acids: L-Histidine, D-Tryptophan, L-Alanine, L-Tryptophan, D-Phenylalanine and L-Lysine. The "L" form of an amino acid is the naturally occurring form and often in the nomenclature the "L" is dropped. The "D" form does not occur in nature and is the isomeric form (i.e. mirror image) of the naturally occurring "L" form. GHRP-6 (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) is composed of both natural and isomeric forms of those 6 amino acids.This sequence provides a signal to the body to begin secreting Growth Hormone release while also blocking Somatostatin, a hormone that inhibits the release of Growth Hormone.
Cerebrolysin—also known as FPE 1070—is a synthetic nootropic drug. Nootropic drugs are substances that enhance cognitive functions such as memory, creativity, and motivation in otherwise healthy individuals. This peptide is extremely small, allowing it to penetrate the blood-brain barrier and act directly on the neurons of the central nervous system. Cerebrolysin has been found to improve the metabolic activity of brain tissue, shield neurons from harmful substances, and stimulate the peripheral and central nervous systems. In addition to its utility as a nootropic substance, the drug has potential as part of a treatment plan addressing Alzheimer’s disease, stroke, and moderate to severe head injury.
Conclusions: Subcutaneous administration of CJC 1295 resulted in sustained, dose-dependent increases in GH and IGF-I levels in healthy adults and was safe and relatively well tolerated, particularly at doses of 30 or 60 ug/ kg. There was evidence of a cumulative effect after multiple doses. These data support the potential utility of CJC 1295 as a therapeutic agent.

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

A remarkable specific (125)I-Tyr-Ala-hexarelin binding was observed in the human cardiovascular system where the highest binding levels were detected in ventricles, followed by atria, aorta, coronaries, carotid, endocardium, and vena cava. In other experiments on H9c2, cardiomyocyte-specific GHRP binding was found along with a potent antiapoptotic activity.3 The primarily investigated receptor was the growth hormone secretagogue receptor type 1a (GHS-R1a), which was detected in isolated human cardiomyocytes, myocardium, and aorta samples.17 It has been recently shown that GHS-R1a is a sort of “promiscuous receptor” involved in many systems and behavioral patterns such as reward, feeding, and memory, which makes it an attractive pharmacological target.18 Years later, the synthetic GHRP hexarelin was acknowledged as a ligand of another protein identified as CD36, a scavenger receptor that is expressed in various tissues, including monocytes/macrophages and the endothelial microvasculature. Activation of CD36 in perfused hearts by hexarelin was shown to increase coronary perfusion pressure in a dose-dependent manner. Contrariwise, this effect was lacking in hearts from CD36-null mice and hearts from spontaneous hypertensive rats genetically deficient in CD36.19,20 Thus, it is currently accepted that two cardiac receptor subtypes mediate the pharmacological actions of GHRP-6, GHRP-2, and hexarelin.21,22

CJC-1295 increases the production of growth hormone as well as IGF-1 – which has anabolic effects in adults. However, it does not increase the levels of prolactin – high levels of which can create impotence and mental health problems in men. By increasing these two hormones, it enhances protein production in the body, which in turn, boosts muscle mass. It also induces lipolysis – the breakdown of fat tissue, boosts recovery from injuries, increases bone density, and also reduces aging factors like skin wrinkles. It can also stimulate cell growth, due to which it can be used to treat withered tissue or organs.

Similar to other enhancers, it is observed that administrating GHRP-6 along with insulin gets an increased GH response. However, in presence of elevated glucose levels, GHRP-6 does not work well. As a result, consuming carbohydrates or dietary fats before administrating GHRP-6 is a bad idea. Thus the dose should be taken two hours after your last meal and at least thirty minutes before your next meal. Also, GHRP-6 has saturation points. As a result, you want to put a healthy interval between two doses so that your receptors are clear. The best schedule is one dose upon waking up, one post workout, and one before sleeping.
Another benefit of CJC 1295 is its ability to promote slow wave sleep. Slow wave sleep is also known as deep sleep and is the portion of sleep responsible for the highest level of muscle growth and memory retention. SWS decreases significantly in older adults and also with people who tend to exercise later in the evening. Clinical studies have shown that a once-daily administration of CJC 1295 normalizes the GHRH response and can induce significantly deeper sleep.

The final verdict is to go for it. GHRP-6 is not your garden-variety performance enhancer. One of the most important aspects of it is that it does not cause desensitization. This means that it will not cause overdose and that works best for athletes. Also since it increases appetite, it forces you to make more calories available to your body for exercise and for recovery. It does not boost unnatural muscle growth like other performance enhancers and the result does not put extra pressure on your tendons and ligaments.

By increasing our own growth hormone levels (which normally decrease as we age), there is an increase in protein synthesis which subsequently stimulates muscle growth.  It leads to an increase in muscle mass, an increase in fat metabolism (fat loss), and increase in physical strength.  It is also helpful in skin ageing, and effective in reducing wrinkles.


Our group recently demonstrated the antifibrotic effects of the growth hormone-releasing peptide 6 (GHRP-6) in a rat model of liver cirrhosis. GHRP-6 prevented parenchymal fibrotic induration in more than 85% and removed in about 75% the accumulated fibrotic material in both preventive and therapeutic administration schemes. Differentially expressed genes in a microarray experiment indicated that GHRP-6 modulates the expression of genes involved in the redox metabolism, as in the mesenchymal cells response to injury [7].
Five of the submissions did not support the proposal while the sixth submission did. The former contend that potential risks of inadvertent use of caffeine in those at risk of an adverse event will be increased if selection of an analgesic is made without the assistance or intervention of a healthcare professional. There was also concern that the proposed exemption may result in an increase in liver damage due to excessive consumption of such a product. This was likely to result from people abusing these products as a source of stimulants.
In June 2011, the delegate decided to reschedule from Schedule 2 to Schedule 3, combination ibuprofen+paracetamol preparations (up to 200 mg of ibuprofen and 500 mg of paracetamol) when in packs of 30 dosage units or less. The delegate also decided that combination ibuprofen+paracetamol preparations in packs of more than 30 dosage units are to be captured by Schedule 4.
Prolactin, or estrogen gynecomastia issues: Those that are sensitive to prolactin based gynecomastia are open to problems with GHRP-6. Luckily, this is a rare occurrence, and it can be easily combated with dostinex. However, those who stack this compound with anabolic androgenic steroids may have a greater chance of getting gynecomastia. Thats why an AI (aromatase inhibitor) should be used during this kind of cycles.
But let’s say you’ve already implemented the IGF-1 boosting strategies of adequate calories, sufficient protein, weight training, plenty of sleep, smart supplementation, mineral intake and alcohol moderation. Should you take the next step, wander into an anti-aging clinic, find an online pharmacy, lurk in the depths of bodybuilding forums, and begin IGF-1 injections?
Five public submissions were received. Many of the submissions referred to the article published in the New England Journal of Medicine (NEJM) when giving their reasons for either supporting or rejecting the proposal. Some submissions also noted that a similar proposal is to be considered by an upcoming meeting of the Medicines Classification Committee (MCC) in New Zealand.
Immunohistochemical determination of CD31 expression (platelet endothelial cell adhesion molecule-1, PECAM-1) was conducted as this is a marker protein of mature vascular endothelium [19]. Sections (5 μm) were mounted on chromalum-coated slides, dewaxed, rehydrated, rinsed, and washed in PBS 1x solution for 30 min. Once endogenous peroxidase was quenched, the specimens were treated with target retrieval solution (Dako) equilibrated at 99°C. Tissue samples were then incubated for 40 min with 1/50 dilution of anti-CD31 antibody (Abcam 28364, USA) in background reducing solution (Dako). The immunohistochemical reactions were carried out using the labelled streptavidin/biotin-horseradish peroxidase conjugate method, according to the manufacturer’s instructions (Dako). The peroxidase reaction was developed with diaminobenzidine and counterstained with hematoxylin.
Extreme hunger stimulation: It has been previously mentioned in this profile already that almost all GHRPs will stimulate hunger simply by virtue of the fact that they are Ghrelin mimetics (they mimic the action of the hormone Ghrelin in the body), but GHRP-6 has demonstrated both anecdotally as well as clinically to stimulate the largest hunger increases in comparison to all other GHRPs[2]. GHRP-6 tends to stimulate what can only be described as agonizing hunger, and is commonly misconceived as a hypoglycemic episode. The hunger resultant from GHRP-6 is, in fact, simply the peptide acting on Ghrelin receptors that signal hunger to various regions in the brain. No studies or any anecdotal evidence demonstrates hypoglycemic blood glucose readouts following GHRP-6 administration. Following a meal, the hunger should subside. Many users have also reported the intensity of the hunger diminishing several weeks into GHRP-6 cycles but not completely disappearing.

However, after the administration, Mod GRF 1-29 starts breaking down soon. This happens because peptides have a strong affinity for bonding with amino acids. The administered peptide has to travel a long distance between the point of administration and the pituitary gland. On the way, the enzymes act on it making it break down and bond with the amino acids. The peptides that are secreted by the body on its own do not have to face this problem because they do not have to travel this long.
Finally, an exciting medical opportunity could be opened for synthetic GHRP to treat the threatening cancer-associated anorexia–cachexia syndrome in advanced-stage cancer patients. Although the mechanistic bases of this syndrome are not fully understood, it represents a major impediment for the course of chemotherapy. In a rodent model of cancer-bearing chemotherapy, GHRP-2 administration increased appetite/food intake and prolonged median survival time, which certainly suggests that GHRP-2 may improve the quality of life of cancer patients by correcting its nutritional and metabolic states.61 These data may also incite to further studies in the search for a potential niche for GHRP to counteract the catabolic states of prolonged critical illness, invasive surgeries, severe burn traumas, etc.
The final verdict is to go for it. GHRP-6 is not your garden-variety performance enhancer. One of the most important aspects of it is that it does not cause desensitization. This means that it will not cause overdose and that works best for athletes. Also since it increases appetite, it forces you to make more calories available to your body for exercise and for recovery. It does not boost unnatural muscle growth like other performance enhancers and the result does not put extra pressure on your tendons and ligaments.
The best way to summarise how well SARMs (and peptides for that matter) work is to point out that they have been banned by WADA (the world anti-doping authority) for competitive sports because they give an unfair advantage to athletes. Luckily they are legal to purchase so if Sarms can do that for athletes imagine how much they can help ordinary folk.
Ghrelin has been linked to inducing appetite and feeding behaviors. Circulating ghrelin levels are the highest right before a meal and the lowest right after. Injections of ghrelin in both humans and rats have been shown to increase food intake in a dose dependent manner. So the more ghrelin that is injected the more food that is consumed. However, ghrelin does not increase meal size, only meal number. Ghrelin injections also increase an animals’ motivation to seek out food, behaviors including increased sniffing, foraging for food, and hoarding food. Ghrelin also readies the body for the incoming nutrients by stimulating gastrointestinal motility and gastric acid secretions.
Results: After a single injection of CJC 1295, there were dose dependent increases in mean plasma GH concentrations by 2- to 10-fold for 6 d or more and in mean plasma IGF-I concentrations by 1.5- to 3-fold for 9–11 d. The estimated half-life of CJC 1295 was 5.8–8.1 d. After multiple CJC 1295 doses, mean IGF-I levels remained above baseline for up to 28 d. No serious adverse reactions were reported.
These studies on human subjects were paralleled by contemporary experimental progresses in basic science, which demonstrated that hexarelin enhanced H9c2 cardiomyocyte proliferation in a dose-dependent manner. Since these were in vitro experiments, they completely excluded a potential intervention of the GH axis and clearly indicated a direct GHRP binding to cardiac cells membranes.32 Weekers et al33 demonstrated that 14 days of pretreatment with GHRP-2, but not GH, selectively protected against the postischemic diastolic dysfunction and myocardial stunning of excised hearts submitted to ischemia/reperfusion in isolated, perfused rabbit hearts.
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