More than a decade ago, CD36 was identified as one of the GHRP-6 receptors [12]. This is a scavenger receptor endowed with multiligand and multifunctional capabilities and is expressed by a broad constellation of mammalian cells [13]. Granulation tissue neovascularization is perhaps the most renowned physiological role of CD36 in wound healing [14]. Serendipitous observations of our laboratory indicated that CD36 mRNA transcript appeared abundantly represented in clinical samples of granulation tissue of either acute (deep burn injuries) or chronic (pressure ulcers) wounds, as in laboratory rat’s controlled full-thickness wounds. This finding incited us to speculate on the effects associated with CD36 agonistic stimulation beyond that of the angiostatic action via thrombospondin binding [15]. Here we provide the first experimental evidence on the favorable impact of the topical administration of GHRP-6, as a candidate to qualitatively improve the healing process.
GHRP-6 is normally always manufactured as lyophilized (freeze-dried) powder contained in vials in amounts of 5mg. Some companies might manufacture amounts greater or lesser than 5mg per vial, but the standard is generally 5mg/vial. The lyophilized powder contained within the vial will need to be reconstituted with bacteriostatic water in order for it to be injected. After reconstitution, the solution must then be refrigerated in storage. If left in hot environments or in room temperature environments for extended periods of time, the protein structure will degrade and become ineffective. For reconstitution, users will typically mix 3ml of bacteriostatic water with the powder gently. However, users can and do frequently reconstitute the powder with less (or more) water which will yield different concentrations of GHRP-6. For example, reconstitution of 5mg of powder with 3ml of water will yield GHRP-6 doses of 166mcg per 0.1ml (or 10iu on an insulin syringe).
GHRP mechanism of action. GHRPs are endowed with the ability to bind two different receptors that seem to mediate its cytoprotective and other pharmacological properties (GHS-R1a and CD36). The main biological properties/pharmacological actions of GHRP-6 as cyto- and cardioprotective candidates are summarized as follows: Inotropic: mediated by an elevation of Ca2+ influx via PLC/DAG/PKC, through the voltage-gated calcium channel, triggering Ca2+ release from thapsigargin-sensitive intracellular stores, which translated in a positive inotropic response without a chronotropic effect. Anti-fibrotic: via upregulation of PPARγ, which is followed by a transforming growth factor-beta (TGF-β), CTGF, and platelet-derived growth factor (PDGF) downregulation. Anti-inflammatory: blunts NFκB expression and activation. Cell survival: it involves 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). Cardioprotective: as shown, it involves different biological actions that converge to enhance cardiomyocytes survival. Vasodilatory: it seems to involve e-NOS upregulation and endothelin activity reduction. Anabolic: it is mediated by the IGF-1/AKT1 and mTOR pathway activity.
At the time that decision was made, paracetamol/caffeine combinations were available over-the-counter in over 50 other countries and had been exempt from scheduling in a number of major markets that are similar to Australia in terms of population type and regulatory status. Experience with the unscheduled sale of this product was extensive: UK 19 years, Ireland 12 years and New Zealand for 7 years. However, the Committee determined not to consider paracetamol combined with caffeine for exemption from scheduling until market experience had been gained with use as a Schedule 2 product in Australia.

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

"In circumstances where a medicine is widely known to be used in connection with modifying a physiological process in persons (as appears to be the case with some SARMs and other peptide products), that medicine is likely to satisfy the definition of a therapeutic good despite any disclaimer to the effect that it is for research purposes only and/or not for human use."


In 2005, we undertook a porcine model of AMI via left circumflex artery occlusion for 1 hour followed by a 72-hour reperfusion period. GHRP-6 rescued ischemic myocardium from death for over 70% of the area at risk (Figure 3), and that in addition to enhance survival signaling pathways/gene expression of the PI-3K, AKT1, and BCL2 pathways, GHRP-6 decreased reactive oxygen species (ROS) spillover, the inflammatory marker CRP, and preserved the antioxidant defenses.45 These antioxidant and anti-inflammatory properties have also been attributed to GHRP-2 when its antiatherogenic potential was examined in ApoE(−/−) mice so that 12/15-lipoxygenase, interferon gamma, and macrophage migration inhibitory factor (MMF) gene expression were accounted. Furthermore, in cultured aortic smooth muscle cells, GHRP-2 prevented the generation of peroxides, the downregulation of IGF-1 receptor, and the commitment of apoptosis.46

Author Contributions: Conceived and designed the experiments: JBA, AAC, DGBH, YMM, ARU, AGO, VFC, FHB, GGN. Analyzed the data: JBA, AAC, DGBH, YMM, ARU, AGO, VFC, FHB. Wrote the first draft of the manuscript: JBA. Contributed to the writing of the manuscript: JBA, AGO, YMM. Agree with manuscript results and conclusions: JBA, AAC, DGBH, YMM, ARU, AGO, VFC, FHB, QB, GGN. Jointly developed the structure and arguments for the paper: JBA, AGO, GGN. Made critical revisions and approved final version: QB, GGN. All authors reviewed and approved of the final manuscript.


I have questions about combined therapy of CJC 1295 and Ipamorelin at the same time on a daily basis for both. The compounding pharmacies do not clearly state whether the CJC is with or without DAC. If it is the CJC with DAC, which sustains elevated GH and IGF-1 for several days, would taking it nightly in conjunction with the Ipramorelin, that is suggested to be taken TID but is being recommended only once at night, be over-stimulatory? If the CJC is without DAC, why take two pepetides simultaneously ,that have similar effects? I am just not clear why taking a daily dose of CJC with Ipamorelin as a single dose is better than taking the CJC with DAC twice per week alone or take the CJC with DAC for a while then switch to the Ipamorelin for a while?
Healthy male Wistar rats (250–270 g) were purchased from the National Center for Animal Breeding (CENPALAB, Havana, Cuba). Animals were individually housed at the animals’ facility of the Center for Genetic Engineering and Biotechnology, Havana, Cuba, and maintained under controlled environmental conditions and light cycles (12/12 hrs). Rats were fed with standard laboratory rodent’s chow under no restriction. Following an acclimation week, the dorsum of the rats was conditioned to receive two controlled full-thickness wounds, under sodium pentobarbital (30 mg/kg) anesthesia. The cuts were generated with disposable 6 mm diameter punch biotomes (Acuderm, Ft. Lauderdale, USA). Two independent experiments were performed using the above described wound model. Thus, 10 rats ( wounds) were used for either GHRP-6 formulation or vehicle (1% CMC) groups in each experiment. Upon wounds induction the rats were randomly assigned to either group. The wounds were cleansed daily with saline, their contours traced on transparent plastic sheets and treated accordingly. Treatments were topically applied twice a day at the same hours during four days. Wounds closure dynamic was measured by planimetric analysis as described previously [16] using the ImageJ software, version 1.46r. Since the GHRP-6 intervention increased the rate of closure, the animals were terminated by anesthesia overdose on day five after wounding. Ulcers and a surrounding margin of intact skin (~5 mm) were collected and hemisectioned. One hemisection was preserved in RNA Later solution for further gene expression studies. The other hemisection was fixed in 10% buffered formalin, paraffin embedded, and 5-μm sectioned. The specimens were stained with hematoxylin/eosin (H/E) and Mallory trichrome to examine collagen deposit. Other slides were destined for immunohistochemistry (as described below).
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.
The search strategy was based on the PubMed/MEDLINE electronic databases including original research and review articles. The search was progressively date escalated from 1980 and included articles in English only. The search terms were as follows: growth hormone secretagogues (GHS), GHRP, growth hormone secretagogue receptor (GHS-R), CD36, cardiac ischemia/reperfusion, cardiac stunning, heart failure, cytoprotection, and cardioprotection.
GHRP-6 is normally always manufactured as lyophilized (freeze-dried) powder contained in vials in amounts of 5mg. Some companies might manufacture amounts greater or lesser than 5mg per vial, but the standard is generally 5mg/vial. The lyophilized powder contained within the vial will need to be reconstituted with bacteriostatic water in order for it to be injected. After reconstitution, the solution must then be refrigerated in storage. If left in hot environments or in room temperature environments for extended periods of time, the protein structure will degrade and become ineffective. For reconstitution, users will typically mix 3ml of bacteriostatic water with the powder gently. However, users can and do frequently reconstitute the powder with less (or more) water which will yield different concentrations of GHRP-6. For example, reconstitution of 5mg of powder with 3ml of water will yield GHRP-6 doses of 166mcg per 0.1ml (or 10iu on an insulin syringe).

Users get even greater growth hormone release from this peptide than both GHRP-6 and GHRP-2. Much like other GHRP and GHRH peptides, it is believed to be useful for muscle building, fat loss and anti-aging. Hexarelin is stronger than practically all other growth hormone releasing peptides at all dosing levels. But this means it has higher potential to desensitize, regardless of dose or whether breaks are observed.


CJC1295 is a 30 amino acid peptide, which primarily functions as a growth hormone releasing hormone analogue (mimicing the effect of GHRH).  It was initially invented to treat deep fat deposits in people, because it is known that having an increase in our own growth hormone levels will target this.It stimulates production of our own growth hormone from the pituitary gland.  
The ACMS recommended listing 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 in Appendix D, Item 5.
GHRP-6 stands for growth hormone releasing hexapeptide, so it is obviously a peptide hormone. As you can probably guess, it acts in the same manner as all peptides do in the Growth Hormone (GH) class – it increases the amount of GH our bodies produce. This is a very beneficial property, as growth hormone is the fountain of youth, and serves many purposes from fat loss, to muscle gain and anti-aging effects. For this reason many athletes have turned to GHRP-6 in order to get an athletic edge.

In rat stomach, a second type of ghrelin peptide has been purified and identified as des-Gln14-ghrelin (). Except for the deletion of Gln14, des-Gln14-ghrelin is identical to ghrelin, even retaining the n-octanoic acid modification. Des-Gln14-ghrelin has the same potency of activities with that of ghrelin. The deletion of Gln14 in des-Gln14-ghrelin arises due to the usage of a CAG codon to encode Gin, which results in its recognition as a splicing signal. Thus, two types of active ghrelin peptide are produced in rat stomach: ghrelin and des-Gln14-ghrelin. However, des-Gln14-ghrelin is only present in low amounts in the stomach, indicating that ghrelin is the major active form. In addition, n-decenoyl (C10:l)-modified ghrelin exists in the stomach in small amounts.
The prescription form of IGF-1 most often injected is “mecasermin”, which goes by the trade name Increlex. Manufactured using recombinant DNA technology, mecasermin is clinically used to treat IGF-1 deficiency and stunted growth. It is also prescribed to patients who have developed antibody resistance to normal growth hormone therapy. Increlex is actually identical to natural IGF-1, meaning that it has the identical 70 amino acid sequence of IGF-1 that the body produces. In other words, it’s not some kind of growth hormone “precursor”. It’s just straight up IGF-1.
In November 1999, the National Drugs and Poisons Schedule Committee (NDPSC) decided to reschedule mometasone from Schedule 4 to Schedule 3 for use in aqueous nasal sprays for the treatment of seasonal allergic rhinitis, with certain dose and age conditions. The NDPSC considered that this rescheduling was appropriate given mometasone's safety in use based on pharmacokinetic parameters, and that the treatment of seasonal allergic rhinitis has a place in Schedule 3.
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In June 2007, the NDPSC decided to extend the exemption from the limit on paracetamol combinations being allowed as general sale products to include phenylephrine (as long as it also qualified as exempt from scheduling through the phenylephrine entries). At that time, the NDPSC considered that the safety profile of these substances was such that allowing a fixed combination to be unscheduled was reasonable.
These substances come in form of powder that has to be reconstituted with sterilized water and injected. The injections are given either subcutaneously or intramuscularly, but the former option is more common. The advice is to use an insulin syringe for administration purpose. You need to be extra careful when self-injecting peptides. Make sure you do not strike a vital blood vessel.

CJC 1295 can be compounded in two forms (DAC and non-DAC). Drug affinity complex (DAC) prevents enzymatic degradation thus increasing the half-life. Consequently CJC 1295-DAC can be dosed as a single weekly injection. Administration of CJC 1295-DAC provides a GHRH-like stimulation around the clock. A potential drawback when using a weekly protocol can be attributed to ineffective GHRH stimulation when the body is due for a GH spike (usually 1:00am). This is referred to as a GH-bleed and the overall result is inferior to using CJC 1295-NON-DAC daily for 5 days out of 7. Therefore using CJC 1295-NON-DAC daily (between 6-8pm) provides a more effective GH spike at 1:00am.


CJC-1295 is also known by the names of Modified GRF 1-29, Mod GRF 1-29, CJC-1295 without DAC (DAC stands for Drug Affinity Complex) and also by its chemical name tetrasubstituted GRF (1-29). This variety of names makes it difficult for the average consumer to select or even research upon this compound. Since some manufacturers list all of its names and others list only one, it also becomes very confusing. However, there is a reason for this wide variety of names.
Among the other reasons why bodybuilders use peptides is its ability to help you recover faster. They assist in making oxygen available to the muscle cells in sufficient amount. They also improve user’s level of endurance. These benefits make them popular among athletes generally. Peptides further help to burn body fat, which is another reason they are considered beneficial in bodybuilding.
There’s no question this is a slightly safer version than GH, but it’s got plenty of athletes in hot H2O for testing the waters. Famously, this is the peptide the Essendon footballers were caught out using which led to the government shutting down regulatory loopholes used to legally get it into Australia. So assess all your risks before you take it then be honest with a doctor if you are considering it, particularly if you want to heal an injury, because your health is far more valuable than any improvements to your reflection.
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