Various experiments have been conducted to test the effectiveness of CJC 1295-DAC in vivo and the Journal of Clinical Endocrinology & Metabolism has reported dose-dependent increases in mean plasma GH concentrations by 2-10 fold for more than 6 days and increased IGF-1 concentrations 1.5-3 fold for 9-11 days after a single injection. Mean half-life was shown to be 5.8-8.1 days, also after multiple doses mean IGF-1 levels remained above baseline for up to 28 days. No serious adverse reactions were reported in any group.

Although the history of some of the foremost biomedical discoveries is permeated by serendipity,4 we deem that the well-established pivotal role of the GH/insulin-like growth factor-1 (IGF-1) axis for cardiomyocyte physiology, and the subtle alterations of this axis within the pathogenicity of dilated cardiomyopathy (DCM) and left ventricular (LV) dysfunction, ignited the idea of assessing the potentiality of GHRP to alleviate cardiac pathologies.5 It was far to be anticipated on those early days, however, that the GHRP-mediated cardiotropic and cytoprotective effects are superior to those shown by the exogenous administration of GH and are not shared by GH-releasing hormone (GHRH) and that, importantly, GHRPs exert their pharmacological actions via GH-independent pathways that obviously represented another turning point in this history.3


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
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:
Phenylephrine is a direct alpha-1 adrenergic agonist, with weak alpha-2 adrenergic agonist activity. It also has very weak beta-adrenergic effects, but at therapeutic doses there are no significant stimulating beta-1 adrenergic effects on the heart, or on the bronchial airways, or on peripheral blood vessels. This contrasts with pseudoephedrine, which has greater beta-adrenergic activity. The effect on the alpha-adrenergic receptors leads to local vasoconstriction and shrinking of mucous membranes. There is no anti-histamine effect. The drug is readily and completely absorbed following oral administration, undergoing extensive first pass metabolism in the intestinal wall and in the liver leading to some variability in individual pharmacokinetics. Nasal decongestion is apparent within 15 to 20 minutes and persists for up to 4 hours (AHFS 2007).
To amend Schedule 2 entry to exempt paracetamol when compounded with caffeine, in a powder or granule product containing 1000mg or less of paracetamol and in tablets or capsules containing 500mg or less of paracetamol when paracetamol is the only therapeutic active constituent and when supplied in primary packs of not more than 20 tablets/caplets or 10 sachets of powders/granules.
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.
I stopped the colostrum and my ” symptoms ” subsided, seems I have a moderately enlarged prostate which doesn’t run in my family on either side, my question is could the colostrum possibly cause the prostate to enlarge due to the igf-1 at a certain age,? due to a possible decline in testosterone, or could the benefits of colostrum outweigh the prostate issue?

I have been using sermorelin (bioidentical growth hormone releasing hormone) for 2 months now to help heal a nasty right quad tendon rupture suffered the end of December. I’m 52 years old with 7% bodyfat and am a lifetime strength trainer and former high level bike racer. 2 months ago, in spite of months of religious rehab, I couldn’t do a single right leg bench stepup. Yesterday I was doing 20lb DB’s for repeated sets of 15. I get complete blood panels every 6 months, and my last labs in May showed my IGF-1 levels off the reference range low. I get my next bloods in a couple of weeks. I was initially afraid to try this hormone due to the cancer implications, and I didn’t need it to be lean and fit, but I was desperate and for my injury recovery, and it has made a significant difference. Plus, I believed supplementing the releasing hormone vs, IGF-1 limits the possibility of increasing the levels too much, as well as causing a negative feedback loop. By the way, I also tried TB-500 previous to the sermorelin, and it seemed to make some other achy joints in the gym go away, but didn’t seem to help the quad injury.
Like all other steroidal drugs, GHRP-6 too has a few side effects which will be discussed below. It is because of these side effects, the drug is not available over the counter without a prescription. The most common side effect users report is aggravated hunger. All GHRP's are known to escalate hunger in users and GHRP-6 is no exception. Studies show that GHRP-6 has the highest potential when it comes to increasing hunger among users. This agonizing hunger is said to subside, after the consumption of an appropriate meal. Users have reported the gradual diminishing of this side effect but it remains throughout the entire cycle of administration.
The Work around is GHRH + GHRP. If GHRH help stimulate growth hormone and GHRP can stimulate twice as much, once you combine the two you are going to increase the amount of growth hormone that can be secreted by 12 times. GHRH will increase the amount of growth hormone that is secreted at the natural times when your body is ready to release the GH. GHRP will selectively send a pulse forcing GH to be secreted. Taking the two together, the GHRP will force a pulse and the GHRH will increase the power of that pulse. Basically, the power of that pulse will be greater, and with more frequency, when using GHRP and GHRH together. This combination gives the option for users to mix and match; thereby, finding which peptides work best for them.
Our peptide therapies are also known as secretagogues – a substance that promotes secretion.  These amino acid chains communicate with the body to produce or release growth hormone.  The increased volume of human growth hormone produced by the pituitary gland causes an increase in the production of Insulin-Like Grow Factor-1 (IGF-1) by the liver and results in several health benefits such as:
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.
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.
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.
Exercise and sports have, in recent times gained the credit it is due. Not only are these sports a testament to the fortitude of the athletes, but they are also a science in themselves. Each sport has different exercise regimes and different dietary requirements. While some athletes face the same environment in each competition, there are those who have to face a different environment every time they compete. What remains constant however is the importance of growth hormone and the effect it has on the athlete’s body.
A multicenter study comparing the oral GH secretagogue macimorelin with arginine/GHRH found it to be safe, convenient, and of comparable efficacy (82% sensitivity, 92% specificity, and 87% accuracy in diagnosing adult GHD), with a GH cut-off point of 6.8 μg/L for patients with a body mass index (BMI) <30 kg/m2 and 2.7 µg/L for patients with a BMI >30 kg/m2 [268].
Y.-T. Shen, J. J. Lynch, R. J. Hargreaves, and R. J. Gould, “A growth hormone secretagogue prevents-ischemic-induced mortality independently of the growth hormone pathway in dogs with chronic dilated cardiomyopathy,” Journal of Pharmacology and Experimental Therapeutics, vol. 306, no. 2, pp. 815–820, 2003. View at Publisher · View at Google Scholar · View at Scopus
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

Statistical analyses were carried out using GraphPad Prism 6 for Windows, version 6.01. For clinical response, histomorphometric parameters, and gene expression data, normal distribution (Kolmogorov-Smirnov) and variance homogeneity (Brown-Forsythe) tests were performed. Once normality was demonstrated, differences between GHRP-6-treated and placebo-treated animals were determined using two-tailed unpaired Student’s -test. For non-Gaussian distributed data, Mann-Whitney U test was performed. For analyzing closure kinetics of rat wounds, two-way ANOVA was performed, followed by Sidak’s multiple comparisons test. In all cases, values of were considered statistically significant. The values shown represent mean ± SD (error bars).
Growth Hormone Releasing Peptides (GHRP) are a class of compounds, which stimulate the release of growth hormone. GHRP variants include GHRP-2, GHRP-6, hexarelin, ipamorelin (Thomas et al, 2011) and agents with similar actions including CJC-1295 (Teichman et al, 2006, Acherman et al, 1999, Walker et al, 2006). These agents are considered peptide hormones. GHRPs are thought to act by stimulating the release of endogenous human growth hormone leading to pharmacological effects such as increased bone mineral density, increased lean muscle mass, modest improvements in strength and improved recovery from injuries such as fractures (Smith, 2005).
The authorities have branded it as a banned substance in the competitive athletics and bodybuilding to prevent the unfair advantage users are likely to gain from this drug. But many athletes and bodybuilders continue to pursue the drug actively. Then there are those people who are ready to try just about anything to lose all of their extra weight. There is always heavy demand for fat cutters and the demand for GHRP-6 is no exception. A majority of the demand groups don't have prescriptions for this drug and are likely to procure this from the black market or the internet. This is where the authorities need to step in.
"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
GHRP-6 can effectively provide substantial increases in GH production. It’s typically taken 2-3 times per day by injection at times when blood sugar is not elevated. Cost is generally moderate. The only common potential adverse side effect is increased hunger. Common alternates include GHRP-2, hexarelin, ipamorelin, or GH itself. GHRP-6 also may provide benefits which GH does not, via its action at the ghrelin receptor in various tissues of the body.
For example, studies have shown that people deficient in IGF-1 have an increased chance of dying from a heart attack. This is because IGF-1 prevents the death of heart cells and offers protection to heart cells when the cells are stressed, such as during a heart attack or long amount of time without oxygen. IGF-1 has a similar protective effect on brain cells.
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.
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.

Basic molecular pathophysiological cascade of acute myocardial infarction. Hypoxia triggers an acute failure in mitochondrial respiratory function when the diffusible oxygen stores become exhausted. Adenosine triphosphate reserves are rapidly depleted, and there is a respiratory shift toward an anaerobic profile. Lactate, H+ ions, CO2, and potassium accumulate may lead to arrhythmias, microendothelial damage, myocardiocytes stunning, and cell death. Adenosine triphosphate (ATP) depletion is irrevocably ligated to the inability of maintaining the normal negative resting membrane potential, to an alteration of calcium homeostasis (intracellular Ca2+ ([Ca2+]i) overload), which may eventually lead to different patterns of abnormal cardiac contraction. Mitochondrial functionality becomes abnormal, establishing the so-called “open pore” (mitochondrial permeability transition pore [mPTP]), leading to local cell death. In this scenario, mitochondria turn into an active ROS manufacturing plant that increases and perpetuates mitochondrial damages and dysfunction. The failure of myocardial contractility (contractility depression) is a precocious and multifactorial consequence of ischemia, which may eventually lead to reduced cardiac output and heart failure. This situation may translate into a self-perpetuated vicious circle, thus amplifying the ischemic episode and the myocardial wall stress. The local inflammatory reaction is a useful but critical operator within the myocardial ischemia/reperfusion damage process. Hypoxia itself activates the HIF-α/MIF axis and the consequent downstream inflammatory cascade. The locally secreted pro-inflammatory cytokines are involved in a self-perpetuating process in the ROS chain reaction, inflammation, and cellular damage.
Remember the GHRP you select is used for a few reasons. One is to prompt the release of the increase pulse in GH you have initiated with the GHRH you have selected to use. This is by inhibition of Somatostatin. So you are actually selecting the timing of the release of your natural production of  still physiologic amount of GH.  Another reason is to actually contribute a little more to the amplitude of you GH pulse.
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.
The response to GHSs is not gender related, except during puberty, when girls exhibit a greater response than do boys. The GH responses to both GHSs and ghrelin are similar during the early-follicular, late-follicular, and luteal phases of the menstrual cycle, suggesting that they are not affected by changes in estrogen levels. However, estrogen as well as estrogen-progestin supplementation enhances the GH response to ghrelin after menopause.
Peptides is from the latin word pepsis which means digestion. So in reality they cover anything in the body that aids digestion and since we get all our nutrients from this process the use of peptides is seemingly limitless. Recently biologically active peptides have been discovered in the heart, brain and skin so the potential uses and benefits of peptides in the future is really exciting.
A peptide is an amino acid chain (amino acids being the building blocks of proteins), responsible for signalling different responses in the body. These amino chains already exist in the body in one form or another, which is why some consider them as ‘natural’ compounds (although testosterone exists in the human body too, adding extra is considered cheating in most cases). Peptides have been classified in research and manufacture according to a number sequence in many cases, which is why some are just numbers and letters (see later).
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.
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.
This is the most popular variant of IGF-1 that buyers will find on the market today. IGF-1 LR3 comprises 83 amino acids. That means it adds extra 13 amino acids to the sequence of the standard insulin-like growth factor-1. The polypeptide boasts qualities that make it much more powerful than normal IGF-1. It boasts a longer half life of up to 30 hours, compared to the latter’s 15 hours. In addition to bodybuilding, IGF-1 LR3 helps with fat burning, quicker recovery and slowing aging.
Myocardial ischemia/reperfusion damage entails multiple molecular and biochemical mechanisms that each alone is sufficiently injurious to disturb an organ whose mechanical performance is dependent upon the stability of ionic/electrical pumps. Oxidative stress, intracellular calcium overload, pH changes, mitochondrial dysfunction, inflammation, and excessive neurohormones are part of an interactive and self-perpetuating continuum of the myocardial injury cascade (Figure 1). The evidences obtained along the years of experimental screening of the synthetic GHRP suggest that each single member of this family of peptides is able to simultaneously counteract different injurious operators in the myocardial ischemic event.
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