# The questions people actually arrive with > Growth Hormone Axis Research Peptides FAQ — Ipamorelin, CJC-1295, Tesamorelin — steroidnpeptides — Frequently asked questions about Growth Hormone Axis research peptides: what ipamorelin, CJC-1295 and tesamorelin are, what the trials measured, what the risks are, and what this desk deliberately does not cover. **QUESTIONS AND ANSWERS** Answered from the published record, with the citation attached to every number and the gaps named where they exist. ## What is ipamorelin? Ipamorelin is a synthetic peptide five amino acids long, with the sequence Aib-His-D-2-Nal-D-Phe-Lys-NH2. It was derived from the earlier growth-hormone-releasing peptide GHRP-1 and acts as a selective agonist of the ghrelin receptor, GHS-R1a, on pituitary cells. Activating that receptor produces a discrete pulse of growth hormone release. It has never been approved as a drug in any jurisdiction and is handled as a research chemical. In older literature it appears as NNC 26-0161. ## What is ipamorelin peptide, and how is it different from the older GHRPs? It belongs to the same family as GHRP-1, GHRP-2 and GHRP-6, all of which release growth hormone through the ghrelin receptor. Its distinguishing feature is selectivity: unlike those earlier compounds, ipamorelin does not meaningfully raise ACTH, cortisol or prolactin. That property is what made it the reference compound of the class in the pharmacological literature, and it is a claim about the receptor pharmacology rather than a claim of general safety. ## What does ipamorelin do, according to the published studies? In humans, the published record shows two things. It produces a single growth hormone pulse peaking about 40 minutes after administration, with a terminal half-life of approximately 2 hours and dose-proportional kinetics across the range tested in healthy male volunteers [4]. And in the only controlled trial of a clinical outcome — 114 adults recovering from bowel resection — it did not shorten the time to a first tolerated meal, at 25.3 hours against 32.6 hours on placebo, p=0.15 [3]. In animals it increased longitudinal bone growth in rats from 42 to 52 micrometres per day at the highest dose tested [5] and reduced chemotherapy-associated weight loss in ferrets by about 24% [1]. That is the whole published picture. ## What are the risks of ipamorelin? The largest one is the size of the evidence base. Controlled human exposure amounts to a seven-day perioperative intravenous trial in 114 patients [3] and acute single-dose infusions in eight volunteers per dose level [4]. There is no Phase 3 trial and no long-term human safety database. Beyond that, three mechanistic concerns recur in the literature: growth-hormone-axis activation raises IGF-1, a known mitogen, which is a theoretical issue for anyone with a pre-existing or occult tumour; growth hormone reduces peripheral insulin sensitivity while ipamorelin separately stimulates insulin release from pancreatic islet tissue in ex vivo work, making the net glycaemic effect unpredictable; and a 28-day study of a different GHS-R1a agonist in rats found dose-dependent myocardial degeneration, a class-level cardiovascular signal that has never been ruled out for ipamorelin because the equivalent study has never been done [2]. Material obtained outside pharmaceutical supply chains also has unverified purity, identity and sterility. ## What is CJC-1295? CJC-1295 is a synthetic analogue of growth-hormone-releasing hormone built on the first 29 residues of human growth-hormone-releasing factor, with four amino-acid substitutions that block enzymatic breakdown. In its long-acting DAC form it also carries a linker that bonds covalently to circulating serum albumin, giving it a half-life estimated at 5.8 to 8.1 days [9]. It is not approved for human use anywhere, and the original commercial development programme was discontinued. ## What is the difference between CJC-1295 DAC and Modified GRF 1-29? They are two pharmacologically different molecules sold under overlapping names. The DAC form carries the albumin-binding handle and therefore acts for days; the no-DAC form, usually labelled Modified GRF 1-29 or Mod GRF 1-29, keeps the four protective substitutions but omits that handle and is short-acting. The albumin-conjugate design was demonstrated in rats to give a four-fold increase in growth hormone area-under-curve over the unconjugated peptide, with the compound still detectable in plasma beyond 72 hours [12]. Because sustained exposure is what drives fluid retention, glycaemic drift and cumulative IGF-1, any reported effect is uninterpretable without knowing which form produced it — and the two are routinely conflated in commercial listings and in discussion. ## What does CJC-1295 do to growth hormone and IGF-1? In healthy adults aged 21 to 61, single subcutaneous doses of 30 or 60 micrograms per kilogram produced dose-dependent two- to ten-fold increases in mean plasma growth hormone lasting six days or more, and one-and-a-half- to three-fold increases in IGF-1 lasting nine to eleven days; after repeated dosing IGF-1 remained above baseline for up to 28 days [9]. In a separate study of healthy men aged 20 to 40, a single dose raised trough growth hormone approximately 7.5-fold, mean growth hormone by about 46% and IGF-1 by about 45% one week later, with the frequency and magnitude of pulsatile secretion unaltered [10]. ## Is CJC-1295 safe? There is no dataset that could answer that question. Published human exposure consists of a small number of early pharmacology studies [8][9][10]; no large or long-term trial in healthy adults has ever been conducted. What the record does contain: the Food and Drug Administration cited immunogenicity among the safety concerns underlying its 2024 decision not to recommend the compound for the Section 503A compounding bulks list, and the current class review notes that long-acting albumin-binding designs raise such considerations [6]. The original Phase 2 programme in HIV-associated visceral obesity was discontinued, and a patient death during the development era is frequently cited alongside it — the public record does not establish that CJC-1295 caused it, and this desk does not claim that it did. Sustained IGF-1 elevation carries the standard class concern, since population epidemiology links higher circulating IGF-1 to modestly increased risk of certain cancers. ## How much CJC-1295 is used in the published studies? This desk does not provide dosing and does not tell anyone what to take. It can report what the trials administered, because that is part of the finding. The human pharmacology studies used single subcutaneous doses of 30 or 60 micrograms per kilogram [9] and 60 or 90 micrograms per kilogram [10] in healthy adults, under supervision, with hormone concentrations as the measured outcome. The animal work used 2 micrograms every 24 hours in GHRH-knockout mice [11]. Those figures describe experiments; they are not a schedule, and nothing here should be read as one. Almost every protocol circulating online is derived from something other than a controlled human trial, because there are only a handful of controlled human trials to derive anything from. ## What is tesamorelin? Tesamorelin (Egrifta) is a synthetic 44-amino-acid analogue of human growth-hormone-releasing hormone with a trans-3-hexenoic acid group on the N-terminus that resists cleavage by dipeptidyl peptidase-IV. It is the only compound on this desk with an approved medical use: the United States approved it in November 2010 to reduce excess abdominal fat in HIV-infected adults with lipodystrophy [14]. Every other application is off-label. ## What does tesamorelin do, and how does it work? It binds the growth-hormone-releasing hormone receptor on anterior-pituitary somatotroph cells, activating a Gs-coupled cAMP and protein kinase A cascade that stimulates synthesis and pulsatile release of endogenous growth hormone. That growth hormone drives hepatic IGF-1 production, and the two together promote lipolysis preferentially in visceral adipose tissue. Because it amplifies the body's own pulsatile rhythm rather than supplying hormone from outside, its metabolic profile differs from recombinant growth hormone: in 13 healthy men, two weeks of 2 milligrams daily raised mean overnight growth hormone by 0.5 micrograms per litre (p=0.004) and IGF-1 by 181 micrograms per litre (p<0.0001) while leaving fasting glucose (p=0.93) and insulin-stimulated glucose uptake (p=0.61) unchanged [16]. ## Does tesamorelin reduce visceral fat, and does the effect last? Yes to the first, with qualifications on the population, and no to the second without continued treatment. Pooled across five randomised controlled trials in HIV-associated lipodystrophy, tesamorelin reduced visceral adipose tissue by 27.71 square centimetres (95% CI -38.37 to -17.06), trunk fat by 1.18 kilograms and hepatic fat fraction by 4.28 percentage points, and increased lean body mass by 1.42 kilograms, all at p<0.001 [13]. A six-month randomised trial in 50 adults found a -42 square centimetre treatment effect (p=0.005) [15]. Over 52 weeks in 273 participants the reduction was sustained at 18% (p<0.001 against baseline) — and visceral fat reaccumulated on discontinuation [17]. Those results are in adults with a specific fat-redistribution syndrome; generalisation to other populations is mechanistically plausible but has not been established by large randomised trials. ## Are these peptides anabolic steroids? No, and the two categories are not related in mechanism, chemistry or regulatory status. Anabolic-androgenic steroids are lipid-derived molecules acting on the androgen receptor and are a controlled-substance class. The compounds on this desk are short amino-acid chains acting on two receptors of the pituitary gland to change how much of the body's own growth hormone is released. This site does not cover the anabolic-androgenic class at all: no protocols, no comparisons for use, no sourcing, no legality guidance, and no framing of any peptide here as an alternative to, a substitute for, or a partner to anything in that category. ## Are growth hormone secretagogues allowed in competitive sport? No. Ipamorelin, CJC-1295 and tesamorelin are all prohibited at all times — in and out of competition — under category S2 of the World Anti-Doping Agency Prohibited List, which covers peptide hormones, growth factors, related substances and mimetics. The class is detectable by accredited anti-doping laboratories, and CJC-1295 has been structurally identified by high-resolution tandem mass spectrometry as the active ingredient of an unlabelled preparation seized in an anti-doping context [7]. This is stated as a fact about the compounds' regulatory status, not as advice about competing. ## Why do the trials measure such different things from what forums discuss? Because they were designed to answer different questions, funded by different people, for different purposes. A trial must pre-specify an endpoint that a regulator will accept, which pushes towards measurable clinical outcomes in defined patient populations: time to a first tolerated meal after bowel surgery [3], square centimetres of visceral adipose tissue in HIV-associated lipodystrophy [13][15][17], hormone concentrations in supervised volunteers [9][10]. Community discussion is organised around subjective experience over weeks in people who are generally healthy — a population no trial in this reference list enrolled. Neither literature is worthless, but they answer different questions and the answers do not transfer between them. Keeping that boundary visible is the editorial purpose of this desk. ## Does this site sell peptides or recommend a supplier? No. It sells nothing, links to no vendor, and names no supplier. It is a literature digest: it summarises published research, cites every source by number, and states where evidence is missing. It also gives no dosing guidance and no medical advice of any kind. Anyone with a clinical question should take it to a licensed clinician, who is the only person positioned to answer it. --- A reference desk on the growth hormone axis: it reports what the trials measured and names the species they measured it in, and it covers neither anabolic pharmacology nor any way of obtaining anything.