# Growth Hormone Axis research peptides, mapped by receptor > Growth Hormone Axis research peptides, mapped by receptor — Precision Peptide Planner — Growth Hormone Axis research peptides mapped at the receptor: CJC-1295 and sermorelin at GHRHR, ipamorelin at GHS-R1a, MOTS-c nowhere near the pituitary. An independent, cited literature digest with no doses and no protocols. **GH / IGF-1 axis — receptor map** Four compounds, three distinct molecular targets, one shared output. This desk plots where each one actually binds — and marks the places where the marketing quietly stops matching the pharmacology. ### [CJC-1295](/cjc-1295) A GHRH(1-29) scaffold with four protease-resistant substitutions and, in the DAC form, a covalent handle onto serum albumin. Long plasma residence, measured pulsatility preserved, human data limited to early pharmacology. ### [Ipamorelin](/ipamorelin) A selective ghrelin-receptor (GHS-R1a) agonist — a different door into the same somatotroph. Short, discrete GH pulse; the only controlled human trial missed its primary endpoint. ### [Sermorelin](/sermorelin) GHRH(1-29) itself: the shortest fragment of the native hormone that retains full receptor activity. The one compound here with an approval history, a pediatric efficacy trial, and a thin adult evidence base. ### [MOTS-c](/mots-c) A mitochondrially encoded 16-residue peptide acting on the folate cycle, AMPK and casein kinase 2. Filed with the GH peptides by retailers; it does not touch the pituitary. ## Start here Growth hormone is made in the pituitary, a gland about the size of a pea at the base of the brain. It is not released steadily. It comes out in bursts, called pulses, mostly during deep sleep. The liver answers those bursts by making IGF-1, a second hormone that carries out much of growth hormone's work in muscle, bone and fat. The four compounds catalogued on this site get filed under one shopping-cart heading — "growth hormone peptides" — but they do not do the same thing. Two of them, CJC-1295 and sermorelin, imitate the body's own release signal and press the same button on the pituitary. A third, ipamorelin, presses a different button on the very same cell. The fourth, MOTS-c, never reaches the pituitary at all; it works inside muscle cells on an energy sensor. That set of differences is the whole subject of this desk. What follows is a map of mechanisms and published findings. It is not a schedule, not a protocol, and not a dose. ## One axis, three places to intervene The growth-hormone axis is a relay. The hypothalamus releases growth-hormone-releasing hormone (GHRH). GHRH acts on somatotroph cells in the anterior pituitary. Those cells release growth hormone (GH) in pulses. The liver converts that signal into insulin-like growth factor 1 (IGF-1). Somatostatin, an opposing hypothalamic hormone, sets the troughs between pulses, and IGF-1 feeds back to damp the loop. Three of the four compounds here intervene at the same stage — the pituitary somatotroph — without using the same receptor: - **GHRH-receptor agonists.** Sermorelin is GHRH(1-29), the shortest fragment of the native 44-residue hormone that retains full activity at the GHRH receptor [1]. CJC-1295 is that same 1-29 scaffold carrying four amino-acid substitutions and, in the DAC variant, a maleimidopropionyl handle that bonds covalently to circulating serum albumin [7]. Both dock at GHRHR and drive the Gs/cAMP/PKA cascade inside the somatotroph. - **Ghrelin-receptor agonist.** Ipamorelin is a synthetic pentapeptide that binds GHS-R1a, the growth-hormone-secretagogue receptor for ghrelin, on that same somatotroph. Different receptor, different intracellular route, same secretory output. - **Neither of the above.** MOTS-c is a 16-amino-acid peptide encoded inside the mitochondrial 12S rRNA gene [19]. Its characterised targets are the folate cycle and de novo purine synthesis, AMPK, NRF2-regulated stress genes, and — since a 2024 report — casein kinase 2, which it binds directly [17]. The pituitary is not on that list. A fourth position on the axis exists and none of these compounds occupies it: recombinant growth hormone itself, which is supplied from outside and bypasses the pituitary and the feedback that governs it. Everything mapped here sits upstream of GH, which is the reason pulsatility and feedback remain part of the discussion at all. ## GHRHR and GHS-R1a: two doors into the same room The two pituitary receptors converge on GH release. They are not interchangeable, and the difference is measurable. GHRHR is the receptor the body's own signal uses. An agonist arriving there raises cyclic AMP through Gs and protein kinase A, increasing both GH synthesis and GH release. Because the input enters the axis exactly where the endogenous input enters it, somatostatin tone and IGF-1 feedback continue to shape the output — a GHRH analog raises the height of the pulses rather than flattening them into a plateau. The clearest demonstration is a single-dose study in healthy men aged 20 to 40: CJC-1295 raised trough GH roughly 7.5-fold and lifted mean GH by about 46% and IGF-1 by about 45% one week later, while the frequency and magnitude of pulsatile secretion were unaltered [5]. GHS-R1a is the receptor for ghrelin, the stomach-derived hunger signal, and it reaches the same secretory machinery by a different intracellular route. Ipamorelin's effect there is short and discrete: population pharmacokinetic-pharmacodynamic modelling in healthy male volunteers put its terminal half-life at roughly 2 hours, with the GH response peaking about 40 minutes after administration as a single distinct pulse [11]. It also does something the older growth-hormone-releasing peptides do not — it releases GH without meaningfully raising ACTH, cortisol or prolactin, and that selectivity is the compound's defining pharmacological feature. Because the two doors are genuinely separate, opening both is additive rather than redundant, and that is the entire pharmacological argument behind the widely discussed pairing of a GHRH analog with ipamorelin. It is worth stating the argument precisely: it rests on single-agent pharmacology at two receptors, not on any controlled trial of the combination against an outcome. ## Where the map stops matching the marketing Four places where the category language and the pharmacology come apart, all of them documented in the literature this desk reads: **"CJC-1295" names two different drugs.** The DAC variant binds albumin and has an estimated half-life of 5.8 to 8.1 days, with IGF-1 still above baseline as long as 28 days after repeated administration [4]. The no-DAC form, sold as Modified GRF (1-29), keeps the four stabilising substitutions but has no albumin handle and is short-acting. Product listings and forum threads routinely treat the two as one compound. They are not pharmacokinetically comparable, and every duration figure on this site is tagged to the form it was measured in. **The combination is inferred, not tested.** The pharmacology behind pairing a GHRH-receptor agonist with a ghrelin-receptor agonist is sound and is spelled out above. What does not exist is a trial of that combination against any clinical outcome. The evidence is two single-agent literatures set side by side. **MOTS-c is filed in the wrong drawer.** It is sold alongside the secretagogues and described in the same breath, but its published mechanism runs through AMPK, the folate cycle and CK2 in skeletal muscle [17][19], not through the pituitary. Grouping it with GH secretagogues is a retail convention, not a mechanistic one. **Sermorelin's regulatory history is routinely misstated.** It was an approved drug for pediatric growth-hormone deficiency and was withdrawn from the US market in 2008 for commercial reasons, not for safety or efficacy failures — a distinction that gets lost in both directions. Separately, an *Annals of Internal Medicine* editorial concluded that using growth-hormone secretagogues to prevent or treat the effects of aging is not yet justified by the evidence, calling it "not yet ready for prime time" [14]. That verdict has not been overturned by anything catalogued here. ## What "research peptide" means here, and what "planner" does not mean Three of the four compounds on this site — CJC-1295, ipamorelin and MOTS-c — have no approved human indication anywhere and are sold by suppliers for laboratory research use only. Sermorelin is the exception: it held a US approval for pediatric growth-hormone deficiency, and after that product's withdrawal it is handled through compounding pharmacies under the FDA's interim Section 503A Category 1 policy. Ipamorelin travelled in the opposite direction, being removed from Category 2 of that interim list in 2024 and reviewed at the October 2024 Pharmacy Compounding Advisory Committee meeting. All four are prohibited in sport at all times by the World Anti-Doping Agency, and validated detection methods exist for the class. Material sold as research-grade peptide is not manufactured under pharmaceutical quality assurance; identity, purity and sterility are supplier-dependent and unverified, and critical reviews of the gray market report frequent mislabelling and contamination. Any figure on this site describes what was measured in a cited study, in the material and species that study used. One clarification the name of this site earns. The planning done here is editorial: what gets planned is a route through the published record — which paper answers which question, and which claim rests on a mouse. This desk publishes no protocols, no cycles, no stacks, no schedules and no quantities intended for a person to follow. Where a dose appears in these pages it belongs to a cited experiment and is reported as a description of that experiment, never as guidance. --- Precision Peptide Planner charts where four growth-hormone-axis compounds bind and what the studies actually measured — a receptor map drawn from the literature, not a clinic, not a supplier, and not a protocol anyone can follow.