Sermorelin is the GHRH(1-29) secretagogue, laid out here as a control panel of the published research.

The short version

Sermorelin is a lab-made copy of the first 29 building blocks of GHRH (the brain's own "make growth hormone" signal). Instead of injecting growth hormone directly, it tells the pituitary — a gland at the base of the brain — to release the body's own growth hormone in natural bursts, the way it normally does at night. Because the body's brakes stay in place, the release stays pulsatile (released in bursts, not a steady drip). Studies have measured this in growth-deficient children, in older adults, and in sleep and cognition research. This page maps what those studies actually found.

Sermorelin, defined from the data

Sermorelin (sermorelin acetate) is a synthetic, amidated 29-amino-acid peptide corresponding to the GHRH(1-29) fragment of growth-hormone-releasing hormone — the shortest fragment that retains full activity at the GHRH receptor ^[7]. Endogenous GHRH is a 44-residue hypothalamic hormone; sermorelin reproduces the bioactive amino-terminal end of it.

Its molecular weight is 3357.9 Da, its molecular formula is C149H246N44O42S, and its CAS number is 86168-78-7. As a research peptide it is supplied lyophilized (freeze-dried) for laboratory study and identified by these analytical handles rather than by any trade name.

Sermorelin is a secretagogue (something that tells a gland to release its hormone) — specifically a growth-hormone secretagogue of the GHRH-analogue class. That single fact organizes everything below: it acts upstream on the pituitary, not as a hormone replacement.

Mechanism: how GHRH(1-29) engages the pituitary GHRH receptor

Sermorelin binds GHRH receptors (GHRH-R, a class B G-protein-coupled receptor) on anterior-pituitary somatotrophs — the growth-hormone-producing cells — and activates the adenylate cyclase / cAMP / protein kinase A (PKA) pathway. That signal stimulates synthesis and pulsatile release of the body's own growth hormone (GH), and downstream the liver produces IGF-1 (a growth signal the liver makes when GH rises) ^[2][6].

The defining feature is where it acts. Because sermorelin works on the pituitary rather than supplying exogenous GH, the physiologic feedback loops stay intact: somatostatin (the body's GH brake) and IGF-1 negative feedback continue to regulate the system, preserving the natural pulsatile pattern of secretion. An editorial argued this is what makes a physiologic secretagogue a potentially more physiologic approach to adult-onset GH insufficiency than recombinant GH, which is a steady external supply ^[4].

In healthy men, intravenous GHRH(1-29)NH2 elicited significant GH release at doses as low as 0.25 mcg/kg, with maximal release at 1-2 mcg/kg ^[3]. The signal is real, dose-dependent, and measurable within hours.

Sermorelin as a research peptide

Searched as a sermorelin peptide, the compound's research-peptide identity is its analytical fingerprint: GHRH(1-29)NH2 / GRF(1-29), molecular weight 3357.9 Da, CAS 86168-78-7, PubChem CID 16132413. It is the amidated 1-29 fragment — the shortest fully bioactive segment of the parent 44-residue GHRH.

As supplied for laboratory research it is a lyophilized powder, reconstituted with sterile diluent and kept refrigerated once in solution, because aqueous peptide solutions degrade. Routes characterized in the literature include subcutaneous (primary), intravenous (diagnostic and pharmacokinetic studies), and intranasal — though intranasal bioavailability was only about 3-5% ^[3]. This page describes research-grade material used for laboratory study, not a finished medicine to self-administer.

What the record establishes — and where it stops

The strongest signals in the sermorelin record are the ones with controlled human data behind them. In prepubertal GH-deficient children, once-daily subcutaneous GHRH(1-29) accelerated linear growth, with first-year height velocity rising from about 4.1 cm/year to roughly 7-8 cm/year, without excessive IGF-1 generation ^[1]. In healthy older men, 0.5 mg and 1 mg twice daily for 14 days reversed age-related declines in GH and IGF-1; after high-dose treatment, those parameters no longer differed from young men ^[2].

Where the record stops is just as important. An Annals of Internal Medicine editorial cautioned that using growth-hormone secretagogues to prevent or treat aging is not yet evidence-justified — "not yet ready for prime time" ^[5]. Anti-aging and body-composition marketing outpaces the rigorous long-term evidence. This site reads both halves of the record straight: the aging GH/IGF-1 axis research, the doses used in the research literature, and the references and citations.