Reference Desk · Sermorelin · GHRH(1-29)
A layered read on sermorelin.
29 amino acids, 11-12 minute half-life, six landmark adult trials, one canonical receptor. Three decades of GHRH-axis research, condensed into glanceable panels with the math left legible underneath.
The short version
Sermorelin is a 29-amino-acid peptide — the shortest fragment of the brain's own growth hormone-releasing hormone (GHRH) that still fully activates the pituitary receptor. Unlike injecting growth hormone (GH) directly, sermorelin tells the pituitary to release the body's own GH in its natural pulses, with the body's brakes (somatostatin, IGF-1) still intact [7].
It was an FDA-approved prescription drug (Geref) from 1990 to 2008 — pulled from the US market for commercial reasons, not safety failures [6]. Today it is compounded under 503A pharmacy rules, Category 1 status [8]. The trials that exist are real and show modest, reproducible changes in GH/IGF-1, body composition, and cognition; the long-term anti-aging evidence is thin [1][5]. It is banned in sport (WADA S2.2.4) [14]. What people report in research-use settings — benefits and side effects — is on the effects page.
The compound, at a glance
Sermorelin is a 29-amino-acid peptide that corresponds to the N-terminal fragment of human growth hormone-releasing hormone (GHRH), the 44-residue neuropeptide produced in the hypothalamic arcuate nucleus. The 1-29 fragment is the shortest sequence that retains full GH-releasing activity at the pituitary GHRH receptor (GHRHR) [6]. Sequence: YADAIFTNSYRKVLGQLSARKLLQDIMSR-NH2. Molecular formula C149H246N44O42S. Molecular weight 3357.93 Da. CAS 86168-78-7.
C-terminal amidation stabilizes receptor binding. The N-terminal tyrosine-alanine bond is the cleavage site for dipeptidyl peptidase IV (DPP-IV), which is why the parent peptide carries an 11-12 minute plasma half-life [8] and why later analogs (tesamorelin, CJC-1295, MR-409) were engineered with DPP-IV-resistant N-terminal modifications [10].
The FDA approved the original commercial formulation (Geref, Serono Laboratories) in 1990 for diagnostic use and in 1997 for treatment of idiopathic growth hormone deficiency in children [6]. Serono voluntarily discontinued commercial production in 2008 for business reasons; the FDA published the formal withdrawal notice in 2013. Sermorelin currently exists in the US market as a 503A compounding-pharmacy substance, not as an FDA-approved finished drug.
What the adult research shows
Across the modern adult-aging literature, the headline numbers cluster within a recognizable range. In the largest controlled trial — Baker 2012, 20 weeks of 1 mg/day subcutaneous tesamorelin (a DPP-IV-stable GHRH(1-29) analog) in 152 adults aged 55-87 — serum IGF-1 rose 117% while remaining within the physiological range, body fat dropped 7.4%, lean mass increased 3.7%, and executive function improved (p=0.005) in both healthy and mild-cognitive-impairment participants [1].
Five months of nightly subcutaneous sermorelin ~14 µg/kg (~1 mg) in 89 older adults — Vitiello 2006 — doubled 24-hour GH secretion, raised IGF-1 by ~40%, reduced body fat ~5%, and improved psychomotor processing-speed scores by 5-7% [5]. Six weeks of 2 mg nightly in 11 elderly men — Vittone 1997 — significantly raised nocturnal GH pulse area (p<0.006) and measured upper-body strength (upright row p<0.02) without reaching DEXA-detectable composition changes in the short window [2]. Sixteen weeks of [Nle27]GHRH(1-29) 10 µg/kg nightly in 19 men and women — Khorram 1997 — produced +1.26 kg lean mass in men and measurable skin-thickness increases in both sexes [3].
The direction is consistent across studies; the magnitudes are modest, not transformative.
Why GHRH agonism, and not GH itself
The pharmacological argument for stimulating the GHRH axis rather than delivering recombinant growth hormone directly is mechanistic. Sermorelin binds GHRHR on pituitary somatotrophs, raises intracellular cAMP via Gs-adenylyl cyclase, activates protein kinase A, phosphorylates CREB, upregulates GH1 gene transcription, and triggers exocytosis of pre-formed GH-containing secretory granules [7].
Because the entire cascade still passes through the pituitary, two feedback mechanisms remain intact: somatostatin (which inhibits GH release) and IGF-1 (which feeds back at both hypothalamic and pituitary levels). The result is pulsatile, self-limiting GH release that approximates the physiological pattern — rather than the flat, tonic exposure produced by direct GH injection [7]. In Vitiello 2006, 24-hour GH secretion doubled but IGF-1 rose only 40% and never exceeded the physiological range, consistent with feedback-capped output [5].
What this site is
MD Sermorelin is an independent editorial project that publishes summaries of the peer-reviewed research literature on sermorelin and the broader GHRH(1-29) analog family. The site is not a clinic. It does not employ clinicians. It does not provide medical advice. It does not manufacture, sell, distribute, or recommend sermorelin or any related compound.
The 'MD' in the domain name signals editorial framing — the panels are organized the way a medical reference desk is organized — not a claim about services. The seven pages of this site read top to bottom: mechanism on /research, dose context on /dosage, common questions on /faq, the eighteen primary citations on /references, the publisher's editorial standards on /about. A research disclaimer rides every page footer.