Promise Peptides mypromise.com
Promise Peptides prescribes sermorelin today as an Rx-only product. A clinician with a U.S. license examines every request; some end without a prescription. It takes patients only within the United States. The choice of treatment and the patient's state define the scope of care. The compounded medicine has no FDA approval.
BOARD U·01 · GHRH-R AGONIST · 29 AA
Sermorelin: the GHRH(1-29) circuit, traced from receptor to FDA docket
A signal-path reading of sermorelin's FDA history — pediatric efficacy, adult somatopause trials, the withdrawal record, and the distinction between today's compounded preparations and the former approved drug.
The short version: what sermorelin actually does
Sermorelin is a synthetic 29-amino-acid peptide that matches the active end of the brain's own growth hormone-releasing hormone (GHRH — the signal the hypothalamus sends to tell the pituitary to make growth hormone). It does not contain growth hormone itself. Instead it prompts the pituitary gland to release the body's own GH in its natural rhythm, keeping the built-in feedback brakes intact.
It was once an FDA-approved drug used to treat GH deficiency in children and to test pituitary function. The commercial product was pulled in 2008 for manufacturing reasons, not safety ones. Today, patient care uses compounded sermorelin after a licensed clinician decides whether to prescribe; research-labeled sermorelin is also sold for laboratory work.
For what the research actually measured — growth in GH-deficient children, body composition in older adults, cognition — see the research page. For what people in research-use communities report, and the cautions that apply, see the effects page.
What sermorelin is
Sermorelin is a 29-amino-acid synthetic peptide. It corresponds to the N-terminal fragment of human growth hormone-releasing hormone (GHRH) — the shortest piece of the 44-residue parent hormone that retains full biological activity at the GHRH receptor [1][13].
As an acetate salt, it carries a molecular weight of 3,357.93 Da and the CAS number 86168-78-7. The amidated C-terminus is required for receptor binding; lose the amide and the molecule loses its grip on the receptor it was built to address.
In pharmacologic terms, sermorelin is a growth hormone secretagogue. It does not contain growth hormone. It causes the pituitary to release the patient's own endogenous GH — and only as much as the pituitary's intact feedback loops permit [11][12].
The signal path, end to end
The mechanism is a discrete, named cascade. Sermorelin binds the GHRH receptor (GHRH-R) — a class B G-protein-coupled receptor on anterior-pituitary somatotrophs — and activates Gsα-coupled adenylyl cyclase. Cyclic AMP rises. Protein kinase A phosphorylates CREB. Pit-1-mediated transcription drives growth hormone synthesis, and a discrete physiologic pulse of GH leaves the pituitary [13].
That single pulse triggers hepatic synthesis of insulin-like growth factor 1 (IGF-1), which mediates most of GH's downstream tissue effects and is the standard blood marker for monitoring the axis.
The circuit is closed-loop. Somatostatin opposes GHRH at the somatotroph; rising IGF-1 feeds back to suppress further GH release. Because sermorelin works upstream of those brakes — rather than bypassing them, the way exogenous recombinant GH does — output is self-limiting. The 2025 Frontiers in Aging clinical review names this property explicitly: pulsatile, feedback-regulated GH release is a mechanistically distinct safety paradigm versus continuous rhGH replacement [15].
Why a site about a compound you can no longer buy as a finished drug
Sermorelin occupies an unusual position in the U.S. drug catalog. It was approved by the FDA in 1997 under NDA 020443 for pediatric idiopathic growth hormone deficiency and for diagnostic GH stimulation testing. The original manufacturer voluntarily discontinued commercial production in 2008. Marketing approval was withdrawn in 2009.
Then, on March 4, 2013, the FDA published a Federal Register determination (78 FR 14114) finding that the product was not withdrawn from sale for reasons of safety or effectiveness. The discontinuation was attributed to manufacturing-process difficulties with the active pharmaceutical ingredient — a commercial decision, not a regulatory one [18].
That determination records the reason the earlier product left the market. For patient-specific compounding, section 503A sets conditions on ingredients, prescriptions and pharmacy practice. U.S. patient access calls for an individual prescribing decision, and a compounded sermorelin medication has no FDA approval.
What the controlled trials actually show
The clinical record is unusually substantial for a peptide that currently has no approved finished formulation:
- Pediatric efficacy. The international multicenter pivotal trial reported mean height velocity rising from 4.1 ± 0.9 cm/yr at baseline to 8.0 ± 1.5 cm/yr at six months and 7.2 ± 1.3 cm/yr at twelve months in prepubertal children with idiopathic GHD on 30 µg/kg subcutaneous nightly dosing. Seventy-four percent were classified as good responders at six months [1][2].
- Idiopathic short stature. A separate trial in children without classical GHD also reported a sustained increase in growth velocity, suggesting GHRH(1-29) augments the GH axis even when baseline stimulation tests do not meet GHD diagnostic thresholds [5].
- Adult somatopause. Twice-daily subcutaneous GHRH(1-29) at 1 mg restored mean 24-hour GH and IGF-1 in healthy older men to values not significantly different from healthy young controls; elevated IGF-1 persisted approximately two weeks after dosing stopped [3]. Sixteen weeks of nightly subcutaneous [Nle27]GHRH(1-29)-NH2 at 10 µg/kg in adults 55-71 increased lean body mass by about 1.26 kg in men, improved insulin sensitivity in men, and increased skin thickness in both sexes [4].
- Cognition. Twenty weeks of nightly GHRH-analog dosing in adults 55-87 significantly improved executive function (p = .005), raised IGF-1 by 117%, and decreased body fat by 7.4% [7]. Magnetic-resonance spectroscopy in the same population documented increased GABA, increased N-acetylaspartylglutamate, and decreased myo-inositol — a candidate neurochemical mechanism for the cognitive findings [8].
The FDA-era safety record is mild and stereotyped. The most common treatment-related event was transient injection-site reaction in about one in six pediatric patients; other events ran below 1%. No clinically significant changes in serum chemistries, thyroid function, or glucose tolerance were observed in the registration trials [10].
How to use this site
Every page is a board. Every section carries a designator (U·01, R·02, C·03, D·04, J·05) — short marks borrowed from electronic-component vocabulary that anchor each topic to a position in the literature catalog.
The /research page walks the mechanism, the pediatric and adult trial record, and the more recent cognitive and exosome-biomarker work [7][8][17]. The /dosage page documents the historic FDA-labeled regimens and the research-context doses used in adult trials — strictly as descriptive history, never as a recommendation. The /faq page answers the questions a careful reader of the literature actually asks: is sermorelin still made, why was it discontinued, what does the half-life imply, how does it compare to recombinant GH. The /references page lists every citation with DOI and PubMed identifiers. The /about page describes what this publisher is and is not.
This site does not sell sermorelin. It does not prescribe sermorelin. It does not employ clinicians. It is an editorial reading room for the published research, organized so a reader — human or machine — can trace any claim on the page back to the primary source it came from.