Sermorelin Research, Specifications & Scientific Information

Sermorelin is the first 29 amino acids of human growth hormone-releasing hormone, synthesised as a C-terminal amide. It is the shortest fragment of that hormone with full biological activity, and it was formerly approved in the United States as a pharmaceutical product; that product is no longer marketed.

By Elegance Peptides Editorial TeamPublished September 22, 2026Updated September 22, 2026

Category: GHRH analogues and GH secretagogues

Introduction

Sermorelin is the reference point for everything else in this family. It is not an analogue, not a conjugate and not a designed molecule: it is simply the first 29 amino acids of human growth hormone-releasing hormone, made as a C-terminal amide, and it is the shortest fragment of that hormone that retains its full biological activity ^[8]. Every growth hormone-releasing hormone analogue offered as a laboratory reagent is either a substituted version of this chain, a version with something bolted to its C-terminus, or an extension of it back towards the native 44-residue sequence.

It is also the only member of the family on this site that reached a regulatory approval and then lost it. Sermorelin acetate was approved in the United States, sold as Geref, and is no longer marketed. Its clinical literature is real, it is largely thirty years old, and it was conducted in children — a population and a set of endpoints that have nothing to do with laboratory reagent use. This page sets out what those trials measured and where the evidence stops.

What Is Sermorelin?

Sermorelin is a synthetic 29-residue peptide, sequence YADAIFTNSYRKVLGQLSARKLLQDIMSR, terminating in an amide. Positions 1 through 29 are identical to the native human hormone; the amide at the C-terminus is the only structural difference the chemical register records.

Its pharmacology follows from that identity. Administered intravenously or subcutaneously, it stimulates growth hormone secretion from the anterior pituitary ^[8], and because it acts on the pituitary rather than replacing the hormone the pituitary makes, it only works where the pituitary is intact. That is the clinical rationale on which its whole literature rests: in growth hormone deficiency of hypothalamic origin, where the pituitary is capable but under-stimulated, a releasing-hormone fragment is a plausible substitute for growth hormone itself. Where the deficit is pituitary, it is not.

Two uses were pursued. As a diagnostic agent, the growth hormone response to a single intravenous administration was assessed as a provocative test for growth hormone deficiency. As a therapy, repeated subcutaneous administration was studied in children with growth failure ^[8].

Sermorelin Specifications

Compound name: Sermorelin
Full chemical name: Human growth hormone-releasing factor (1-29) amide
Aliases: GHRH(1-29)NH2, GRF(1-29)NH2, Geref, growth hormone-releasing factor (human)-(1-29)-peptide amide, Groliberin
Development code: Not publicly characterised
CAS number: 86168-78-7
PubChem CID: 16132413
UNII: 89243S03TE
Compound type: Synthetic peptide (hormone fragment)
Peptide family: Glucagon / secretin peptide superfamily (growth hormone-releasing hormone)
Amino acid sequence: YADAIFTNSYRKVLGQLSARKLLQDIMSR
Sequence length: 29 residues
Molecular formula: C149H246N44O42S
Molecular weight: 3357.9 g/mol
Primary target: Growth hormone-releasing hormone receptor (GHRHR)
Secondary targets: Not publicly characterised
Receptor family: Class B1 (secretin-like) G protein-coupled receptors
Agonist / antagonist status: Agonist at the GHRH receptor

Sermorelin is not an analogue in the usual sense; it is a fragment. The 29 residues above are the first 29 amino acids of the 44-residue human growth hormone-releasing hormone, unmodified, terminating in a C-terminal amide rather than a free acid. That amide is the one structural modification the FDA/NCATS Global Substance Registration System records for the substance under UNII 89243S03TE: an amino acid substitution at arginine 29 with L-argininamide. The register describes this as the shortest synthetic peptide retaining the full biological activity of the parent hormone, and every other growth hormone-releasing hormone analogue offered as a laboratory reagent is a modification of this chain or an extension of it. CAS registry number 86168-78-7 and PubChem compound identifier 16132413 both resolve to this substance, and the molecular formula and mass agree across those registers and the supplier catalog. Any figure on this page is a reference value: the certificate of analysis supplied with a laboratory order is the record for a given lot.

Values that a public register does not carry are shown as not publicly characterised rather than estimated. Identifiers are reference values; the certificate of analysis supplied with a laboratory order is the record for a given lot.

How Does Sermorelin Work?

The receptor is the growth hormone-releasing hormone receptor, cloned from human anterior pituitary in 1993 and characterised there as a G protein-coupled receptor of the class that signals through Gs and cyclic AMP ^[3]. It belongs to the class B1, or secretin-like, family — structurally related to the receptors for glucagon, GLP-1 and secretin, and unrelated to the growth hormone secretagogue receptor that ipamorelin and the GHRP hexapeptides engage.

Receptor occupancy on a somatotroph raises intracellular cyclic AMP and leads to growth hormone release. Circulating growth hormone in turn drives hepatic production of insulin-like growth factor 1, which is why both hormones are measured across this literature.

The limitation that shaped the whole family is clearance. Sermorelin disappears from plasma quickly, and the analogues that followed it exist because of that fact rather than because of any deficiency in its receptor activity.

Sermorelin Mechanism of Action

In vitro research

The clearance mechanism was characterised in 1989, and the 1-29 amide was one of the forms tested. Plasma degradation of growth hormone-releasing hormone proceeds primarily by dipeptidylpeptidase IV cleavage at the 2-3 amino acid bond. The native 44-residue amide, the 40-residue acid, and the shortened 1-32 and 1-29 amides were all rapidly cleaved at that site; a fragment beginning at residue 2 was not; and conversion was blocked by a competitive inhibitor of the enzyme. Substituting a D-amino acid at position 1 or 2 prevented the hydrolysis entirely ^[2].

The same study reported a secondary, trypsin-like cleavage. Native growth hormone-releasing hormone was cleaved at the 11-12 position, while cleavage at 12-13 occurred only with the shortened 1-32 and 1-29 forms — so the shortened fragment is not merely a smaller version of the hormone with respect to metabolism ^[2].

A modern analytical study worked out the in vitro metabolism of four of the larger growth hormone-releasing hormone analogues, sermorelin among them, identifying nineteen major metabolites across the set, synthesising and characterising them, and building a liquid chromatography-tandem mass spectrometry method that also targets the sermorelin(3-29) amide metabolite — the product of exactly the dipeptidylpeptidase IV cleavage described above ^[9].

What Is Sermorelin Being Researched For?

Published research on sermorelin covers:

Diagnosis of growth hormone deficiency — the growth hormone response to a single intravenous administration as a provocative test ^[8].
Growth hormone deficiency of hypothalamic origin in children — repeated subcutaneous administration, with height velocity as the endpoint ^{[1, 5]}.
Idiopathic short stature — a 12-month treatment study ^[6].
Radiation-induced growth hormone deficiency — a multicentre study in children treated for brain tumours or leukaemia ^[7].
Pharmacokinetics and alternative routes of administration — intravenous and intranasal work in healthy men ^[4].
Analytical detection — anti-doping method development ^[9].

All of the clinical work above studied a pharmaceutical product under a protocol, mostly in children, in the late 1980s and 1990s. None of it is research into, or evidence about, research-grade material supplied for laboratory use.

Human Research on Sermorelin

Human clinical research

Results from pharmaceutical clinical trials describe the investigational material and populations used in those studies and should not be interpreted as establishing the effects of research-grade materials offered for laboratory use.

First sustained treatment study in growth hormone-deficient children

Population. 18 prepubertal children with growth hormone deficiency ^[1].

Endpoint and duration. Twice-daily subcutaneous administration of the 1-29 amide, with height velocity assessed over the first six months and continued follow-up to 18 months in responders ^[1].

Result. Height velocity rose in 12 of the 18 children, and 8 were judged to have shown a worthwhile response — an increase of more than 2 cm/year, with a range of 2.7 to 11.2 cm/year. Those 8 were followed for 6 to 18 months with the increase maintained. Among the 14 who had previously received human growth hormone, height velocity on growth hormone correlated with height velocity on the 1-29 amide; 4 of those decelerated on the fragment for reasons the authors could not explain. A pretreatment peak serum growth hormone above 30 mU/l on an intravenous test predicted a good response, though a lower peak did not preclude one ^[1].

Adverse events. Anti-GHRH antibodies developed in 14 patients; the authors reported no apparent adverse effect on growth or on growth hormone responses ^[1].

Limitations. 18 children, no control group, and an explicit conclusion that suitable administration regimens remained to be established.

Randomised comparison against growth hormone

Population. 43 prepubertal children aged 4.3 to 18.9 years (mean 10.4 ± 2.9) with growth hormone deficiency of hypothalamic origin ^[5].

Endpoint and duration. Random assignment to three regimens for six months: a lower amount of the 1-29 amide (30 µg/kg per day subcutaneously, divided three times daily; n = 15), a higher amount (60 µg/kg per day, divided three times daily; n = 12), or growth hormone at 0.1 IU/kg per day (n = 16). Assessment included anthropometry, bone age, intravenous and subcutaneous provocative tests, and IGF-1 ^[5].

Result. An increase in height velocity of 2 cm/year or more occurred in all but two children. Height velocity was lowest in the lower-amount group and comparable between the higher-amount and growth hormone groups. An increase in height standard deviation score for bone age occurred only in the growth hormone group. Growth hormone responses to intravenous testing showed a priming effect in the lower-amount group and a decrease in the growth hormone group ^[5].

Limitations. Six months, 43 children across three arms, and a divergence between the two endpoints: height velocity was comparable in two arms while height standard deviation score for bone age improved in only one.

Pharmacokinetics and route comparison in healthy men

Population. 30 healthy men aged 19 to 43 ^[4].

Endpoint and duration. Intravenous and intranasal administration, with peptide and growth hormone concentrations measured ^[4].

Result. The lowest intravenous amount tested, 0.25 µg/kg, elicited significant growth hormone release; maximal release, with mean peaks of about 90 mU/l, came at 1 to 2 µg/kg. The peptide was eliminated rapidly, but growth hormone remained elevated for about three hours. Nasal bioavailability was 3 to 5 per cent, and approximately 50 µg/kg intranasally was about as potent as 1 µg/kg intravenously. Repeated intranasal administration produced a sustained response with no suppression of overnight growth hormone secretion ^[4].

Limitations. A single-administration pharmacology study in healthy adult men, with a hormone concentration rather than any clinical measure as its endpoint.

Preclinical Research on Sermorelin

In vitro research

There is no substantial animal literature specific to sermorelin as such, and this page does not manufacture one. The 1-29 amide entered clinical study early, and the preclinical work that bears on it is the enzymology described in the Mechanism of Action section above: it is cleaved in plasma at the 2-3 bond by dipeptidylpeptidase IV, and additionally at the 12-13 position by a trypsin-like activity that does not act at that site on the native hormone ^[2].

The one modern in vitro dataset is metabolic and analytical. Nineteen major in vitro metabolites were identified across sermorelin, tesamorelin and the two CJC-1295 forms, synthesised as reference materials and used to develop detection methods with limits generally at or below 1 ng/ml ^[9].

Where an animal literature would normally sit on a page like this, there is instead a human literature that is older and larger than most compounds in this catalogue can claim. That is unusual, and it is a consequence of sermorelin having been a medicine rather than a research chemical.

Other Areas of Sermorelin Research

Human clinical research

Two smaller clinical programmes extended the work beyond classical growth hormone deficiency.

In idiopathic short stature, 18 short prepubertal children aged 4.3 to 11.0 years, 17 of them male, with height below the third centile and a normal peak growth hormone response to provocative testing, received 20 µg/kg twice daily subcutaneously for one year; one was withdrawn for non-compliance. Mean height velocity rose from 4.8 (SD 0.9) cm/year before treatment to 7.2 (SD 1.6) cm/year at twelve months (p = 0.001), with the children growing most slowly at baseline showing the larger change ^[6].

In radiation-induced growth hormone deficiency, a multicentre study enrolled nine children — six boys — who had received cranial or craniospinal irradiation for a brain tumour distant from the hypothalamic-pituitary axis or as prophylaxis against central nervous system leukaemia, all at least two years from radiotherapy and prepubertal at entry. They received 15 µg/kg twice daily subcutaneously for a year, after which all were switched to growth hormone and followed for a further year. Height velocity rose from 3.3 (SD 1.1) cm/year before treatment to 6.0 cm/year after the year of treatment ^[7].

The review that consolidated this literature reached a measured conclusion: the 1-29 amide was suitable as a provocative test alongside conventional tests, and limited data suggested once-daily subcutaneous administration at 30 µg/kg was effective in promoting growth in some prepubertal children with idiopathic growth hormone deficiency. It also recorded that increases in height velocity were smaller than in children receiving growth hormone at the comparable amount, that the effect on final adult height was undetermined, and that transient facial flushing and injection-site pain were the most common adverse events ^[8].

These were trials of a pharmaceutical product in children with diagnosed endocrine disease, conducted under clinical supervision.

Current Research Status

Regulatory status (United States): Formerly approved, no longer marketed. Sermorelin acetate was approved in the United States and sold as Geref; the product was subsequently withdrawn from commercial sale and there is no currently marketed sermorelin product in the United States. That approval attached to a specific pharmaceutical product and its labelled indications and says nothing about research-grade material.
Investigational status: No active clinical development programme has been identified. The published clinical literature dates chiefly from the late 1980s and the 1990s, when the compound was studied as a diagnostic agent for growth hormone deficiency and as an alternative to growth hormone in children with growth hormone deficiency of hypothalamic origin.
Highest research phase reached: Reached regulatory approval as a pharmaceutical product; that product is no longer marketed
Approved uses: None current. The former United States approval covered use as a diagnostic agent for growth hormone deficiency and treatment of idiopathic growth hormone deficiency in children with growth failure.
Approval is compound-specific: Yes

Status as of September 22, 2026. This block is rendered from maintained fields, not from prose, so it cannot go stale in one place and stay current in another.

Chemical & Molecular Characteristics

Sermorelin is a 29-residue peptide amide, and its chemistry is the least complicated in this family because it contains nothing that is not in the native hormone.

The sequence is the native one. YADAIFTNSYRKVLGQLSARKLLQDIMSR is recorded for sermorelin in the FDA/NCATS Global Substance Registration System under UNII 89243S03TE, and corresponds to residues 1 to 29 of human growth hormone-releasing hormone. Every residue is a standard L-amino acid.

The amide is the modification. The register carries one structural modification: a substitution at arginine 29 with L-argininamide, which is the register's way of recording the C-terminal amide. That amide is not cosmetic — the amidated fragment is the active form, and the 40-residue free-acid form of the native hormone is a separate substance.

The identifiers agree across registers. CAS registry number 86168-78-7 and PubChem compound identifier 16132413 both resolve to this substance, and the molecular formula C149H246N44O42S and molecular weight 3357.9 g/mol are consistent between those registers and the supplier catalog. The single sulphur atom in the formula is the methionine at position 27 — the residue that the CJC-1295 backbone replaces with leucine.

Analytical Specifications

Physical form: Lyophilized powder
Appearance: White to off-white lyophilized solid
Lot number: RP-2609-018
Tested purity: ≥99% by HPLC
Storage: −20 °C, protect from light, desiccate

Analytical figures are lot-specific. Fields the catalog does not carry for the current lot are omitted rather than filled with a typical value. The certificate of analysis and the safety data sheet for the exact lot supplied are provided with a laboratory order; no purity figure on this page is a substitute for that document.

Frequently Asked Questions

What is sermorelin?

Sermorelin is the first 29 amino acids of human growth hormone-releasing hormone, synthesised with a C-terminal amide. It is described in the review literature as the shortest synthetic peptide with the full biological activity of the parent hormone ^[8]. It is a laboratory reagent here; as a pharmaceutical product it was approved in the United States and is no longer marketed.

How does sermorelin work?

It binds the growth hormone-releasing hormone receptor on anterior pituitary somatotrophs — a class B1 G protein-coupled receptor cloned from human pituitary in 1993 and shown to signal through Gs and cyclic AMP ^[3] — and stimulates growth hormone secretion ^[8].

Is sermorelin FDA approved?

Not currently. Sermorelin acetate held a United States approval and was sold as Geref; that product was withdrawn from commercial sale and no sermorelin product is marketed in the United States today. A regulatory approval attaches to a specific pharmaceutical product and its labelled indications, not to a molecule in the abstract, and it never extends to research-grade material.

What was sermorelin studied for?

Two things. As a diagnostic agent, the growth hormone response to an intravenous administration of 1 µg/kg was evaluated as a provocative test for growth hormone deficiency ^[8]. As a therapy, it was given by subcutaneous injection to children with growth hormone deficiency of hypothalamic origin and to children with idiopathic short stature, with height velocity as the measured endpoint ^{[1, 5, 6]}.

How long does sermorelin last in plasma?

It is eliminated rapidly, but the hormonal response outlasts the peptide. In 30 healthy men aged 19 to 43, growth hormone concentrations remained elevated for about three hours after intravenous injection despite rapid elimination of the peptide itself ^[4]. The native hormone is cleaved at the 2-3 amino acid bond by dipeptidylpeptidase IV, and the 1-29 amide is cleaved at the same site ^[2].

How does sermorelin differ from CJC-1295?

Sermorelin is the unmodified fragment. CJC-1295 no DAC is the same 29-residue length with four substitutions; CJC-1295 DAC adds a thirtieth residue carrying an albumin-binding group. The substitutions and the conjugation both address the enzymatic clearance that limits the unmodified fragment ^[2]. Sermorelin is also the only one of the three that reached a regulatory approval.

How does sermorelin differ from tesamorelin?

By length and by an added group. Tesamorelin is the full 44-residue growth hormone-releasing hormone sequence with a hexenoyl group on the N-terminal tyrosine; sermorelin is the unmodified first 29 residues. Both act at the same receptor. Tesamorelin has a currently approved product in a defined indication; sermorelin does not.

Why is sermorelin no longer marketed?

The commercial withdrawal is a matter of regulatory record rather than of published science, and no peer-reviewed source states a reason, so none is asserted here. What the literature does show is that the clinical programme was small and dated: the trials that supported it were conducted in the late 1980s and 1990s, and growth hormone itself produced larger increases in height velocity than sermorelin at the amounts compared ^[8].

Scientific References

Ross RJ, Rodda C, Tsagarakis S, et al.. Treatment of growth-hormone deficiency with growth-hormone-releasing hormone Lancet (London, England); 1987. PMID 2879138 doi:10.1016/s0140-6736(87)90699-4
Frohman LA, Downs TR, Heimer EP, et al.. Dipeptidylpeptidase IV and trypsin-like enzymatic degradation of human growth hormone-releasing hormone in plasma The Journal of clinical investigation; 1989. PMID 2565342 doi:10.1172/JCI114049
Gaylinn BD, Harrison JK, Zysk JR, et al.. Molecular cloning and expression of a human anterior pituitary receptor for growth hormone-releasing hormone Molecular endocrinology (Baltimore, Md.); 1993. PMID 7680413 doi:10.1210/mend.7.1.7680413
Wilton P, Chardet Y, Danielson K, et al.. Pharmacokinetics of growth hormone-releasing hormone(1-29)-NH2 and stimulation of growth hormone secretion in healthy subjects after intravenous or intranasal administration Acta paediatrica (Oslo, Norway : 1992). Supplement; 1993. PMID 8329825 doi:10.1111/j.1651-2227.1993.tb12827.x
Neyzi O, Yordam N, Ocal G, et al.. Growth response to growth hormone-releasing hormone(1-29)-NH2 compared with growth hormone Acta paediatrica (Oslo, Norway : 1992). Supplement; 1993. PMID 8329826 doi:10.1111/j.1651-2227.1993.tb12828.x
Kirk JM, Trainer PJ, Majrowski WH, et al.. Treatment with GHRH(1-29)NH2 in children with idiopathic short stature induces a sustained increase in growth velocity Clinical endocrinology; 1994. PMID 7955460 doi:10.1111/j.1365-2265.1994.tb02580.x
Ogilvy-Stuart AL, Stirling HF, Kelnar CJ, et al.. Treatment of radiation-induced growth hormone deficiency with growth hormone-releasing hormone Clinical endocrinology; 1997. PMID 9231053 doi:10.1046/j.1365-2265.1997.1790998.x
Prakash A, Goa KL. Sermorelin: a review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy; 1999. PMID 18031173
Memdouh S, Gavrilović I, Ng K, et al.. Advances in the detection of growth hormone releasing hormone synthetic analogs Drug testing and analysis; 2021. PMID 34665524 doi:10.1002/dta.3183

Every identifier above is resolved against PubMed, Crossref or ClinicalTrials.gov at build time, and the title returned by the register is compared with the title stored here. A page does not publish if a reference fails to resolve.

Research-Use Information

For in vitro research use only. This material is a laboratory reagent. It is not a drug, food, dietary supplement, or cosmetic and is not for human or veterinary use, including ingestion, injection, or any other administration. No information on this page describes or implies any effect in humans or animals. Sold only to researchers under our Terms of Sale.