Sermorelin: Complete Guide to the GHRH(1-29) Peptide

Minutes. Native GHRH is inactivated in plasma when dipeptidylpeptidase IV (DPP-IV) removes its first two amino acids; the resulting GHRH(3-44) retains less than a thousandth of the biological activity. After intravenous injection in healthy people, intact GHRH(1-44) had a half-life of 6.8 minutes. The shortened 1-29 amide is cut at the same bond, and it is also open to trypsin-like cleavage further along the chain.^[4][5]

Human measurements of sermorelin itself agree. During constant intravenous infusion in ten healthy men, GHRH(1-29)-NH2 had a disappearance half-time of 4.3 minutes. In 30 healthy men it was eliminated rapidly after an intravenous injection, yet GH stayed elevated for about three hours, and its bioavailability through the nasal mucosa was only 3-5%. Its DPP-IV product, GHRH(3-29), has been detected in human plasma after a subcutaneous dose.^[6][7][3]

The short plasma life is the design problem that later analogues set out to solve. A D-alanine at position 2 lengthened the half-time only modestly, to 6.7 minutes; CJC-1295 stacked four substitutions onto the same 29-residue chain, and tesamorelin kept the full 44-residue chain with an N-terminal hexenoyl group. The family is compared side by side in a separate article.^[6][3]

Sermorelin's strongest clinical data come from children with growth-hormone deficiency. In an open-label multicentre study, 110 previously untreated prepubertal GH-deficient children received sermorelin once daily at bedtime for up to a year, and 86 were eligible for the efficacy analysis. Mean height velocity rose from 4.1 cm per year at baseline to 8.0 cm per year at six months and 7.2 cm per year at twelve months, 74% were rated good responders at six months, bone age did not advance faster than height age, and no adverse changes in chemistry, glucose or IGF-1 were seen.^[9]

The comparison with growth hormone itself is less flattering. In a randomised study of 60 children with GH deficiency of hypothalamic origin, six months of continuous GHRH(1-29)-NH2 at either of two doses produced mean height velocities of 9.2 and 9.3 cm per year, against 14.6 cm per year with GH. IGF-1 rose at first and then fell back, and 39 of the 40 children given GHRH developed antibodies to it, which had almost disappeared nine months after treatment stopped.^[10]

A 1999 drug review summarised the position: limited data showed once-daily sermorelin was effective in some prepubertal children with idiopathic GH deficiency, the sermorelin regimens compared directly with once-daily somatropin gave smaller gains in height velocity, and its effect on final adult height had not been determined.^[8]

Because it acts directly on the pituitary, a single intravenous dose of sermorelin became a rapid and relatively specific test of the gland's capacity to release GH. Fewer children without GH deficiency gave false-positive results with sermorelin than with other provocative tests, and in adults the combination of sermorelin with arginine was considered more specific still.^[8]

The test had a built-in blind spot. A normal GH response to sermorelin shows that the pituitary works, so it cannot exclude GH deficiency caused by a problem higher up, in the hypothalamus; other stimulation tests were needed to confirm that diagnosis.^[8]

The arginine-plus-GHRH test disappeared with the product. An FDA medical review from 2017 records that Geref (sermorelin acetate) was withdrawn from the US market in 2008 because of a business decision by the manufacturer, as the active ingredient used to produce the diagnostic was no longer being made. The same review describes Geref as an amidated synthetic peptide corresponding to the first 29 amino acids of the 44-amino-acid GHRH.^[15]

It raises GH in older adults; whether that turns into anything more is unproven. In a study of ten healthy older men who took two dose levels in random order, 14 days of twice-daily GHRH(1-29) at the higher dose raised 24-hour GH and IGF-1 to the levels of nine young men, without changing fasting glucose or blood pressure.^[11]

A single nightly dose did less. Eleven healthy men aged 64 to 76, with low baseline IGF-1, self-administered GHRH(1-29) each night for six weeks in an uncontrolled study. Nocturnal GH release and peak amplitude increased, but IGF-1, IGFBP-3, weight, DEXA measures of muscle and fat, glucose and lipids did not change. Two of six strength measures and one endurance test improved, and the authors concluded that single nightly doses are less effective than multiple daily doses.^[12]

A close analogue, [Nle27]GHRH(1-29)-NH2, given nightly for 16 weeks after a placebo run-in to 19 men and women aged 55 to 71, raised nocturnal GH and IGF-1 within two weeks, but IGF-1 drifted back toward baseline by week 16. A retrospective chart review of 14 men prescribed sermorelin together with GHRP-2 and GHRP-6 reported higher IGF-1, but it had no control group and cannot isolate sermorelin's effect.^[13][14]

In the clinical programme, single intravenous doses and repeated once-daily subcutaneous doses were well tolerated. Transient facial flushing and pain at the injection site were the most commonly reported adverse events. In the one-year paediatric study, no adverse changes appeared in general biochemistry or hormone panels, fasting glucose did not change, and IGF-1 was not generated in excess.^[8][9]

Immunogenicity is the signal most often missed. In the randomised six-month comparison with growth hormone, 39 of the 40 children receiving continuous GHRH(1-29)-NH2 developed antibodies to it. The antibodies did not correlate with the change in height and had almost disappeared nine months after treatment stopped, but they show that the body can recognise this peptide as foreign.^[10]

The safety record has clear limits. It comes from GH-deficient children and from small adult studies lasting days to weeks. There are no long-term safety data in healthy adults, and a 2026 endocrine review describes the human evidence for sermorelin outside its original indications as limited and largely indirect.^[12][16]

Not any more in the United States. Sermorelin acetate was FDA-approved and marketed as Geref for the evaluation and treatment of GH deficiency in children. According to an FDA medical review, the manufacturer told the agency in July and December 2008 that it was discontinuing production, and the approvals of the two new drug applications containing Geref were withdrawn in June 2009.^[16][15]

In the European Union, a search of the EMA medicines database on 22 September 2026 returned no entry for sermorelin, so there is no centrally authorised sermorelin medicine and no European public assessment report.^[17]

In sport, the WADA 2026 Prohibited List names sermorelin alongside CJC-1293, CJC-1295 and tesamorelin as a GHRH analogue under S2.2.4, growth hormone releasing factors. Substances in class S2 are prohibited at all times, in and out of competition.^[18]

Peptyds supplies sermorelin as a lyophilised research peptide with a batch certificate of analysis, for in-vitro laboratory research only. We do not present it as an anti-ageing therapy, a growth-hormone replacement or a body-composition product.

The evidence is worth knowing precisely because it is unusual for this field: a molecule with a real regulatory history, randomised and open-label trials in GH-deficient children, a validated diagnostic role, and a handful of small adult studies. It is also plainly bounded: the paediatric trials used a clinical population, the adult studies were small and short, and no controlled trial in healthy adults has shown a durable benefit.^{[9][10][12][16]}

Tesamorelin, the GHRH analogue with the most extensive modern trial record, has its own complete guide, and CJC-1295, the substituted 29-residue analogue usually paired with ipamorelin, is covered in the CJC-1295 + ipamorelin guide.^[3][16]