What is Sermorelin sold for here?

This product is sold exclusively as a laboratory research chemical, not as a medicinal product, and is not intended for use in humans or animals. In the European Union, Sermorelin does not hold marketing authorization as a medicinal product.

What exactly is Sermorelin?

Sermorelin is GHRH(1-29)-NH₂, the amino-terminal 29-amino-acid fragment of human growth hormone releasing hormone (GHRH), which carries the full receptor-activating activity of the native 44-amino-acid hormone. It is a linear peptide with C-terminal amidation and a molecular mass around 3358 Da.

How are Sermorelin's identity and purity confirmed?

Identity is verified by mass spectrometry, including confirmation of C-terminal amidation, together with an HPLC purity result on the batch certificate. The report comes from Janoshik and is submitted by the manufacturer; current batch values are on our CoA page.

How does Sermorelin differ from Tesamorelin?

Sermorelin is unmodified GHRH(1-29) with a short half-life in the range of minutes. Tesamorelin is a GHRH(1-44) analog stabilized with a trans-3-hexenoyl group, protected against breakdown by dipeptidyl peptidase-4, and backed by an extensive clinical trial program. Both are research chemicals; Sermorelin does not hold marketing authorization as a medicinal product in the EU.

How does Sermorelin differ from CJC-1295?

CJC-1295 combines a multiply substituted GHRH(1-29) backbone (Mod GRF(1-29)) with a drug affinity complex (DAC): a maleimidopropionamide group attached to an extra C-terminal lysine, which binds covalently to cysteine-34 of serum albumin and extends the duration of action. The variant without DAC ("CJC-1295 no-DAC," i.e., Mod GRF(1-29)) does not have this extension. Sermorelin carries none of these modifications and acts through brief, pulsatile stimulation of the GHRH receptor.

What did the Khorram 1997 study show?

Khorram et al. (JCEM 1997, PMID 9141536) conducted a single-blind study in 19 healthy older adults (55-71 years); the study used the closely related analog [Nle27]GHRH(1-29)-NH₂, 10 µg/kg subcutaneously each evening for 16 weeks (after a 4-week saline baseline). Reported outcomes included a significant IGF-1 increase, increased nocturnal GH output (predominantly through the injection-induced peak; spontaneous pulsatility remained unchanged), and, in the male subgroup, higher lean mass and insulin sensitivity. The sample is small at n=19 and has not been replicated at modern scale.

Are there large controlled human studies in adults?

The controlled adult evidence is limited, but Khorram 1997 (n=19, [Nle27] analog) is not the only study. A randomized, double-blind study in HIV patients with lipodystrophy used GHRH(1-29)/GEREF (Koutkia et al., JAMA 2004, n=31, 1 mg subcutaneously twice daily for 12 weeks) and reported an IGF-1 increase, a significant decrease in trunk fat, and an improved visceral-to-subcutaneous fat ratio. Beyond that, the published evidence consists mainly of observational series and pharmacological studies; pediatric stimulation-test data concern a different population. Large, modern adequately powered randomized trials are lacking; claims in this area should be weighed accordingly.

What doses have been used in research?

In controlled studies, the [Nle27]GHRH(1-29) analog was administered at 10 µg/kg subcutaneously in the evening (Khorram 1997), and GHRH(1-29)/GEREF at 1 mg subcutaneously twice daily in HIV lipodystrophy (Koutkia et al., JAMA 2004). These are reported study doses, not recommendations. Non-validated community reports mention figures around 100-300 µg per application; these figures are self-reported, not collected under controlled conditions, and do not constitute a recommendation. There is no treatment regimen approved in the EU for human use.

What side effects have been reported in research?

In the controlled study (Khorram 1997, the [Nle27]GHRH(1-29) analog, n=19), the only reported side effect was transient hyperlipidemia, which resolved by the end of the study. The controlled adult data set is small, and no large long-term human safety data exist; any statement about tolerability should be treated as preliminary.

How is Sermorelin stored?

The lyophilized powder is stored at -20 °C. After reconstitution, it is stored refrigerated at 2-8 °C and protected from light. Without a batch-specific stability study, no fixed shelf life after reconstitution can be guaranteed; lab practice follows general discard conventions, and for protocols lasting longer than a week, aliquoting is recommended.

What is Sermorelin reconstituted with?

Bacteriostatic water is commonly used in lab practice. Let the liquid run slowly down the vial wall and swirl gently, do not shake. This does not establish validated compatibility or stability with Sermorelin; the specific protocol should specify a suitable, validated solvent.

Is it legal to buy Sermorelin for research in the EU?

There is no single EU-wide category for research peptides; the legal situation depends on presentation, intended use, and the national law of the relevant member state. We sell exclusively for laboratory research and not for human consumption. Check the rules with your national competent authority and your institution, seek qualified legal advice if needed, and treat this as general information, not legal advice.

How quickly is Sermorelin delivered?

Shipping is from the EU with tracking, typically within 2-3 business days within the EU. Current delivery times, countries, and conditions are on our shipping page.

Buy Sermorelin: What Researchers Need to Know About the GHRH(1-29) Analog

Q: Why was GEREF withdrawn from the market?

From 1990, Sermorelin held US approval under the brand name GEREF, mainly for pediatric growth hormone stimulation testing and pediatric growth hormone deficiency. The manufacturer withdrew the product from the US market in 2008; the FDA stated that the market withdrawal was not for reasons of safety or efficacy.

Sermorelin is one of the earliest synthetic analogs of growth hormone releasing hormone (GHRH). Long before Tesamorelin, CJC-1295, or modern ghrelin mimetics existed, Sermorelin (GHRH(1-29)) served as a reference tool for studying the somatotropic axis. It carried FDA approval in the early 1990s, was withdrawn from the US market in 2008, and has since remained a compounded research peptide of ongoing academic interest. This long history matters for researchers: the mechanism is well described, but the controlled human evidence in adults remains narrow.

Sermorelingrowth

GHRH(1-29) analog for physiological growth hormone stimulation research

Background: GHRH(1-29) and the History of GEREF

Human growth hormone releasing hormone is a 44-amino-acid peptide from the hypothalamus. The first 29 residues carry the entire biological activity of the native molecule. Sermorelin is simply GHRH(1-29)-NH₂, synthesized as the acetate salt, and reproduces the receptor-binding pharmacophore of the native hormone without any stabilizing modification.

This makes Sermorelin the structural starting point for the entire GHRH analog class. CJC-1295 adds a drug affinity complex for albumin binding, and Tesamorelin adds a trans-3-hexenoyl cap to prevent cleavage by dipeptidyl peptidase-4. Sermorelin carries none of these modifications. Its plasma half-life is in the range of minutes, and it acts through brief, pulsatile stimulation of the GHRH receptor on somatotropic cells of the pituitary.

Sermorelin received US Food and Drug Administration approval in 1990 under the brand name GEREF (EMD Serono), initially for pediatric growth hormone stimulation testing and later for the treatment of pediatric growth hormone deficiency. The product was withdrawn from the US market in 2008. The FDA stated that the market withdrawal was not for reasons of safety or efficacy. Sermorelin subsequently moved into the compounding pharmacy space and the research peptide market, where it remains available today.

What the Research Shows

Khorram 1997: The Central Adult Human Study

A widely cited study of GHRH(1-29) in older adults comes from Khorram and colleagues, published in the Journal of Clinical Endocrinology and Metabolism (Khorram O et al., JCEM 1997, PMID 9141536). It was a single-blind, sequential study (saline baseline, then active drug) with the closely related analog [Nle27]GHRH(1-29)-NH₂ (not Sermorelin itself); it therefore provides class evidence in the adult indication area.

Design: Single-blind study in 19 healthy older adults (10 women, 9 men, 55-71 years). Four weeks of evening saline injection (placebo baseline) were followed by 16 weeks with the analog [Nle27]GHRH(1-29)-NH₂, 10 µg/kg subcutaneously each evening.

Key findings: The analog increased nocturnal GH output (AUC), predominantly through the GH peak triggered by the evening injection; spontaneous GH pulse frequency and amplitude did not change. Serum IGF-1 rose significantly compared with the placebo phase. Skin thickness, measured by Harpenden caliper, increased. In the male subgroup, lean body mass (DXA) and insulin sensitivity (measured by intravenous glucose tolerance test, FSIGT) increased. The only adverse effect reported was transient hyperlipidemia, which resolved by the end of the study.

The important honest caveat is the sample size. Nineteen participants is small by today's standards, an adequately powered replication has not followed, and the substance tested was an analog, not Sermorelin itself. The study is still cited because it is one of the few controlled aging studies with a short GHRH(1-29) analog.

Khorram 1997 JCEM - The Reference Dataset

Design: Single-blind study, n=19 (10 women, 9 men), age 55-71. Intervention: 4 weeks saline baseline, then 16 weeks [Nle27]GHRH(1-29) analog, 10 µg/kg subcutaneously every night. Results: IGF-1 significantly increased, nocturnal GH output (AUC) increased, predominantly through the injection-induced peak (spontaneous pulsatility unchanged), skin thickness measured by Harpenden caliper increased, lean body mass and insulin sensitivity (measured by FSIGT) improved in the male subgroup. Caveat: Small sample, no modern replication, and the substance was the [Nle27] analog, not Sermorelin itself.

Mechanism: Feedback-Regulated Pulsatile Release

The mechanistic argument for GHRH(1-29), as discussed in the review literature (including Walker, Clin Interv Aging 2006, PMC2699646, a review/commentary; Prakash & Goa, BioDrugs 1999, PMID 18031173, a predominantly pediatric review), rests on a distinction from exogenous recombinant GH administration. Direct rhGH use can produce a sustained, supraphysiological GH elevation. It acts downstream of hypothalamic-pituitary control and does not require involvement of the pituitary somatotropes; the downstream GH/IGF-1 feedback loop remains active.

Sermorelin acts upstream. It binds the GHRH receptor on somatotropic cells and stimulates endogenous GH release. Because pituitary somatostatin tone remains intact, the resulting GH output remains subject to negative feedback from IGF-1 and somatostatin. Several consequences follow from this:

Pulsatile, not continuous, GH elevation. Endogenous release remains episodic.
No pronounced tachyphylaxis was reported in the early literature within the dose ranges studied.
An IGF-1 rise that, depending on dose, may stay within or near the physiological range, in contrast to the supraphysiological levels that can occur with rhGH administration.
A mechanistically potentially more favorable side-effect profile, since the GH rise remains subject to negative feedback; however, the controlled data available for a direct comparison with rhGH cohorts is limited.

This mechanistic profile is why Sermorelin remained of research interest even after its market withdrawal. GHRH receptor stimulation preserves elements of endogenous feedback but does not guarantee physiological GH or IGF-1 levels.

Recent Review Articles

Two more recent reviews situate GHRH analogs within the modern GH-axis literature. Fernández-Garza (Frontiers in Aging 2025, PMID 40260058) surveys the somatotropic axis in older adults, the associated changes in body composition and metabolism, and the evidence for GHRH-based interventions. Ishida and colleagues (JCSM Rapid Communications 2020) review the growth hormone secretagogue class as a whole and place GHRH analogs within its development.

Alongside Khorram 1997 (the [Nle27] analog), the controlled adult evidence includes a randomized GEREF study in HIV lipodystrophy (Koutkia et al., JAMA 2004, n=31) and shorter pharmacological studies with GHRH(1-29) (e.g., Corpas et al., 1992, n=10). Beyond that, the literature consists mainly of observational series. A large-scale, modern adequately powered randomized trial does not exist. Researchers should read claims in this area with this evidence limitation in mind.

Sermorelin in Context: The Two GHRH Analogs in Our Range

Within the GHRH analog class, PeptidesDirect carries two substances, and they occupy different research roles.

Sermorelin is unmodified GHRH(1-29). It has a simple, unmodified profile: short half-life, pulsatile GHRH stimulation, feedback regulation still in place. The controlled adult evidence includes Khorram 1997 (n=19, the [Nle27] analog) and the randomized GEREF study by Koutkia et al. (JAMA 2004, n=31), along with shorter pharmacological studies.

Tesamorelin is a hexenoyl-stabilized GHRH(1-44) analog with FDA approval for HIV-associated lipodystrophy. Its pivotal phase 3 program (Falutz et al., NEJM 2007) led to FDA approval; a later pooled randomized analysis (Falutz et al., JCEM 2010, PMID 20554713) included 806 patients. Smaller exploratory studies examined additional endpoints (including Stanley, Lancet HIV 2019, liver fat; Baker, Arch Neurol 2012; and Ellis, 2025, a phase 2 study with n=73, cognitive endpoints). Among the GHRH analogs, it has the most extensive clinical trial program.

The two are complementary, not interchangeable. Sermorelin is the structural baseline with unmodified pulsatile kinetics, while Tesamorelin is the more extensively studied, longer-acting analog. Head-to-head research protocols are rare in the published literature.

Quality Criteria for Purchase

Sermorelin is a 29-residue linear peptide with C-terminal amidation. The synthesis is chemically well understood, but deletion sequences, aspartimide formation, and oxidation of Met27 remain the main byproduct risks. C-terminal amidation is part of Sermorelin's identity and affects potency and stability.

Purity Testing

Research-grade Sermorelin should show high HPLC purity; the purity value for each batch appears on the Certificate of Analysis (see the CoA page). At PeptidesDirect, a lab report from Janoshik Analytical is available for every batch (submitted by the manufacturer). A Certificate of Analysis like this typically documents HPLC purity, mass spectrometry confirming molecular mass (around 3358 Da for GHRH(1-29)-NH₂), and peptide content; residual solvent and counterion are sometimes listed as well. C-terminal amidation can be confirmed by MS. A report of this kind, focused on identity and purity, does not include sterility, endotoxin, or microbiological testing.

Storage

Sermorelin is supplied as a lyophilized powder. Store at -20 °C before reconstitution; in lyophilized form, the peptide is stable under these conditions. After reconstitution, store refrigerated at 2-8 °C and protected from light; without a batch-specific stability study, no fixed shelf life can be guaranteed, and lab practice follows general discard conventions. Unlike hexenoyl-stabilized Tesamorelin, unmodified Sermorelin has no additional protection against enzymatic breakdown in plasma; validated stability data for the refrigerated solution are not available. For longer protocols, divide the solution into single-use aliquots to reduce repeated opening and temperature fluctuations.

EU shipping: For European researchers, PeptidesDirect ships from within the EU. For deliveries within the EU there is no customs and no import fees, with delivery in two to three business days with tracking.

Reconstitution

Use Bacteriostatic Water

Bacteriostatic water (0.9% benzyl alcohol) is commonly used in lab practice as a reconstitution agent. This does not establish validated compatibility or stability with Sermorelin; the specific protocol should specify a suitable, validated solvent. Without a batch-specific stability study, no fixed shelf life can be guaranteed.

Add Slowly Down the Vial Wall

Let the solvent run slowly down the inside wall of the vial. Do not inject it directly onto the lyophilized cake, to avoid mechanical stress on the peptide.

Swirl Gently, Do Not Shake

Rotate the vial slowly until the powder has fully dissolved. The solution should be clear and colorless. Vigorous shaking can cause foaming; gentle swirling is preferred.

Store Cold and Protected From Light

Store the reconstituted vial at 2-8 °C in a dark container or the original packaging. For longer protocols, divide into single-use aliquots to reduce repeated opening and temperature fluctuations.

Regulatory Context

Sermorelin (GEREF) received US Food and Drug Administration approval in 1990, with a clinical indication focused on pediatric GH stimulation testing and pediatric growth hormone deficiency. The manufacturer withdrew the product from the US market in 2008. The FDA stated that the market withdrawal was not for reasons of safety or efficacy. After 2008, Sermorelin moved into the compounding pharmacy space in the US and into the research peptide supply chain worldwide.

Sermorelin is prohibited in sport at all times, both in and out of competition, under WADA S2 (peptide hormones, growth factors, and related substances), together with the entire GHRH analog class.

In the European Union, Sermorelin is not currently approved as a medicinal product. It is supplied exclusively as a reference substance for in vitro and preclinical research. It is not a drug, is not for human consumption, and is not intended for diagnostic or therapeutic use.

An Honest Assessment of the Evidence Base

Sermorelin occupies an unusual scientific position. The mechanistic argument for GHRH(1-29) as a physiological secretagogue is strong and widely cited. The FDA history documents a peptide that passed regulatory review more than three decades ago. And yet the controlled adult evidence remains limited: it rests mainly on Khorram 1997 (n=19, the [Nle27]GHRH(1-29) analog, thus class evidence rather than direct Sermorelin evidence) and a small HIV lipodystrophy study with GHRH(1-29)/GEREF (Koutkia et al., JAMA 2004, n=31). The remaining literature is dominated by observational series, pediatric stimulation-test data (the original GEREF indication), and review articles that revisit the original findings.

That is not a reason to ignore Sermorelin. It is a reason to read it correctly: as a structural and historical reference peptide of the GHRH analog class, with a well-described mechanism, a solid pharmacological track record, and a narrow controlled adult dataset that includes both class evidence from the [Nle27] analog (Khorram 1997, single-blind, sequential) and direct GEREF evidence (Koutkia 2004, randomized, double-blind, placebo-controlled). Researchers designing protocols should weigh the Khorram 1997 evidence (n=19) for what it actually is, not for what the subsequent popular literature has occasionally extrapolated it into.

Among the GHRH analogs available today, Sermorelin is an unmodified mechanistic probe: the original GHRH(1-29) pharmacophore, without half-life extensions or receptor-affinity modifications. This status, together with its long research history, keeps it relevant for research programs studying the somatotropic axis in aging.