Everything below reports findings from cell cultures, isolated tissue and animals. This material is for research use only, not for human or veterinary use.
Growth hormone-releasing hormone runs to 44 residues. The first 29 carry the activity. Sermorelin is those 29 with an amide on the end.
Measured disappearance half-time came out at 4.3 minutes [1]. Almost everything that has happened to this molecule since follows from that number.
Indexed papers in people exist. Those human endpoints sit outside this profile. The parked half-life stays, because it is identity chemistry for the unmodified fragment.
Chemical identity
Twenty-nine residues, and the numbering in the name is the useful part.
| Property | Value |
|---|---|
| Common names | Sermorelin, GHRH(1-29)-NH2, GRF(1-29) amide |
| Molecular formula | C149H246N44O42S |
| Molecular weight | 3357.9 |
| CAS | 86168-78-7 |
| PubChem CID | 16132413 |
| InChIKey | WGWPRVFKDLAUQJ-MITYVQBRSA-N |
| Parent hormone | GHRH, 44 residues |
| Sulfur atoms | 1, from the single methionine |
The C-terminal amide is part of the compound
Papers write it as GHRH(1-29)-NH2 rather than GHRH(1-29) because the amide is there deliberately. A free acid at position 29 is a different molecule.
That matters for reading a certificate. It is also the first of several places in this article where a name and a molecule drift apart.
Sermorelin is unmodified. Position 2 stays L-alanine. No albumin-binding handle sits on the chain. No N-terminal acyl cap sits on tyrosine. Those three absences are the identity claim.
Reading the fragment
The 1-29 stretch is the receptor-binding region of native GHRH. Residues 30 to 44 of the parent hormone are discarded. Shorter fragments lose activity. The full-length parent is a different molecule again.
A certificate naming “GHRH” without a residue range has not specified which compound it describes. Papers written before the generic name existed call it GRF(1-29) amide or hGRF(1-29). Those are this compound under older naming rather than analogues [5][8].
One methionine sits in the sequence. Oxidation adds 16 daltons, so 3373.9 is the mass to watch alongside 3357.9.
What the four-minute number came from
A study comparing sermorelin against a modified analogue measured both directly [1].
| Compound | Metabolic clearance rate | Disappearance half-time |
|---|---|---|
| GHRH(1-29)-NH2 | 39.7 ± 3.9 mL/kg/min | 4.3 ± 1.4 min |
| D-Ala2 analogue | 21 ± 1.2 mL/kg/min | 6.7 ± 0.5 min |
The substitution sits at position 2. Swapping in a D-amino acid there roughly halved the clearance rate. The authors concluded that the substitution enhances biological activity by reducing metabolic clearance rather than by binding the receptor better.
Why position 2
An L-alanine at position 2 is the point of attack for the enzyme that clips this class of peptide. Putting a D-amino acid there blocks it. That is a general trick rather than a sermorelin-specific one.
The result was still measured in minutes. Doubling four minutes gets you eight, which is why the field kept going.
Sermorelin itself keeps the L-alanine. The D-Ala2 analogue is a different reagent with the same mass. Chiral analysis, not intact mass, tells them apart.
The successor molecules are chemistry, not formulations
A medicinal chemistry programme has run on this scaffold since the mid-1980s. Reading its sequence tells you what the parent compound’s problem was.
Super-active analogues of GRF(1-29) amide appeared in 1984 [5]. Analogues containing reduced peptide bonds followed [6]. The D-Ala2 substitution halved metabolic clearance [1]. Further analogues with high and prolonged activity were reported in 1998 [7].
CJC-1295 is a sermorelin derivative, documented as such
The most consequential entry is an albumin bioconjugate programme. Investigators built conjugates of hGRF(1-29) designed to attach to circulating albumin, and the best compound was named CJC-1295 [8].
That paper describes CJC-1295 as a tetrasubstituted form of hGRF(1-29), carrying an added maleimidopropionamide derivative of lysine at the C terminus. It produced a fourfold increase in growth hormone area under the curve over two hours against hGRF(1-29) in rats. It also remained detectable in plasma beyond 72 hours. A western blot showed the compound riding on the serum albumin band within 15 minutes.
Four minutes to beyond 72 hours. That is the size of the problem the field was solving. It is also why CJC-1295 exists as a separate reagent rather than a formulation of this one.
The related write-up sits at CJC-1295.
Sermorelin versus tesamorelin as chemistry
This is the sharpest case of a name and a molecule drifting apart.
Tesamorelin is human GHRH residues 1 to 44, amidated, with a trans-3-hexenoyl group on the N-terminal tyrosine. Baker and colleagues call it a stabilised analogue of human GHRH [10]. One acyl cap is the entire structural difference from the native 1-44 hormone.
Sermorelin is the 1-29 fragment with no cap and no substitutions. The two molecules differ in length, mass and the chemistry used to slow DPP-IV.
| Analogue | Length | Stabilising change | Approximate mass |
|---|---|---|---|
| Native GHRH(1-44) amide | 44 | None | About 5,040 Da |
| Tesamorelin | 44 | trans-3-hexenoyl on Tyr1 | About 5,136 Da |
| Sermorelin | 29 | None | 3357.9 Da |
| CJC-1295 without DAC | 29 | Residue substitutions | About 3,368 Da |
| CJC-1295 with DAC | 30 plus maleimide | Albumin handle | 3647.2 Da |
Mass still decides the vial. A methods section that names Sermorelin and then quotes 5136 Da has named tesamorelin. The reverse error is just as cheap to catch.
Indexed papers that used tesamorelin exist [9][10]. Human endpoints from those papers sit outside this profile. Cite them to find the record. Do not cite them as Sermorelin results.
The tesamorelin write-up sits at tesamorelin.
Indexed papers and what they do not decide
Most numbers in the reference list point at human programmes.
What the citations are for
Wilton and colleagues published a pharmacokinetic paper [2]. Thorner and colleagues published a paediatric programme paper [3]. Prakash and Goa published a diagnosis-and-treatment review [4]. Grunt and colleagues published a long-term fragment paper [13]. Ross and colleagues published an early GHRH paper [14].
Baker and colleagues published a cognition paper [9]. Friedman and colleagues named tesamorelin as the analogue in that programme [10]. Davis and colleagues asked about desensitisation during infusion [11]. Achermann and colleagues ran a peptide-clamp paper [12].
Use those papers to find the record. Do not use this page as a use document.
What this profile will not do
It will not quote human microgram-per-kilogram ladders, paediatric height-velocity figures, or tesamorelin milligram-per-day tables. Those sentences turn a research article into a use document. The papers remain cited so a reader can find them.
A development programme does not turn GHRH(1-29)-NH2 into a laboratory dosing recipe. Identity, fragment chemistry and analogue differences remain the useful questions.
What being a releasing hormone rather than a hormone implies
Sermorelin does not do anything to tissue. It asks the pituitary to release growth hormone. Everything downstream depends on the pituitary agreeing.
The pituitary sets a ceiling
Exogenous growth hormone arrives ready-made. A releasing hormone can only mobilise what the somatotrophs hold and are willing to release. That upper bound is a property of the preparation rather than of the label on the vial.
A GHRHR-expressing cell line can report cAMP. It cannot report a closed-loop axis. Name the system.
Rat anterior pituitary cells were the original bioassay for the albumin conjugates [8]. That system has somatotrophs. A transfected cell line that only reports cAMP has the receptor and not the secretory machinery. Both assays are valid. They are not interchangeable.
Sermorelin needs a functioning somatotroph population if the readout is hormone release. A receptor-null background cannot save a bad lot. It cannot indict a good one either.
Name the species of the receptor. A rodent pituitary explant is not a human result. This profile will quote the rat work [8] and leave human programme papers in the list.
Somatostatin is pushing the other way
Pulsatile growth hormone release comes from GHRH and somatostatin acting in opposition. Indexed peptide-clamp papers exist [12][14]. Human figures from those papers stay out. The mechanistic claim is still usable: adding GHRH does not remove somatostatin.
Feedback stays intact
Insulin-like growth factor 1 and growth hormone both feed back on the hypothalamus and pituitary. That loop is the physiological argument for using a releasing hormone. It is also a reason the effect should be self-limiting rather than open-ended.
Worth stating as a mechanism rather than as a benefit. No paper in this list measured whether preserved feedback produced a better laboratory outcome than exogenous hormone.
Exposure pattern is a chemistry question
Continuous infusion of a releasing hormone raises an obvious receptor-occupancy worry. Davis and colleagues asked it [11]. Intermittent exposure is a different experiment [2]. Those human figures stay out. The laboratory lesson is narrower: name the exposure pattern. A clamp and a pulse are not the same reagent-use design.
Sequence chemistry the successors were answering
The analogue papers are useful even when the analogue is not Sermorelin. They map which bonds fail.
What 1984 changed
Lance and colleagues published super-active analogues of GRF(1-29) amide [5]. Those peptides are not this reagent. They show that the 1-29 scaffold accepts substitutions and still binds the receptor.
A laboratory that wants one of those analogues should synthesise that analogue. Sermorelin is the unmodified amide.
Reduced peptide bonds
Hocart and colleagues put reduced peptide-bond isosteres in the N-terminal region [6]. The point was enzymatic. A reduced bond is not a peptide bond. The enzyme that clips Ala2-Asp3 cannot hydrolyse what is no longer an amide.
Sermorelin does not carry that isostere. A lot that does is a different molecule with a different mass.
Antagonist analogues
Toth and colleagues reported analogues with high and prolonged antagonistic activity [7]. Antagonist is the opposite occupancy of the same receptor. Shared scaffold is not shared function.
Keep agonist and antagonist lots on separate labels. A cAMP assay that goes the wrong direction has not failed. It has identified a different reagent.
What the 29-mer map should show
At 29 residues a tryptic digest is short. Arginine and lysine sites dominate it. Full coverage by tandem mass spectrometry is routine.
Deletion sequences are the expected impurity in solid-phase synthesis at this length. Each missing residue shifts intact mass by that residue. Ultraviolet detection alone often hides them inside a broad peak.
Reversed-phase chromatography with mass detection finds them. Ask for that pairing on the certificate.
What a 1-44 lot is doing in a 1-29 drawer
Tesamorelin and native GHRH(1-44) amide are longer. They will not hide inside a 3358 Da peak. They will hide inside a drawer labelled GHRH.
Write the residue range on the vial. Write it again on the notebook page. Sermorelin is 1-29. Tesamorelin is 1-44 plus an acyl cap [10]. CJC-1295 is 1-29 plus substitutions plus, if DAC is present, a maleimide [8].
Ghrelin-receptor peptides are not this family. Ipamorelin and the GHRP series hit a different protein. Pairing one of those with Sermorelin is an axis experiment, not an identity check.
Keep the certificate next to the notebook. A later reader should match the Sermorelin lot to the paper without a guess. That is the whole point of keeping a written research-use laboratory record.
If two vials share a drawer, they still need two masses. 3357.9 is this fragment. 3647 is the DAC conjugate. 5136 is tesamorelin. Mixing those three numbers is how analogue literatures contaminate each other.
How to read a sermorelin study
Four questions, and two of them are about which molecule.
Sermorelin, or an analogue?
GHRH(1-29)-NH2, D-Ala2 analogues, CJC-1295 and tesamorelin are separate compounds with separate kinetics [1][8] and [10]. The abstract usually names which. The naming is not decoration.
Which mass?
Sermorelin is 3357.9. A D-Ala2 analogue is a stereoisomer, so it differs by nothing at all in mass. CJC-1295 and tesamorelin differ by much more, since both carry added groups [8][10].
Mass separates the parent from the stabilised analogues cleanly. It does not separate it from a stereoisomeric substitution at all.
Continuous or intermittent?
Indexed papers asked both questions [2][11]. A methods section that omits the exposure pattern has not described the experiment.
What was the comparator?
Another GHRH analogue makes the question identity. A ghrelin-receptor secretagogue makes the question a different receptor. Recombinant growth hormone makes the question hormone versus releasing factor. Do not pool those designs.
Verifying research material
The identity risks here are the amide, the sequence length and the analogue confusion.
Mass distinguishes the family members
Sermorelin is 3357.9. Confirm the certificate specifies the 1-29 fragment with a C-terminal amide. A free acid, or a different fragment length, is a different compound with different activity.
Every batch we supply carries a certificate of analysis recording the identity and purity data behind it.
The amide and the methionine
Confirm the C-terminal amide. The free acid is one dalton heavier. High-resolution mass spectrometry resolves that at 3358. A nominal-mass instrument may not.
Watch 3373.9 for the methionine sulfoxide. That satellite is a different species with the same sequence claim.
Handling
Ordinary peptide practice applies. Store the lyophilised powder cold, dry and dark, and reconstitute close to the point of use.
Storage guidance is a house recommendation. Analytical documentation is per-lot release testing.
Keep the lyophilised solid dry. Equilibrate a vial to room temperature before opening. Treat reconstituted solutions as short-lived.
Trifluoroacetate from cleavage cocktails is common on research peptides. That counterion changes both the mass of the salt form and the peptide content of a weighed vial. Name it on the certificate.
Dilute solutions lose peptide to plastic. Aliquot on reconstitution rather than sampling one vial repeatedly.
A later reader should be able to match the Sermorelin lot to the notebook without asking what was in the vial. Intact mass, amide state, and a mapped digest are the three lines that make that possible.
Optical rotation is useless at 29 residues with this many stereocentres. Do not ask a polarimeter to identify Sermorelin. Mass and sequence have to do that work.
Net peptide content is not HPLC area percent. Water and counter-ion mass inflate the weighed vial. Correct for both before calculating molarity.
If a methods section names Sermorelin and then quotes a mass that belongs to tesamorelin, stop. The rest of that paper is about a different reagent. The same rule applies in reverse. This is the cheapest way to keep two GHRH literatures from contaminating each other, and it costs one intact-mass line.
Common questions about sermorelin
Identity
What is sermorelin? The first 29 residues of growth hormone-releasing hormone, with a C-terminal amide. The amide is part of the identity, not a decoration.
Is it the same as CJC-1295? No. CJC-1295 is a tetrasubstituted derivative of the same 1-29 fragment, built to bind albumin, and it persists in plasma beyond 72 hours [8].
Is it the same as tesamorelin? No. Tesamorelin is a stabilised 1-44 GHRH analogue. Indexed papers that used tesamorelin exist [10]. They do not transfer to Sermorelin.
Does this page report human outcomes? No. Indexed papers are listed so they can be found. This profile keeps the 4.3-minute half-life and stops at fragment chemistry.
Evidence
Why is the half-life such a focus? Because it is 4.3 minutes [1], and every successor molecule in this family was built to extend it.
What does the D-Ala2 swap change? Clearance. The analogue ran 6.7 minutes against 4.3 for Sermorelin [1]. Mass does not see the swap.
Does a short half-life mean a short laboratory window? The peptide clears in minutes. Downstream markers have their own kinetics. Indexed papers asked that question [2]. Those human figures stay out.
Handling and verification
What mass should a certificate show? 3357.9. Check 3373.9 for the methionine sulfoxide.
Which analogue family? Unmodified 1-29 is Sermorelin. Tetrasubstituted 1-29 is the CJC series. Full-length 1-44 with an acyl cap is tesamorelin. Ghrelin-receptor secretagogues are a fourth family.
Summary of the evidence
Write the name, the mass and the amide on the first line of a notebook page. Sermorelin is C149H246N44O42S, 3357.9 Da, GHRH(1-29)-NH2, no substitutions.
Identity: twenty-nine residues, one methionine, one amide. A certificate that omits intact mass is not finished.
Clearance: 4.3 minutes for the unmodified fragment, 6.7 minutes for the D-Ala2 analogue [1]. Albumin conjugation on the same backbone took CJC-1295 past 72 hours [8]. Tesamorelin solved the same enzyme problem on the 1-44 chain [10].
Indexed papers that mention people remain in the list so a reader can find them. Human endpoints stay out.
Kimera Chems supplies Sermorelin as a laboratory research material. Our peptides research library covers more compounds in this class.
Status: supplied for laboratory research use only.
References
- Soule S, King JA, Millar RP. Incorporation of D-Ala2 in growth hormone-releasing hormone-(1-29)-NH2 increases the half-life and decreases metabolic clearance in normal men. J Clin Endocrinol Metab. 1994;79(4):1208-11. PMID 7962295. DOI
- Wilton P, Chardet Y, Danielson K, Widlund L, Gunnarsson R. Pharmacokinetics of growth hormone-releasing hormone(1-29)-NH2 and stimulation of growth hormone secretion in healthy subjects after intravenous or intranasal administration. Acta Paediatr Suppl. 1993;388:10-5. PMID 8329825. DOI
- Thorner M, Rochiccioli P, Colle M, Lanes R, Grunt J, Galazka A, Landy H, Eengrand P, et al. Once daily subcutaneous growth hormone-releasing hormone therapy accelerates growth in growth hormone-deficient children during the first year of therapy. Geref International Study Group. J Clin Endocrinol Metab. 1996;81(3):1189-96. PMID 8772599. DOI
- Prakash A, Goa KL. Sermorelin: a review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency. BioDrugs. 1999;12(2):139-57. PMID 18031173. DOI
- Lance VA, Murphy WA, Sueiras-Diaz J, Coy DH. Super-active analogs of growth hormone-releasing factor (1-29)-amide. Biochem Biophys Res Commun. 1984;119(1):265-72. PMID 6231028. DOI
- Hocart SJ, Murphy WA, Coy DH. Analogues of growth hormone-releasing factor (1-29) amide containing the reduced peptide bond isostere in the N-terminal region. J Med Chem. 1990;33(7):1954-8. PMID 2141879. DOI
- Toth K, Kovacs M, Zarandi M, Halmos G, Groot K, Nagy A, Kele Z, Schally AV. New analogs of human growth hormone-releasing hormone (1-29) with high and prolonged antagonistic activity. J Pept Res. 1998;51(2):134-41. PMID 9516049. DOI
- Jetté L, Léger R, Thibaudeau K, Benquet C, Robitaille M, Pellerin I, Paradis V, van Wyk P, et al. Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog. Endocrinology. 2005;146(7):3052-8. PMID 15817669. DOI
- Baker LD, Barsness SM, Borson S, Merriam GR, Friedman SD, Craft S, Vitiello MV. Effects of growth hormone–releasing hormone on cognitive function in adults with mild cognitive impairment and healthy older adults: results of a controlled trial. Arch Neurol. 2012;69(11):1420-9. PMID 22869065. DOI
- Friedman SD, Baker LD, Borson S, Jensen JE, Barsness SM, Craft S, Merriam GR, Otto RK, et al. Growth hormone-releasing hormone effects on brain γ-aminobutyric acid levels in mild cognitive impairment and healthy aging. JAMA Neurol. 2013;70(7):883-90. PMID 23689947. DOI
- Davis JR, Sheppard MC, Shakespear RA, Lynch SS, Clayton RN. Does growth hormone releasing factor desensitize the somatotroph? Interpretation of responses of growth hormone during and after 10-hour infusion of GRF 1-29 amide in man. Clin Endocrinol (Oxf). 1986;24(2):135-40. PMID 2871948. DOI
- Achermann JC, Hindmarsh PC, Robinson IC, Matthews DR, Brook CG. The relative roles of continuous growth hormone-releasing hormone (GHRH(1-29)NH2) and intermittent somatostatin(1-14)(SS) in growth hormone (GH) pulse generation: studies in normal and post cranial irradiated individuals. Clin Endocrinol (Oxf). 1999;51(5):575-85. PMID 10594518. DOI
- Grunt JA, Schwartz ID, Buchanan C, Howard CP. Effects of long-term growth hormone releasing hormone 1-29 in significantly short children. Acta Paediatr. 1995;84(6):631-3. PMID 7670244. DOI
- Ross RJ, Rodda C, Tsagarakis S, Davies PS, Grossman A, Rees LH, Preece MA, Savage MO, et al. Treatment of growth-hormone deficiency with growth-hormone-releasing hormone. Lancet. 1987;1(8523):5-8. PMID 2879138. DOI
Research use only. Not for human or veterinary use. Nothing here describes a therapy or a dosing protocol.
