Preloaded Autoinjector | GHRP-2 | 3ml Pen | 10mg

The GHRP-2 pen is a preloaded 3ml autoinjector holding pralmorelin in solution at 3.33 mg/ml, 10 mg of hexapeptide in total, drawn in 0.01 ml graduations of 33.3 µg each. One synthetic residue, D-3-(2-naphthyl)alanine at position 2, gives this molecule a second near-UV chromophore beside its single tryptophan and makes it the most surface-adsorbent secretagogue of the series.

Specification Table

What Changes When GHRP-2 Ships in Solution?

Putting pralmorelin into water leaves one tryptophan, one synthetic naphthylalanine and a C-terminal amide in continuous contact with dissolved oxygen, trace metals and light for the whole shelf life, while the deamidation routes that limit most peptide solutions are absent from this sequence entirely.

Trp4 is the residue that moves first. Indole is the most oxidation-prone side chain in the proteinogenic set, and it converts under peroxide, leached metal ions or near-UV illumination to hydroxytryptophan at +16 Da, N-formylkynurenine at +32 Da and kynurenine at +4 Da. Those products are yellow and they appear as new peaks ahead of the parent on reversed-phase chromatography. In a lyophilized cake the same residue sits in a rigid, nearly anhydrous matrix and the reaction runs orders of magnitude slower.

The residue at position 2 is the part of this molecule that has no counterpart elsewhere in the catalogue. D-3-(2-naphthyl)alanine is not a proteinogenic amino acid: it has no codon, no one-letter code, and a fused bicyclic aromatic side chain of formula C₁₃H₁₁NO. That ring absorbs strongly between 270 and 290 nm and is an efficient triplet sensitiser, so a cartridge under bench lighting contains a chromophore that can absorb energy and pass it to the tryptophan four residues away. Two independent near-UV absorbers in a six-residue chain is unusual, and it is the reason light protection here is a mechanism rather than a habit.

The same naphthalene ring decides where the material goes when it is not being oxidised. With no aspartate or glutamate and an amide in place of the C-terminal carboxylate, the calculated net charge is +1.91 at pH 7.0 and the molecule stays cationic to roughly pH 11. No isoelectric point in the usable range means no pH at which it precipitates and no pH at which it stops binding ionised silanols on borosilicate glass. On top of that permanent charge sits the most hydrophobic residue set of any common growth hormone secretagogue, driving partition into polypropylene, PVC, silicone oil and elastomer stoppers. The substitution that made this compound a more potent releaser than its predecessor also made it stickier.

The C-terminal amide is the slow route. Hydrolysis to the free acid changes the molecule by roughly one dalton and removes one unit of positive charge, which is enough to separate parent from product on reversed-phase chromatography and trivial to see on a modern mass spectrometer. The reaction is acid- and base-catalysed and slowest near neutral pH, so the unpublished formulation pH sets its rate.

What the sequence lacks narrows the problem usefully. No asparagine and no glutamine, so no deamidation. No Asp-Gly and no Asp-Pro, so no isomerisation and no acid-catalysed cleavage. No methionine, cysteine, disulfide or tyrosine. Six residues is far too short for the extended beta-structure amyloid requires. Three D-residues make the chain resistant to proteolysis, which protects it from none of the chemistry above, because none of that chemistry is enzymatic.

The one company that had to answer this question left its decision on the record. The only regulator-reviewed pralmorelin product is a single-use 100 µg intravenous unit, prepared as the hydrochloride and given once. Nobody has marketed this molecule as a stored multi-dose solution.

GHRP-2 Solution Stability: What Has Actually Been Measured?

GHRP-2 solution stability has never been measured. No forced-degradation, photostability, pH-dependence or freeze-thaw study of this compound in water appears in the peer-reviewed literature, so every stability statement about it, including the ones on this page, is residue-level inference.

The nearest published analytical work is doping control. Okano et al. 2010 developed an LC-ESI tandem mass spectrometry method for pralmorelin and its major urinary metabolite, which establishes that parent and degradation-adjacent species can be resolved and quantified at trace level. It says nothing about a sealed cartridge on a shelf at 5°C for six months.

Freezing is excluded for reasons specific to a solution rather than a powder. As ice forms, the remaining liquid phase concentrates peptide and buffer together while its pH moves, because individual salts crystallise out at different points. Both effects push oxidation and interfacial loss, and a frozen cartridge also loads its seal. GHRP-2 pen stability over the device shelf life is therefore an open question, and the storage and stability article covers the general principles that apply while it stays open.

Concentration and Increment Arithmetic for the GHRP-2 Pen

The GHRP-2 pen holds 10 mg in 3 ml, which is 3.33 mg/ml and 33.3 µg per 0.01 ml graduation, but the molar concentration is 4.08 mM as the free base and 3.74 mM as the dihydrochloride, an 8 percent difference decided entirely by the counter-ion.

The arithmetic is short. 10 mg divided by 3 ml is 3.3333 mg/ml. Divided by the free-base average mass of 817.98 g/mol and multiplied by 1,000 that is 4.08 mM. Repeat the division with the dihydrochloride mass of 890.89 g/mol and the same solution is 3.74 mM, because 10 mg of the dihydrochloride carries only about 9.2 mg of peptide base. One 0.01 ml graduation on a U-100 scale holds 33.3 µg, which is 40.8 nmol of base; 0.1 ml holds 333 µg, or 408 nmol. The peptide calculator reproduces these figures for any fill, and the certificate of analysis is the only place the salt and net peptide content will be stated.

Set against the one regulator-reviewed human exposure, the cartridge is very large. The entire approved Japanese diagnostic dose is 100 micrograms intravenously, which at 3.33 mg/ml occupies 0.03 ml, three graduations on an insulin scale. A single GHRP-2 pen therefore carries 100 whole diagnostic doses, and one 0.1 ml increment at 333 µg is 3.3 times the complete registered human dose. Set against receptor pharmacology the cartridge is enormous in the other direction: GHSR-1a agonism operates in the low nanomolar range, and reaching 10 nM from 4.08 mM is a 408,000-fold serial dilution, performed in plastic, on a peptide that partitions into plastic.

GHRP-2 Pen vs Vial: What Does the Format Suit?

The GHRP-2 pen vs vial question comes down to whether the work needs many equivalent draws of a permanently cationic, strongly aromatic hexapeptide from one lot over weeks, or a few freshly dissolved samples measured on the day they are prepared.

The format suits the first case. Concentration is fixed at manufacture, so diluent measurement, incomplete dissolution and transfer loss stop being per-session variables, and for this molecule every transfer step removed is one fewer surface for a peptide that binds surfaces by two mechanisms at once. The preloaded autoinjector category page sets out the general case.

It suits the second case badly. For a single assay against a reference standard, the lyophilized 10 mg vial dissolved that morning has spent minutes in water rather than months, so the GHRP-2 solution vs lyophilized comparison favours the dry cake wherever residence time in water is the variable. A vial also allows buffer, ionic strength and pH to be chosen rather than inherited from an unpublished formulation.

The GHRP-2 pen or vial decision otherwise follows the general trade-offs in the pen versus vial article. What is particular here is that no stability figure exists to put against the convenience, so a device used across many weeks runs an uncharacterised chemistry experiment alongside the intended one. A nasal spray presentation exists where the route rather than the metrology is the question.

What the Product Record Does Not State

The product record does not state the excipient system, the solution pH, the salt form, the net peptide content or the fill date, and every one of those five changes what 3.33 mg/ml means at the bench.

Excipients matter first because of the indole. Polysorbates carry peroxide as a degradation product of their own, and peroxide oxidises tryptophan; a preservative such as phenol or benzyl alcohol, standard in multi-draw cartridges, enters every assay the solution is added to; a chelator would suppress the metal-catalysed route. A surfactant would also change adsorption, which for this peptide is the dominant loss mechanism. Whether any of them is present is unknown.

Solution pH sets the amide hydrolysis rate and little else, because the molecule has no titratable acidic group and its charge barely moves across the usable range. Salt form and net peptide content decide how much pralmorelin base sits inside the 10 mg, a gap of roughly 8 percent between the two documented salts, and the fill date decides how much of the degradation clock has already run on arrival. Ask for all five on the certificate of analysis before the quantitative work starts, not once a result has stopped making sense.

Verifying the Device and Confirming the Contents Are Intact

Look at the solution against white before each draw is taken. Intact material is clear and colourless, and a yellow tint is the kynurenine chromophore of oxidised tryptophan rather than harmless colour drift.

Ultraviolet absorbance works here but needs one correction, and this is where a habit carried over from other peptides misleads. The sequence has no tyrosine, so nothing masks the tryptophan, but the naphthalene ring at position 2 absorbs strongly across the same window, so an extinction coefficient calculated from tryptophan content alone under-reads concentration. A falling value at 280 nm with a rising shoulder between 320 and 360 nm is the signature of photo-oxidation regardless of the absolute figure.

Tryptophan fluorescence, excited near 280 nm and read at about 350 nm, falls before absorbance does, which makes it the earlier indicator. Mass spectrometry then settles what the optical measurements suggest: +4, +16 and +32 Da at the tryptophan, roughly one dalton at the C-terminal amide, doubled mass for a photo-crosslinked dimer. The mass-silent changes are epimerisation at the three D-centres, never measured for this compound, and adsorptive loss, visible only as a shortfall in peak area against a freshly reconstituted vial standard run the same day.

Allow the device to reach ambient temperature before actuating, since cold solution is more viscous and a spring mechanism delivers less of it per stroke. Verify delivered volume gravimetrically once per device across five or more actuations.

What Is GHRP 2 and What Does the Literature Report?

GHRP-2 is pralmorelin, a synthetic hexapeptide of sequence D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH₂ developed under the codes KP-102 and GPA-748, and it is an agonist at the growth hormone secretagogue receptor 1a, the receptor later identified as the target of ghrelin.

The short answer to what is GHRP 2 at the level of mechanism: receptor activation in pituitary somatotrophs signals through Gq and phospholipase C, mobilising intracellular calcium and releasing growth hormone by a route separate from, and additive to, GHRH. It was the first compound of the class to reach clinical use, and it got there because preclinical work reported it as a more potent releaser than the earlier hexapeptide (Doi et al. 2004). The differences between the two are set out in the GHRP-2 versus GHRP-6 comparison.

The human record is four studies, none of them a therapeutic trial. Pihoker et al. 1998 is a phase I pharmacokinetic and pharmacodynamic study in children given the compound intravenously, and it is the registration-relevant work. Its numeric half-life, clearance and volume of distribution could not be read for this page, so no half-life figure is published here; the figures circulating on vendor sheets have no traceable source in this dossier. Laferrère et al. 2005 reported that pralmorelin, like ghrelin, increased ad libitum food intake in healthy men, a small acute study. Mericq et al. 2003 followed appetite and body weight in growth-hormone-deficient children on long-term oral administration. Okano et al. 2010 built the urinary detection method used in doping control.

The animal record is Doi et al. 2004 and its companion papers, which characterised KP-102 and separately documented CRF-mediated ACTH-releasing activity in rats. The unstudied list is longer: no controlled human trial of chronic subcutaneous administration, none with a body-composition or muscle-mass endpoint, no multi-dose stability data, no bioequivalence work. Registry status could not be verified for this page.

What Does the GHRP-2 ACTH Cortisol Response Record Show?

The GHRP-2 ACTH cortisol response is documented in rats rather than in a published human study: KP-102 released ACTH in rodents by a mechanism attributed mainly to CRF, so activation of the stress axis is a class property of this receptor rather than something this compound was shown to escape.

That distinction matters because the marketing claim runs the other way. The proposition that pralmorelin is cleaner than its hexapeptide predecessor rests on preclinical selectivity data, and no human head-to-head study of the two compounds exists. The rodent ACTH data sit in the same journal as the potency data used to make the claim.

The appetite finding is the one class effect measured directly in people. Laferrère et al. 2005 recorded increased food intake in healthy men, the ghrelin-receptor effect appearing where receptor pharmacology predicts it. Sustained agonism would be expected to raise IGF-1, but that is inference from the axis rather than a measurement on chronic administration, which has never been run.

What Is the Safety and Regulatory Position?

Pralmorelin holds a marketing authorisation in Japan and nowhere else, and that authorisation is for a diagnostic reagent given as a single 100 microgram intravenous dose, not for any therapeutic use.

The Japanese product is GHRP Kaken 100 from Kaken Pharmaceutical, used in the assessment of growth hormone deficiency. KEGG records it under entry D02040 with Japanese therapeutic category 7223 and efficacy listed as diagnostic, formulated as the dihydrochloride, CAS 158827-34-0, molecular weight 890.89. The approval year and exact indication wording could not be confirmed against PMDA records for this page. This research preparation is not that product: it is a multi-draw solution at 3.33 mg/ml, of unstated salt form, with no authorisation of any kind. Calling a research pen approved in Japan without the words diagnostic, single dose and intravenous is materially misleading.

There is no approved pralmorelin product in the United States, the European Union, Australia or Canada, and no approved therapeutic formulation anywhere in the world. FDA placed growth hormone releasing peptide-2 in Category 2 of the section 503B bulk drug substances list, the category for substances identified as presenting significant safety risks, on 29 September 2023. It is absent from the 503A bulks list, so no lawful compounded preparation exists in the United States. WADA prohibits it at all times as a non-specified substance under S2.2.4, growth hormone releasing factors, where “GHRP-2 (pralmorelin)” is the first named example.

The human record consists of single diagnostic administrations, one paediatric oral study and two small acute studies. There is no chronic exposure database and no published adverse-event table for a multi-draw injectable solution. The device is sold into laboratory research and nothing else; administration to humans or animals is outside what it is offered for.

What Is GHRP-2 and How Does GH Release Work Here?

Pralmorelin, written H-D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2, is one of a series of synthetic peptides built from the original growth-hormone-releasing peptide work of Bowers in the 1980s. Along with hexarelin and GHRP-6, it binds GHS-R1a, the receptor that was later shown to be the ghrelin receptor. Ipamorelin is the selective member of the same family. All are gh-releasing peptides in the pharmacological sense, and none is a GHRH analogue. Growth hormone releasing peptide-2 is the second of the numbered series and the one with the largest human endocrine record.

GH release from this class works by two routes at once. Agonism at GHS-R1a on the anterior pituitary gland directly triggers secretion, and agonism at the same receptor in the hypothalamus suppresses somatostatin tone, which lifts the brake holding the next pulse back. Growth hormone secretion is pulsatile by nature, so what a secretagogue does is add a pulse rather than raise a baseline. Growth hormone releasing hormone acts on a different receptor entirely, and giving both together produces a larger release than either does alone.

The readable downstream marker is insulin-like growth factor-1. Serum GH samples a pulse at an arbitrary moment and is close to uninterpretable alone, while IGF-1 integrates exposure over hours. The endpoints most people are looking for, muscle growth, protein synthesis and tissue repair, sit below that and have not been measured in any trial of this hexapeptide. Muscle growth in particular has never been an endpoint for the GHRP-2 peptide in a controlled human study.

What Is Documented About Side Effects and Selectivity?

This compound is the least selective of the commonly sold secretagogues, and that is its defining pharmacological feature rather than an incidental one. In the published human work it raises prolactin and, more notably, ACTH and cortisol alongside growth hormone, because GHS-R1a agonism reaches more than the somatotroph population. The page above sets out that ACTH and cortisol record in detail. Appetite stimulation is the other consistent finding, since this is a ghrelin receptor agonist and ghrelin is the hunger signal.

Water retention is the side effect most often reported across the class, dose-related, presenting as peripheral oedema and joint discomfort. Reduced insulin sensitivity appears at higher HGH exposures in the recombinant literature. Claims about sleep quality come from small studies of slow-wave sleep with GH secretagogues and are not established for this molecule specifically.

Growth hormone deficiency is a diagnosed clinical condition, confirmed by stimulation testing, and it is treated with recombinant human growth hormone under specialist supervision. This research chemical is not a treatment for it. Pralmorelin has been used as a diagnostic agent in Japan under the name GHRP Kaken 100, which is a test rather than a therapy, and no other regulator has approved it for anything.

What Should a CoA Show and What Does the Format Change?

Tryptophan at position four is the residue that governs handling. It absorbs at 280 nm, giving this compound a real chromophore, and it oxidises readily, with products sixteen and thirty-two daltons above the parent. A certificate should report purity by HPLC at 214 and 280 nm, an accurate mass, water content and the counter-ion percentage. D-amino acids at three positions make the molecule resistant to ordinary peptidases but do nothing to protect the indole ring.

A GHRP-2 5mg vial arrives as a dry cake and is reconstituted with bacteriostatic water at the bench, so the concentration is chosen by the researcher and the solid can be stored cold and dark for a long time. This pen arrives in solution at 3.33 mg/ml, so the tryptophan has been in oxygenated water since a fill date the record does not state. Freeze-dried material protects the indole; a solution does not. Ask for the fill date, and treat it as more informative than the purity figure.

One naming note. The GHRP-2 peptide is prohibited in sport at all times under WADA category S2, along with every other growth hormone secretagogue, and growth performance claims made for the class in livestock or in sport contexts are a separate literature from the human endocrine studies. Neither supports a use for this device, which is supplied for laboratory research only.

Published Literature

Every reference here was confirmed against a publisher page or a primary index. All concern the compound, its detection or its regulatory record; nothing has been published on this delivery format.

1. Pihoker C, Kearns GL, French DC, et al. J Clin Endocrinol Metab. 1998;83(4):1168-1172. DOI: 10.1210/jcem.83.4.4744 PMID: 9543135
2. Doi N, Hirotani C, Ukai K, et al. Arzneimittelforschung. 2004;54(12):857-867. DOI: 10.1055/s-0031-1297041 PMID: 15646370
3. Laferrère B, Abraham C, Russell CD, et al. J Clin Endocrinol Metab. 2005;90(2):611-614. DOI: 10.1210/jc.2004-1719
4. Mericq V, Cassorla F, Bowers CY, et al. J Pediatr Endocrinol Metab. 2003;16(7):981-985. DOI: 10.1515/jpem.2003.16.7.981 PMID: 14513874
5. Okano M, Sato M, Ikekita A, et al. Rapid Commun Mass Spectrom. 2010;24(14):2046-2056. DOI: 10.1002/rcm.4619 PMID: 20552695
6. KEGG DRUG entry D02040, pralmorelin dihydrochloride: C45H55N9O6 · 2HCl, molecular weight 890.89, exact mass 889.3809, CAS 158827-34-0, Japanese therapeutic category 7223, efficacy Diagnostic.

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