$44.99
Buy GHRP-2 Peptide 10 mg Online from SourceTides. Pralmorelin | KP-102 | CAS 158861-67-7 | D-Ala-D-βNal-Ala-Trp-D-Phe-Lys-NH₂ | MW 817.94 g/mol | C₄₅H₅₅N₉O₆ | ≥99% HPLC | D-βNal confirmed | C-terminal amide confirmed | Endotoxin <1 EU/mg (LAL) | Full CoA | Lyophilised | Dry-ice cold chain.
Synthetic hexapeptide GHS-R1a (ghrelin receptor) agonist. Robust pulsatile GH release. Modest cortisol + prolactin (less selective than Ipamorelin). Half-life ~30 min. Japan-approved as Pralmorelin GH stimulation test (2 µg/kg diagnostic dose). Synergistic with CJC-1295/Sermorelin (5–10× GH vs monotherapy). WADA S2 PROHIBITED at all times. For in-vitro laboratory research use only. Not for human consumption.
Buy GHRP-2 Peptide 10 mg Online | Growth Hormone Releasing Peptide-2 | GHS-R1a Agonist | ≥99% Purity | CoA | SourceTides
Buy GHRP-2 Peptide 10 mg Online from SourceTides.
GHRP-2 (Growth Hormone Releasing Peptide-2; Pralmorelin; KP-102; CAS 158861-67-7) is a synthetic hexapeptide GHS-R1a (Growth Hormone Secretagogue Receptor 1a) agonist — the second generation of the GHRP family, developed as a research tool for GH secretion biology and GH axis pharmacology.
Its sequence is D-Ala-D-βNal-Ala-Trp-D-Phe-Lys-NH₂ — six amino acids including two D-amino acids (D-Ala at position 1, D-βNal at position 2) and C-terminal amidation, all contributing to metabolic stability against peptidase degradation.
GHRP-2 activates GHS-R1a on pituitary somatotrophs, hypothalamic neurons, and peripheral tissues, stimulating growth hormone (GH) release through the cAMP/PKA and inositol trisphosphate (IP₃/PKC) second messenger pathways.
The distinguishing pharmacological profile of GHRP-2 within the GHRP family is its potency and relative selectivity.
It produces more robust GH release per dose than GHRP-6 in direct comparison studies, with less appetite stimulation — because GHRP-6’s appetite effects derive partly from ghrelin receptor cross-reactivity at hypothalamic NPY/AgRP circuits, which GHRP-2 activates less potently.
GHRP-2 was selected as the standard clinical research GHRP for GH axis diagnostic and pharmacological studies, including a published Phase 1 clinical trial (Pralmorelin clinical development; Japan).
Unlike Ipamorelin — the highly selective GHS-R1a agonist developed later that produces GH release without cortisol or prolactin elevation — GHRP-2 also stimulates modest cortisol and prolactin secretion alongside GH.
This makes GHRP-2 a less selective but more pharmacologically complete GH secretagogue for research requiring the full spectrum of GHS-R1a activation effects.
GHRP-2 is WADA S2 prohibited as a Peptide Hormone/Growth Factor.
Every SourceTides vial is lyophilised, tested at ≥99% HPLC purity, and ships with a full lot-specific Certificate of Analysis.
For in-vitro laboratory research use only. Not for human consumption.
GHRP-2 Peptide 10 mg — Technical Specifications
| Parameter | Specification |
|---|---|
| Common Names | GHRP-2; Pralmorelin; KP-102; Growth Hormone Releasing Peptide-2 |
| CAS Number | 158861-67-7 |
| Molecular Formula | C₄₅H₅₅N₉O₆ |
| Molecular Weight | 817.94 g/mol |
| Peptide Length | 6 amino acids (hexapeptide); C-terminal amide (–NH₂) |
| Sequence | D-Ala-D-βNal-Ala-Trp-D-Phe-Lys-NH₂ (D-βNal = D-β-(2-Naphthyl)alanine) |
| D-Amino Acids | D-Ala (position 1); D-βNal (position 2); D-Phe (position 5) — three D-configured residues provide metabolic stability against peptidase degradation |
| C-Terminal Amide | –Lys-NH₂ (amidated C-terminus); prevents carboxypeptidase attack; contributes to receptor binding affinity |
| Primary Receptor | GHS-R1a (Growth Hormone Secretagogue Receptor 1a; Ghrelin Receptor); Gq/11 and Gs-coupled GPCR; expressed on pituitary somatotrophs, hypothalamic GHRH neurons, and peripheral tissues |
| Signalling Pathways | GHS-R1a → Gq/11 → PLCβ → IP₃/DAG → Ca²⁺/PKC (primary GH release mechanism) + cAMP/PKA (Gs component); synergises with GHRH → adenylyl cyclase → cAMP → GH secretion |
| GH Release Profile | Stimulates robust pulsatile GH release from pituitary somatotrophs; also stimulates modest cortisol and prolactin elevation (distinguishes GHRP-2 from selective Ipamorelin); synergistic with GHRH/CJC-1295 |
| Plasma Half-Life | ~30 minutes; D-amino acids and C-terminal amide extend stability vs GHRP-6 (~20 min); short half-life reflects typical GPCR hexapeptide pharmacokinetics |
| vs GHRP-6 | More potent GH release per dose; less appetite stimulation (less NPY/AgRP hypothalamic cross-reactivity); slightly longer half-life (~30 vs ~20 min); preferred for GH axis diagnostic research |
| vs Ipamorelin | Less selective (Ipamorelin does not stimulate cortisol/prolactin); more complete pharmacological GHS-R1a activation for research requiring full receptor agonist profile; broader research tool for studying GHS-R1a biology beyond GH axis |
| Physical Form | White lyophilised powder; hygroscopic |
| Purity | ≥99% (RP-HPLC); identity confirmed by ESI-MS (MW 817.94 Da); D-amino acid configuration confirmed |
| Endotoxin | <1 EU/mg (LAL chromogenic assay) |
| Solubility | Freely soluble in sterile water and PBS pH 7.4 (≥5 mg/mL); dissolves readily; reconstitute in BAC water for multi-dose protocols |
| Storage — Lyophilised | −20°C long-term (24 months); 2–8°C short-term; protect from moisture and light |
| Storage — Reconstituted | 2–8°C for up to 14 days in BAC water; −20°C for longer; aliquot before freezing; avoid freeze-thaw |
| Certificate of Analysis | Lot-specific CoA with every order; HPLC + ESI-MS (817.94 Da) + endotoxin |
| WADA Status | WADA S2 PROHIBITED — Peptide Hormones, Growth Factors, Related Substances, and Mimetics; prohibited at all times in and out-of-competition |
What Is GHRP-2?
GHRP-2 belongs to the growth hormone secretagogue (GHS) peptide family — synthetic compounds designed to activate the ghrelin receptor (GHS-R1a) and thereby stimulate pituitary GH secretion.
The first compounds in this family (GHRP-6, GHRP-1) were developed in the late 1980s by the Bowers/Momany laboratories as tool compounds for studying GH regulation.
GHRP-2 was the second-generation optimisation — retaining the D-amino acid/aromatic pharmacophore required for GHS-R1a binding while improving potency and metabolic stability.
The name “Growth Hormone Releasing Peptide” preceded the discovery of the endogenous GHS-R1a ligand, ghrelin, by more than a decade.
When ghrelin was identified in 1999 by Kojima et al., it was recognised that GHRP-2 and related compounds had been acting as synthetic mimetics of this endogenous stomach-derived hormone.
This explains why GHRP-2 activates not just GH release (the originally observed effect) but the full spectrum of ghrelin receptor biology: appetite regulation via hypothalamic circuits, gastric motility, cardioprotection, and anti-inflammatory effects.
The sequence D-Ala-D-βNal-Ala-Trp-D-Phe-Lys-NH₂ encodes the minimum pharmacophore needed for GHS-R1a activation.
D-amino acids at positions 1, 2, and 5 resist peptidase recognition (mammalian peptidases have evolved for L-amino acid substrates).
The D-β-Naphthylalanine at position 2 is the key aromatic residue that occupies the hydrophobic binding pocket of GHS-R1a that also binds the octanoyl-serine of endogenous ghrelin — this aromatic contact is the defining pharmacophoric feature of the GHRP family.
The C-terminal Lys-NH₂ amide contributes to receptor binding and metabolic stability.
GHRP-2 was advanced to clinical development under the name Pralmorelin (INN) by Kaken Pharmaceutical (Japan), where it was studied as a diagnostic agent for GH deficiency assessment — providing a pharmacological GH stimulation test alternative to insulin-induced hypoglycaemia.
This clinical development history gives GHRP-2 a published human pharmacology dataset that most research peptides lack.
When you buy GHRP-2 Peptide 10 mg from SourceTides, you access ≥99% HPLC-pure D-Ala-D-βNal-Ala-Trp-D-Phe-Lys-NH₂ with identity confirmed by ESI-MS.
GHRP-2 vs GHRP-6 vs Ipamorelin vs CJC-1295: The GH Secretagogue Comparison
| Compound | Class / Receptor | GH Release | Cortisol / Prolactin | Appetite Effect | Half-Life | Best Research Use | SourceTides |
|---|---|---|---|---|---|---|---|
| GHRP-2 (this product) | GHS-R1a agonist; hexapeptide | High; robust pulsatile GH | Yes (modest) | Moderate | ~30 min | Full GHS-R1a pharmacology; GH deficiency diagnostic; complete ghrelin receptor biology; GH axis stimulation with clinical precedent | Buy GHRP-2 |
| GHRP-6 | GHS-R1a agonist; hexapeptide | Moderate-high | Yes (modest) | Strong | ~20 min | GH secretagogue + appetite stimulation research; NPY/AgRP hypothalamic effects; ghrelin-like effects combined | Buy GHRP-6 |
| Ipamorelin | GHS-R1a agonist; pentapeptide; selective | Moderate; clean pulse | None | Minimal | ~2 h | Clean selective GH release without cortisol/prolactin; selective GHS-R1a research; most selective GHRP for GH-only endpoints | Buy Ipamorelin |
| Hexarelin | GHS-R1a + CD36 dual agonist; hexapeptide | Highest in class | Yes (substantial) | Moderate | ~30 min | Maximal GH stimulation; cardioprotection via CD36; GHS-R1a + scavenger receptor dual biology | Buy Hexarelin |
| Sermorelin | GHRHR agonist; 29-AA fragment of GHRH | Moderate; physiological pulse | None | None | ~10–12 min | GHRH receptor pharmacology; synergistic with GHRPs; physiological GH pulse; FDA-approved diagnostic precedent | Buy Sermorelin |
| CJC-1295 | GHRHR agonist; modified GHRH(1-29) | Sustained baseline GH elevation | None | None | ~6–8 days (DAC form) | Sustained GHRH receptor activation; chronic GH elevation; IGF-1 axis studies; synergistic with GHRPs | Buy CJC-1295 |
How GHRP-2 Works — Mechanism of Action
GHS-R1a Binding and Gq/11 Signalling
GHS-R1a is a Class A GPCR that couples primarily to Gq/11 heterotrimeric G proteins.
It is expressed at highest density on pituitary somatotroph cells (which produce GH), hypothalamic GHRH-secreting neurons, arcuate nucleus NPY/AgRP neurons, vagal afferent neurons, and cardiac myocytes.
GHRP-2’s aromatic pharmacophore (D-βNal at position 2) occupies the hydrophobic ligand-binding pocket of GHS-R1a — the same pocket that binds the octanoyl chain of endogenous ghrelin.
GHS-R1a activation by GHRP-2 triggers Gq/11 → PLCβ → IP₃/DAG cascade, elevating intracellular Ca²⁺ from ER stores.
In pituitary somatotrophs, this Ca²⁺ surge triggers GH secretory vesicle exocytosis — producing the characteristic pulsatile GH release that defines GHRP pharmacology.
GHRP-2 also activates Gs/cAMP/PKA in some tissues, amplifying the secretory signal.
Synergy with GHRH/CJC-1295
The most important pharmacological property of GHRP-2 for research design is its synergistic interaction with GHRH-class compounds.
GHRH (and its analogs Sermorelin and CJC-1295) act on the GHRH receptor to raise cAMP in somatotrophs — priming the cell for GH release.
GHRP-2 acts through GHS-R1a/Gq/11/Ca²⁺ — a completely different second messenger system in the same cell.
When both pathways are activated simultaneously, GH release is amplified far beyond the simple sum of each compound alone — typically 5–10× more than GHRH or GHRP-2 individually.
This synergy is the mechanistic basis for GHRP + GHRH combination research protocols and is specific to compounds acting through the Ca²⁺ (GHRP) and cAMP (GHRH) arms simultaneously.
Cortisol, Prolactin, and the Non-Selective Profile
Unlike Ipamorelin, which activates GHS-R1a with sufficient selectivity to avoid cortisol and prolactin elevation at standard doses, GHRP-2 produces modest but measurable cortisol and prolactin increases alongside GH release.
These effects occur because GHS-R1a on hypothalamic and adrenal cells activates CRH (corticotropin-releasing hormone) and ACTH pathways in addition to GHRH signalling.
For research design: this non-selective profile makes GHRP-2 a more complete pharmacological representation of GHS-R1a activation — studying all the downstream consequences of full ghrelin receptor engagement.
When studying the isolated GH axis without cortisol or prolactin confounders, Ipamorelin is the preferred tool.
When studying the full spectrum of GHS-R1a biology — including its HPA axis interactions — GHRP-2 is the appropriate choice.
GHRP-2 Research Evidence
| Research Domain | Evidence Level | Key Finding | Source |
|---|---|---|---|
| GH secretion — human pharmacology (Pralmorelin) | Phase 1/2 clinical data (Japan; Pralmorelin/KP-102); multiple published human studies | SC GHRP-2 (2 µg/kg) produces robust GH elevation in healthy adults and GH-deficient patients; GH peak typically 2–5× above baseline; validated as GH stimulation test agent; HPA cortisol elevation modest; well tolerated in human GH axis diagnostic studies | Korbonits et al. 1996; Pralmorelin human data |
| GHRP + GHRH synergy | In vivo (human + rodent); extensively published | GHRP-2 + GHRH combination produces GH release 5–10× greater than either compound alone; Ca²⁺ (GHRP-2/GHS-R1a) + cAMP (GHRH/GHRHR) synergy confirmed mechanistically; this synergy is the fundamental design principle for all GHRP + GHRH combination protocols | Bowers et al.; Ghigo et al. — GHRP/GHRH synergy literature |
| GHS-R1a receptor pharmacology | In vitro + in vivo; standard pharmacological reference compound | GHRP-2 is the primary reference agonist for GHS-R1a characterisation in receptor binding, cAMP, Ca²⁺ flux, β-arrestin, and internalisation assays; published Ki values; standard positive control for GHS-R1a pharmacology | GHS-R1a pharmacology literature; Howard et al. 1996 (ghrelin receptor discovery papers) |
| Cardioprotection (GHS-R1a cardiac) | Preclinical (rodent I/R models) | GHRP-2 reduces infarct size in rodent cardiac ischaemia-reperfusion models; cardiac GHS-R1a activation drives PI3K/Akt survival signalling in cardiomyocytes; distinct from Hexarelin’s CD36-mediated cardioprotection; studied alongside BPC-157 in cardiac protection protocols | Cardiac GHS-R1a GHRP-2 preclinical literature |
| Anti-inflammatory and cytoprotective effects | In vitro + preclinical (inflammation, liver injury models) | GHRP-2 reduces NF-κB-driven inflammatory cytokines (TNF-α, IL-1β, IL-6) in multiple cell types and animal models; hepatoprotective in CCl₄ injury models; cytoprotective effects partly independent of GH axis; GHS-R1a expressed on immune and liver cells | GHRP-2 anti-inflammatory/liver literature |
| GH deficiency diagnosis (Pralmorelin test) | Clinical (Japanese regulatory approval as diagnostic) | Pralmorelin (GHRP-2) approved in Japan as GH stimulation test agent for GH deficiency diagnosis; sensitivity and specificity established vs insulin tolerance test; published cut-off values for GH deficiency diagnosis (peak GH <9 ng/mL indicates GHD); only approved clinical use of a GHRP compound | Pralmorelin GH stimulation test — Japanese clinical data |
What Is GHRP-2 Used for in Research?
| Research Field | Application | Why GHRP-2 |
|---|---|---|
| GHS-R1a receptor pharmacology | GHS-R1a binding assays; cAMP and Ca²⁺ flux; β-arrestin recruitment; receptor internalisation; GHS-R1a inhibitor screening; biased agonism studies | The canonical GHS-R1a full agonist reference; used in every GHS-R1a pharmacology assay as the positive control; compare against selective agonists (Ipamorelin) and partial agonists in biased agonism studies; compare GHRP-2 vs ghrelin for GHRP vs endogenous ligand pharmacophore differences |
| GH axis and somatotroph biology | GH secretion; somatotroph Ca²⁺ signalling; GHRP + GHRH synergy; GH pulsatility; somatostatin inhibition models; feedback regulation | Most potent GH-stimulating GHRP with human pharmacology data; GHRP-2 + CJC-1295 or Sermorelin combination produces maximal pharmacological GH stimulation; compare GH release vs Ipamorelin (selective) and Hexarelin (maximal) for full GHRP potency spectrum |
| GH deficiency models | GH stimulation tests; GHD animal models; somatotroph responsiveness; GH reserve assessment; GH deficiency pathophysiology | Pralmorelin (GHRP-2) is Japan-approved as a GH stimulation test agent — published diagnostic cut-offs and methodology; only GHS-R1a agonist with regulatory approval as a diagnostic; standardised human testing protocol available for direct adaptation to preclinical GHD models |
| Ghrelin receptor biology | Appetite regulation; NPY/AgRP hypothalamic circuits; energy homeostasis; gastric motility; reward and addiction (mesolimbic GHS-R1a); hypothalamic-pituitary axis | GHS-R1a = ghrelin receptor; GHRP-2 activates the full ghrelin receptor programme (not just GH release); studied alongside GHRP-6 to compare appetite/NPY (GHRP-6 stronger) vs GH release (GHRP-2 stronger) dimensions of GHS-R1a pharmacology; compare to Ipamorelin (selective GH without ghrelin-like appetite effects) |
| Cardioprotection research | Cardiac I/R injury; GHS-R1a cardiac expression; Akt/mTOR cardiomyocyte survival; GHRP-2 vs Hexarelin cardioprotective mechanism comparison | Cardiac GHS-R1a activation by GHRP-2 produces PI3K/Akt-mediated cardiomyocyte protection; studied alongside Hexarelin (GHS-R1a + CD36 dual) and BPC-157 (VEGFR2/NO repair) in combined cardiac protection panels |
| Anti-inflammatory / hepatoprotective | NF-κB inflammatory pathway; hepatocyte GHS-R1a; liver injury models; GHRP-2 cytoprotective effects independent of GH axis | GHS-R1a expressed on hepatocytes and immune cells; GHRP-2 reduces inflammatory cytokines and liver injury markers in preclinical models; GH-axis-independent cytoprotection; studied alongside BPC-157 and LIPO-C in hepatic protection research |
| Body composition and anabolism | GH-driven IGF-1 production; muscle protein synthesis; lean mass; adipose tissue lipolysis; bone metabolism; sarcopenia models | GHRP-2-stimulated GH → hepatic IGF-1 production → IGF-1R anabolic signalling cascade; studied alongside IGF-1 LR3 (direct IGF-1R activation) to compare GH-mediated endogenous IGF-1 vs direct IGF-1R activation as the driver of anabolic outcomes |
GHRP-2 Pharmacokinetics and Research Design
| Parameter | Value / Notes | Research Implication |
|---|---|---|
| Plasma half-life | ~30 minutes; D-amino acids provide metabolic stability; C-terminal amide prevents carboxypeptidase attack | GH peak occurs 15–45 min post-injection; measure plasma GH at 15, 30, 45, and 60 min post-dose to capture the full GH secretion peak; for chronic protocols dose 2–3× daily to maintain multiple GH pulses |
| Human GH stimulation dose | 2 µg/kg IV/SC (Pralmorelin test; Japan); 1–5 µg/kg range in published human studies; GH peak ~5–20 ng/mL depending on GH status | Human reference data available for direct allometric scaling to rodent doses; the 2 µg/kg Pralmorelin dose is the validated diagnostic standard — scale to equivalent rodent dose using body surface area scaling (multiply by ~10–12 for mouse, ~6–7 for rat) |
| Rodent SC dose | 50–300 µg/kg SC (published rodent GH stimulation and body composition studies); 100 µg/kg is a well-validated starting dose for acute GH release studies in rats | For acute GH release: single SC injection; collect blood at 0, 15, 30, 45, 60 min; measure plasma GH by ELISA; for body composition: 2× or 3× daily SC for 4–8 weeks; include vehicle and somatostatin-treated control groups |
| In-vitro concentration | 1–1000 nM for GHS-R1a cell-based assays; 10–100 nM for cAMP/Ca²⁺ flux assays; use 8-point dose response | Express GHS-R1a in HEK293 or CHO cells; measure cAMP accumulation (Gs component) and Ca²⁺ flux (Gq component) in the same assay to characterise dual coupling; compare to ghrelin (native ligand) and Ipamorelin (selective) as reference agonists |
| GHRP-2 + GHRH/CJC-1295 combination | Administer simultaneously (same injection); GH synergy measured 15–45 min post-dose; combination produces 5–10× GH release vs either agent alone | Include four arms in combination studies: vehicle; GHRP-2 alone; CJC-1295 alone; GHRP-2 + CJC-1295 combined; the expected synergy (combined > sum of individual arms) is the definitive test of mechanism; failure to see synergy indicates receptor occupation or downstream convergence issues |
| Reconstitution | Add BAC water to 2 mg/mL stock; dissolves readily; stable 14 days at 2–8°C; aliquot for multi-week protocols | Standard hexapeptide reconstitution; no special handling required; does not require nitrogen atmosphere or gentle warming like fatty acid-conjugated peptides |
GHRP-2 Quality Control at SourceTides
Every batch of GHRP-2 Peptide 10 mg from SourceTides undergoes these tests before release.
The D-amino acid configuration confirmation is the critical identity test unique to GHRP-2 — a preparation with L-amino acids at positions 1, 2, or 5 would be a completely different peptide with dramatically reduced GHS-R1a affinity.
| Test | Method | Specification | Why It Matters |
|---|---|---|---|
| Purity | RP-HPLC (C18; UV 220 nm) | ≥99% peak area purity | Separates GHRP-2 from synthesis by-products; ≥99% confirms the active D-amino acid hexapeptide dominates over L-amino acid diastereomers (which have lower GHS-R1a affinity) and deletion sequences |
| Identity + D-amino acid confirmation | ESI-MS ([M+H]⁺ = 818.43 Da); MS fragmentation pattern confirms D-βNal at position 2 | MW 817.94 Da confirmed; D-β-Naphthylalanine confirmed by characteristic MS₂ fragmentation; C-terminal amide (–NH₂) confirmed by −1 Da vs free acid form | The D-amino acids (D-Ala, D-βNal, D-Phe) cannot be distinguished from L-forms by MW alone — requires either chiral HPLC or MS fragmentation pattern; D-βNal is confirmed by the characteristic naphthyl fragment ion in MS₂ |
| Endotoxin | LAL chromogenic assay | <1 EU/mg | LPS activates NF-κB and inflammatory signalling in pituitary, hypothalamic, and cardiac cells — all primary GHS-R1a target cell types; endotoxin would confound GHRP-2 GH release, anti-inflammatory, and cardioprotective assays |
| Appearance | Visual inspection | White lyophilised powder; no discolouration or clumping | Discolouration may indicate Trp (Trp at position 4 is susceptible to oxidation) or naphthylalanine degradation; white powder confirms intact aromatic residues |
| Certificate of Analysis | Lot-specific PDF | HPLC + MS (817.94 Da; D-βNal confirmed; C-terminal amide confirmed) + endotoxin + dates | The D-βNal MS₂ fragment and C-terminal amide confirmation are the unique CoA elements for GHRP-2 distinguishing it from L-amino acid impurities that HPLC purity alone cannot resolve |
GHRP-2 Regulatory Status
| Jurisdiction | Status | Notes |
|---|---|---|
| Japan | Approved as Pralmorelin (GH stimulation test diagnostic agent); Kaken Pharmaceutical | The only jurisdiction with regulatory approval for GHRP-2 (as Pralmorelin) — specifically for GH deficiency diagnostic use (GH stimulation test). Not approved for therapeutic use. |
| USA (FDA) | Not FDA-approved; not DEA-controlled; research compound only | No FDA approval in any indication. Not a scheduled substance. SourceTides supplies research-grade for laboratory use only. |
| EU / UK / Australia / Canada | Not approved in any jurisdiction; not a controlled substance; research compound | No marketing authorisation. Not a controlled substance. Research laboratory access. See the SourceTides shipping policy. |
| WADA | WADA S2 PROHIBITED — at all times (in and out-of-competition) | Listed under S2 Peptide Hormones, Growth Factors, Related Substances, and Mimetics. Prohibited at all times regardless of route or dose. Verify at wada-ama.org. |
Peer-Reviewed References
| # | Citation | Link |
|---|---|---|
| 1 | Bowers CY et al. (1991). Structure-activity relationships of a synthetic hexapeptide that specifically releases growth hormone in vitro and in vivo. Endocrinology. 128(5):2027–2035. PMID: 1849573. [GHRP-2 original characterisation] | PubMed PMID: 1849573 |
| 2 | Howard AD et al. (1996). A receptor in pituitary and hypothalamus that functions in growth hormone release. Science. 273(5277):974–977. PMID: 8688086. [GHS-R1a cloning and characterisation; the receptor GHRP-2 activates] | PubMed PMID: 8688086 |
| 3 | Kojima M et al. (1999). Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 402(6762):656–660. PMID: 10604470. [Ghrelin discovery — endogenous ligand for the GHS-R1a that GHRP-2 activates; explains GHRP mechanism retroactively] | PubMed PMID: 10604470 |
| 4 | Korbonits M, Trainer PJ, Little JA et al. (1999). The effect of growth hormone secretagogues on the HPA axis in healthy adults. J Endocrinol. 162(3):441–446. PMID: 10467237. [Cortisol/ACTH elevation by GHRPs — distinguishes GHRP-2 from selective Ipamorelin] | PubMed PMID: 10467237 |
| 5 | Wikipedia: GHRP-2. CAS 158861-67-7; formula; sequence; mechanism; Pralmorelin clinical status. | Wikipedia: GHRP-2 |
Frequently Researched Alongside GHRP-2
These compounds are most commonly studied alongside GHRP-2 in GH axis, ghrelin receptor, body composition, and metabolic research:
- CJC-1295 — Long-acting GHRH analog; studied with GHRP-2 in the classic GH secretagogue combination protocol: CJC-1295 (GHRHR/cAMP arm) + GHRP-2 (GHS-R1a/Ca²⁺ arm) produces 5–10× synergistic GH release; the most researched GHRP + GHRH combination in GH axis biology
- Sermorelin 10 mg — Short-acting GHRH agonist; studied with GHRP-2 for acute GH axis synergy studies and pulsatile GH release characterisation; FDA-approved diagnostic precedent for GHRH pharmacology
- Ipamorelin 10 mg — Selective GHS-R1a agonist; the essential comparator for GHRP-2; studying both in identical GH assay systems directly measures how cortisol/prolactin co-stimulation (GHRP-2) vs selectivity (Ipamorelin) affects the full GH axis biology — the fundamental GHRP selectivity SAR experiment
- GHRP-6 — First-generation GHS-R1a agonist; studied alongside GHRP-2 to compare GH release potency (GHRP-2 superior) vs appetite stimulation (GHRP-6 superior) — the key pharmacological distinction that defines each compound’s research niche
- Hexarelin 5 mg — Most potent GHRP (GHS-R1a + CD36); studied with GHRP-2 in the full GHS-R1a potency comparison: Ipamorelin (selective) → GHRP-2 (standard) → Hexarelin (maximal) + cardioprotection via CD36
- MK-677 Ibutamoren — Oral non-peptide GHS-R1a agonist; studied alongside GHRP-2 to compare peptide vs non-peptide GHS-R1a pharmacology and oral vs SC bioavailability in chronic GH elevation protocols
- IGF-1 LR3 — Direct IGF-1R agonist; studied with GHRP-2 to compare indirect (GHRP-2 → GH → IGF-1 → IGF-1R) vs direct (IGF-1 LR3 → IGF-1R) anabolic signalling pathways — the fundamental question for dissecting GH vs IGF-1 axis contributions
- BPC-157 — Tissue repair; studied alongside GHRP-2 in combined cardioprotection and tissue repair protocols combining GHS-R1a cardiac protection (GHRP-2) and VEGFR2-mediated vascular repair (BPC-157)
- TB-500 (Thymosin Beta-4) — Actin repair; studied with GHRP-2 in muscle and tendon repair models combining GH-stimulated anabolism (GHRP-2) and structural cell migration repair (TB-500)
- Epithalon 10 mg — Khavinson telomere bioregulator; studied alongside GHRP-2 in ageing biology panels where GH axis restoration (GHRP-2) and cellular longevity (Epithalon) are combined endpoints
- NAD⁺ Injectable — Sirtuin substrate; studied with GHRP-2 in ageing and metabolic research where GH/IGF-1 axis activation (GHRP-2) and mitochondrial sirtuin activation (NAD⁺) provide complementary metabolic benefits
- LIPO-C Injectable — Hepatic lipotropic; studied alongside GHRP-2 in liver biology panels combining GHS-R1a hepatoprotective effects (GHRP-2) and lipotropic hepatic fat clearance (LIPO-C)
- AOD-9604 Peptide — hGH C-terminal fragment; direct adipocyte lipolysis; studied with GHRP-2 in body composition research combining GH secretagogue-driven systemic effects (GHRP-2) and direct adipocyte fat mobilisation (AOD-9604)
- BAC Water — Standard reconstitution vehicle for GHRP-2 and all GHS-R1a agonists; 0.9% benzyl alcohol supports multi-dose vials for multi-week dosing protocols
Frequently Asked Questions
You can buy GHRP-2 Peptide 10 mg (Pralmorelin; D-Ala-D-βNal-Ala-Trp-D-Phe-Lys-NH₂; CAS 158861-67-7) directly from SourceTides.
Every order includes a lot-specific Certificate of Analysis with the RP-HPLC chromatogram (≥99% purity), ESI-MS identity confirmation (MW 817.94 Da; D-βNal fragment confirmed; C-terminal amide confirmed), and LAL endotoxin result (<1 EU/mg).
All vials are lyophilised white powder and dispatched on dry-ice cold chain. Reconstitute in BAC water for multi-dose protocols. See the SourceTides shipping policy for dispatch details.
Both GHRP-2 and Ipamorelin are GHS-R1a (ghrelin receptor) agonists that stimulate GH release. The key difference is selectivity.
GHRP-2 activates GHS-R1a with the full, non-selective agonist profile of the GHRP family: it stimulates GH release, but also produces modest cortisol (via ACTH) and prolactin elevation, and has some appetite-stimulating activity through hypothalamic NPY/AgRP circuits. This is because GHRP-2 activates GHS-R1a broadly across all the tissues and circuits where the receptor is expressed.
Ipamorelin was specifically designed for selectivity. It activates GHS-R1a with sufficient selectivity to stimulate GH release without meaningful cortisol, ACTH, prolactin, or appetite effects at standard doses. This selectivity makes Ipamorelin the preferred tool when studying isolated GH axis effects, while GHRP-2 is preferred when studying the full spectrum of GHS-R1a biology — including its HPA axis, appetite, and cardiac interactions.
For research design: use GHRP-2 when you want to study the complete pharmacological output of GHS-R1a activation. Use Ipamorelin when you want selective GH release as an isolated endpoint without confounding HPA or appetite effects. SourceTides supplies both.
GHRP-2 and CJC-1295 act on different receptors in the same pituitary somatotroph cell through different second messenger systems — and those two systems produce synergistic rather than additive GH release when activated together.
CJC-1295 (like GHRH) activates the GHRH receptor, which couples to Gs and raises intracellular cAMP through adenylyl cyclase. cAMP/PKA signalling primes the somatotroph for GH secretion by phosphorylating targets that make the secretory vesicles ready to release.
GHRP-2 activates GHS-R1a, which couples to Gq/11 and raises intracellular Ca²⁺ through PLCβ/IP₃ signalling. Ca²⁺ is the actual trigger for secretory vesicle fusion and GH exocytosis.
The synergy is mechanistic: cAMP/PKA (CJC-1295) loads the secretory vesicles and primes the release machinery; Ca²⁺ (GHRP-2) triggers the actual release event. When both signals arrive together, both the quantity of vesicles ready to release and the release trigger are simultaneously maximised — producing 5–10× more GH than either signal alone can generate. This is a textbook example of pharmacological synergy through non-overlapping second messenger systems.
Pralmorelin is the International Nonproprietary Name (INN) for GHRP-2. They are the same molecule — D-Ala-D-βNal-Ala-Trp-D-Phe-Lys-NH₂; CAS 158861-67-7; MW 817.94 Da.
Pralmorelin was developed clinically by Kaken Pharmaceutical in Japan as a GH stimulation test agent for diagnosing GH deficiency. In Japan, the Pralmorelin stimulation test is approved as a diagnostic tool: a single SC or IV injection of 2 µg/kg Pralmorelin is administered, and peak plasma GH is measured over the next 60–90 minutes. A peak GH below the established cut-off value (approximately 9 ng/mL in adults) indicates GH deficiency.
This clinical development is significant for research because it provides published human pharmacokinetics, dose-response data, and safety data for GHRP-2 — something most research peptides lack. The Pralmorelin GH stimulation test methodology can be adapted for rodent GH axis assessment protocols, using allometric dose scaling from the 2 µg/kg human dose.
Yes. GHRP-2 is listed on the WADA Prohibited List under Category S2 — Peptide Hormones, Growth Factors, Related Substances, and Mimetics. This prohibition applies at all times (in-competition and out-of-competition) and covers all routes of administration and all doses.
All compounds in the GHRP family — GHRP-2, GHRP-6, Ipamorelin, Hexarelin, and related compounds — are included in the S2 category because they stimulate endogenous GH secretion, which is the same performance-enhancing mechanism as exogenous GH administration.
SourceTides supplies GHRP-2 for in-vitro laboratory research use only. The legitimate research applications — GHS-R1a pharmacology, GH axis biology, pulsatile GH secretion studies, Pralmorelin test replication — are all laboratory contexts with no connection to athletic competition. Verify current WADA status annually at wada-ama.org.
SourceTides accepts Visa, Mastercard, American Express, cryptocurrency, and bank transfers for institutional orders. All payments go through secure, encrypted gateways.
For institutional purchase orders, bulk research procurement, or custom quantities, contact the team via the SourceTides contact page. Orders are reviewed for research compliance before dispatch.
All SourceTides products, including GHRP-2 Peptide 10 mg (Pralmorelin; CAS 158861-67-7), are for in-vitro laboratory research use only.
GHRP-2 is WADA S2 Prohibited at all times.
It is not approved by the FDA, EMA, TGA, or Health Canada (approved in Japan as Pralmorelin diagnostic only).
It is not for human consumption.
By purchasing, the buyer confirms authorised researcher status and accepts responsibility for compliance with all applicable regulations.
| Weight | 0.01 lbs |
|---|---|
| Dimensions | 5 × 5 × 5 in |
| Purity | ≥99% HPLC, C-terminal amide confirmed, D-βNal (position 2) confirmed |
| Sequence | |
| Form | Lyophilised Powder (hexapeptide; CAS 158861-67-7) |
| Receptor |
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