GHRP-6 Peptide For Lab Research
£22.99
Login for member pricesBuy GHRP-6 UK — Research Grade Peptide
GHRP-6 is one of the most searched research peptides in the UK right now. Studied for its role in growth hormone secretion, ghrelin receptor activation pathways, and appetite regulation mechanisms at a cellular level, it remains a staple compound for UK laboratories exploring endocrine and metabolic-related scientific research.
For research use only. Not intended for human consumption.
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Product Description
GHRP-6 Peptide | Buy GHRP-6 UK | Growth Hormone Releasing Peptide-6 | Research Use Only
GHRP-6 (His-D-Trp-Ala-Trp-D-Phe-Lys-NH₂) is a synthetic hexapeptide and the original growth hormone releasing peptide — the founding member of the GHRP class, whose discovery in the early 1980s led directly to the identification of the ghrelin receptor (GHS-R1a) and the endogenous hormone ghrelin itself. It is studied in laboratory research for its dual GHS-R1a and CD36 receptor pharmacology, encompassing GH and IGF-1 secretion, cardioprotection, cytoprotection, wound healing, anti-fibrotic signalling, NPY neuron biology, and gastrointestinal motility — making it one of the most pharmacologically broad research peptides in the GHRP class. Buy GHRP-6 in the UK from Peptides Lab UK with >99% HPLC-verified purity, batch-specific COA, and fast UK dispatch for laboratory and in vitro research use only.
Distributed by Peptides Lab UK in a high-purity lyophilised format, for laboratory research use only. This compound is handled in controlled settings for in vitro and pre-clinical studies, with no applications in human or veterinary medicine. Each batch undergoes rigorous quality analysis to ensure >99% purity (HPLC verified).
What Is GHRP-6?
GHRP-6 is a synthetic hexapeptide with the sequence His-D-Trp-Ala-Trp-D-Phe-Lys-NH₂, first developed by Bowers et al. in the early 1980s as part of a systematic investigation into peptide analogues of met-enkephalin that retained GH-releasing activity without opioid activity. It was the first synthetic GH secretagogue to be characterised and has since become the reference compound of the GHRP class.
GHRP-6’s receptor was originally called the growth hormone secretagogue receptor (GHSR), but due to subsequent discoveries, the hormone ghrelin is now considered the receptor’s natural endogenous ligand — and the receptor has been renamed the ghrelin receptor. This reclassification underscores the historical significance of GHRP-6: its characterisation directly preceded and enabled the discovery of ghrelin as the endogenous ligand for the receptor it was found to activate.
GHRPs are endowed with the ability to bind two different receptors that mediate their cytoprotective and other pharmacological properties — GHS-R1a and CD36. GHS-R1a mediates GH secretion, positive inotropic cardiac effects, and NPY neuron activation; CD36 binding activates prosurvival pathways including PI-3K/AKT1, reduces reactive oxygen species spillover, enhances antioxidant defences, reduces inflammation, and confers anti-fibrotic effects via PPARγ upregulation and TGF-β downregulation.
As a research compound, GHRP-6 UK is the most extensively published founding GHRP in the scientific literature, with decades of peer-reviewed research spanning GH axis biology, cardiovascular science, wound healing, anti-fibrotic pharmacology, neuropeptide biology, gastrointestinal motility, and drug discovery. It is the reference peptide against which all subsequent GHRPs — including GHRP-2, Ipamorelin, and Hexarelin — have been characterised.
How Does GHRP-6 Work?
GHRP-6’s pharmacology is uniquely bifurcated across two receptor systems — the ghrelin receptor (GHS-R1a) and the CD36 scavenger receptor — each conferring distinct and independently meaningful biological activities.
GHS-R1a Receptor Activation — GH Axis Biology
GHRP-6 activates GHS-R1a via phospholipase C/diacylglycerol/PKC signalling, mobilising intracellular calcium in anterior pituitary somatotrophs to trigger GH vesicle fusion and exocytosis. GHRP-6 is a synthetic hexapeptide that releases GH both in vivo and in vitro, with evidence that this peptide acts as a functional somatostatin antagonist at the pituitary level — a mechanism that distinguishes it from the GHRH pathway and contributes to its synergistic GH-releasing effect when combined with GHRH analogues.
GHRH Co-Dependency for Maximal GH Release
Administration of a GHRH antagonist (400 µg/kg i.v.) before GHRP-6 (1 µg/kg i.v.) in healthy men virtually eliminated the GH response to GHRP-6 — reducing the maximal GH increase from 33.8 ± 4.8 to 6.2 ± 1.8 µg/L — demonstrating that endogenous GHRH is necessary for most of the GH response to GHRP-6 in humans. This confirms GHRP-6 functions as a GHRH-amplifier at the hypothalamic level as well as a direct pituitary GHS-R1a agonist.
CD36 Receptor Binding — Cytoprotective and Anti-Fibrotic Activity
GHRP-6’s binding to CD36 activates prosurvival pathways including PI-3K/AKT1, reducing cellular death. The main biological properties mediated through CD36 include: positive inotropic effects via Ca²⁺ influx through PLC/DAG/PKC and voltage-gated calcium channels; anti-fibrotic effects via PPARγ upregulation followed by TGF-β, CTGF, and PDGF downregulation; anti-inflammatory effects via NFκB blunting; and cell survival via PI-3K/AKT1 pathway activation and hypoxia-inducible factor-1 alpha (HIF-1α) induction.
NPY Neuron and IGF-1/Akt Pathway Activation
Chronic systemic administration of GHRP-6 to normal adult rats increases IGF-1 mRNA and phosphorylated Akt (pAkt) levels in various brain regions including the hypothalamus — with GHRP-6 specifically stimulating NPY and IGF-1 mRNA synthesis and activating Akt in neuropeptide Y neurons of the arcuate nucleus, suggesting that some of GHRP-6’s effects involve stimulation of local IGF-1 production and Akt activation in NPY neurons.
ACTH and Cortisol Co-Release — Key Research Distinction from Ipamorelin
In both healthy controls and patients with type 1 diabetes mellitus, GHRP-6 produces significant ACTH and cortisol co-release alongside GH stimulation — a pharmacological profile that distinguishes GHRP-6 from the selective GHS-R1a agonist Ipamorelin, which was specifically developed to eliminate these adrenal axis co-stimulations. This ACTH/cortisol co-release property makes GHRP-6 a valuable research tool for studying hypothalamic-pituitary-adrenal axis interactions with the ghrelin receptor system.
What Does GHRP-6 Do in Research?
In laboratory and pre-clinical settings, GHRP-6 has been studied across a broader range of biological systems than any other GHRP-class peptide. Research has examined its role in:
- GHS-R1a receptor binding, phospholipase C/calcium signalling, and GH vesicle exocytosis studies
- GH and IGF-1 axis stimulation and GHRH co-dependency pharmacology research
- ACTH and cortisol co-stimulation — HPA axis interaction with the ghrelin receptor system
- CD36 scavenger receptor binding, PI-3K/AKT1 prosurvival pathway activation
- Cardiac protection — ischaemia/reperfusion injury, dilated cardiomyopathy, and post-MI models
- Wound healing — closure kinetics, inflammatory cytokine suppression, and hypertrophic scar prevention
- Anti-fibrotic pathway research — PPARγ upregulation, TGF-β1 and CTGF suppression
- NPY neuron activation, arcuate nucleus IGF-1 mRNA upregulation, and hypothalamic Akt signalling
- Gastrointestinal motility research via GHS-R1a and motilin receptor interaction
- Atherosclerosis research via CD36 azapeptide analogue development
- GHRP-class reference compound for SAR studies — Ipamorelin, GHRP-2, and Hexarelin comparisons
GHRP-6 and Cardioprotection Research
GHRP-6 has proved to prevent and attenuate cardiac cell death and left ventricular failure in a variety of experimental scenarios. It activates GHS-R1a and CD36 receptors in cardiac tissue, with CD36 playing a key role in providing the myocardium with its major energy substrate, and agonistic CD36 binding protecting against myocardial damage and dysfunction by ischaemia/reperfusion — with mice deficient for CD36 showing complete loss of GHRP-6-mediated cardioprotection, confirming CD36 as an essential receptor for its cardiac effects.
GHRP-6 and Wound Healing Research
In excisional full-thickness wound models in Wistar rats, topical GHRP-6 at 400 µg/mL accelerated wound closure from the first 24 hours post-injury, significantly reduced proinflammatory and profibrogenic cytokines, and — in a rabbit ear hypertrophic scar model — dramatically reduced the onset of exuberant scarring by activating PPARγ and downregulating fibrogenic cytokines. CD36 was confirmed as abundantly expressed in wound granulation tissue, and RT-PCR data confirmed GHRP-6’s modulation of TGF-β1, CTGF, and PPARγ gene expression at the wound site.
GHRP-6 and Anti-Fibrotic Pathway Research
RT-PCR analysis of GHRP-6-treated wounds confirmed significant reduction of TGFB1 and CTGF expression (p < 0.05) alongside significant elevation of PPARγ expression (p = 0.016) — establishing a PPARγ-mediated antagonism of TGF-β1 signalling as a key mechanism of GHRP-6’s anti-fibrotic activity via CD36, and positioning this pathway as an innovative research target for controlling fibrotic disease.
GHRP-6 and Doxorubicin-Induced Cardiomyopathy Research
Research examining GHRP-6 co-administration with the chemotherapy agent doxorubicin found that GHRP-6 prevented the onset of dilated cardiomyopathy and heart failure alongside multiple organ damage, with sequential echocardiographic evaluation confirming preservation of cardiac contractility and structural myocardial integrity. Preservation of mitochondrial physiology and reduction of oxidative stress were identified as key contributing mechanisms.
GHRP-6 and Gastrointestinal Motility Research
Research confirmed that GHRP-6 enhances neural contractile responses in the rabbit gastric antrum partly through interaction with the motilin receptor on noncholinergic nerves — with tachykinins as the downstream mediator — and partly via a GHS-R subtype on cholinergic nerves. These findings distinguish GHRP-6 from ghrelin, which was found unable to induce contractions via the motilin receptor, and position GHRP-6 as a uniquely valuable research tool for studying the GI motility-ghrelin receptor interface.
GHRP-6 and CD36 Drug Discovery Research
The identification of GHRP-6 as a CD36 ligand has spawned an extensive azapeptide analogue medicinal chemistry programme, producing selective CD36 modulators that reduce macrophage-driven inflammation, mitigate atherosclerosis, inhibit pathological neovascularisation, and protect against ischaemia/reperfusion cardiac injury — with GHRP-6 serving as the foundational pharmacophore scaffold for this research direction.
What Do Studies Say About GHRP-6?
GHRP-6 has one of the most extensive published research profiles of any synthetic peptide in the GH secretagogue class, with peer-reviewed literature spanning more than four decades.
GHRP-6 as the Discovery Peptide for the Ghrelin Receptor
GHRP-6 holds unique historical significance as the synthetic peptide whose characterisation led directly to the identification of the GHS receptor — subsequently renamed the ghrelin receptor upon discovery of its endogenous ligand. This places GHRP-6 at the origin of an entire field of neuroendocrinology and positions it as an irreplaceable reference compound in any research programme studying GHS-R1a biology.
GHRP-6 and the HPA Axis Research Profile
Studies comparing ghrelin, GHRP-6, and GHRH in patients with type 1 diabetes confirmed that GHRP-6 produces ACTH and cortisol release alongside GH stimulation — a profile shared with ghrelin but absent from Ipamorelin — establishing GHRP-6 as the appropriate research tool when HPA axis co-stimulation alongside GHS-R1a activation is the experimental objective, and confirming that the selective GHRP profile introduced by Ipamorelin represents a deliberate pharmacological refinement from the GHRP-6 reference.
GHRP-6 and the GHRH Co-Dependency Research Model
The definitive study establishing GHRP-6’s dependence on endogenous GHRH for maximal GH release found that a GHRH receptor antagonist eliminated 82% of the GH response to GHRP-6 — reducing AUC from 1701 ± 278 to 376 ± 113 µg·min/L. This finding established GHRP-6’s dual hypothalamic-pituitary mechanism — acting both as a direct pituitary GHS-R1a agonist and as an indirect promoter of hypothalamic GHRH release — a mechanistic insight that informed the scientific rationale for GHRH + GHRP combination research models.
GHRP-6 Cytoprotective Evidence Base
A comprehensive review of the peer-reviewed literature from 1980 onwards concluded that GHRPs — with GHRP-6 as the founding and most extensively studied member — exhibit cytoprotective abilities across cardiac, neuronal, gastrointestinal, and hepatic cells through their dual GHS-R1a and CD36 pharmacology, and that the GHRP family represents a class of compounds with broad prosurvival, anti-inflammatory, and anti-fibrotic properties that remain an unmet clinical niche despite a robust pre-clinical evidence base.
GHRP-6 as Foundational Pharmacophore for CD36 Drug Discovery
The CD36 scavenger receptor binds GHRP-6 and its analogues at the lysine-rich domain, with azapeptide GHRP-6 derivatives showing CD36 binding affinities in the 1–2 µM range. This binding mediates anti-angiogenic, anti-atherosclerotic, and cardioprotective activities that are not dependent on GHS-R1a, establishing GHRP-6 as the structural scaffold for an entirely separate and emerging drug discovery programme focused on CD36 biology.
Key cited studies:
- Bowers CY et al. (1984) — On the In Vitro and In Vivo Activity of a New Synthetic Hexapeptide That Acts on the Pituitary to Specifically Release Growth Hormone — Endocrinology 114(5):1537–1545. DOI: 10.1210/endo-114-5-1537
- Pandya N et al. (1998) — GHRH is Required for Most of the GH Response to GHRP-6 in Humans — J Clin Endocrinol Metab 83(2):401–405. PubMed ID: 9543138
- Berlanga-Acosta J et al. (2017) — Synthetic Growth Hormone-Releasing Peptides: A Historical Appraisal of Cytoprotective Effects — PMC5392015
- Mendoza Marí Y et al. (2016) — GHRP-6 Enhances Wound Healing and Reduces Hypertrophic Scarring — Plast Surg Int. PMC4854984
- Berlanga-Acosta J et al. (2024) — GHRP-6 Prevents Doxorubicin-Induced Myocardial and Extra-Myocardial Damage — Front Pharmacol. DOI: 10.3389/fphar.2024.1402138
- Garcia-Ojalvo A et al. (2005) — GHRP-6 Increases IGF-1 mRNA and Activates Akt in NPY Neurons of the Hypothalamus — PubMed ID: 16218998
- Deghenghi R et al. (2001) — GHRP-6 Interacts with the Motilin Receptor in the Rabbit Gastric Antrum — PubMed ID: 12606621
- Proulx C et al. (2020) — Azapeptide Modulators of CD36 for Atherosclerosis and Cardioprotection — PMC7432381
GHRP-6 vs Other GHS-R1a Research Peptides
| Feature | GHRP-6 | Ipamorelin | GHRP-2 | Hexarelin |
|---|---|---|---|---|
| Sequence | His-D-Trp-Ala-Trp-D-Phe-Lys-NH₂ (6aa) | Aib-His-D-2-Nal-D-Phe-Lys-NH₂ (5aa) | D-Ala-D-βNal-Ala-Trp-D-Phe-Lys-NH₂ (6aa) | His-D-2-MeTrp-Ala-Trp-D-Phe-Lys-NH₂ (6aa) |
| GHS-R1a Activity | Potent | Potent (most selective) | More potent than GHRP-6 | More potent than GHRP-6 |
| CD36 Binding | Yes (confirmed) | Not established | Yes (confirmed) | Yes (confirmed) |
| ACTH/Cortisol Release | Yes (significant) | No (selective GH only) | Yes (significant) | Yes (significant) |
| GHRH Co-Dependency | Yes (82% of GH response) | Partial | Partial | Partial |
| GI Motility Research | Yes (motilin receptor interaction) | Not established | Limited | Limited |
| Cardioprotection Research | Extensive | None | Moderate | Extensive |
| Wound Healing Research | Published (PPARγ/TGF-β) | None | None | None |
| CD36 Drug Discovery | Primary scaffold | None | Secondary | Secondary |
| Historical Significance | Discovery peptide (led to ghrelin) | First selective GHRP | More potent GHRP-6 derivative | Most potent classic GHRP |
GHRP-6’s combination of GHS-R1a and CD36 dual-receptor pharmacology, extensive cytoprotective evidence base, foundational historical role in ghrelin receptor discovery, and position as the structural scaffold for CD36 drug discovery makes it an irreplaceable research tool that occupies a uniquely broad niche within the GHRP class — one that neither the more selective Ipamorelin nor the more potent GHRP-2 or Hexarelin can fully replicate.
Quality & Purity Assurance
Every batch of GHRP-6 from Peptides Lab UK is:
- >99% pure — HPLC and mass spectrometry verified
- Supplied with a full Certificate of Analysis (COA) on request
- Lyophilised powder for maximum stability and long shelf life
- Manufactured under strict, controlled laboratory conditions
- Consistent batch-to-batch quality for reproducible research results
Buy GHRP-6 UK — Product Specifications
| Property | Detail |
|---|---|
| Full Name | Growth Hormone Releasing Peptide-6 |
| Sequence | His-D-Trp-Ala-Trp-D-Phe-Lys-NH₂ |
| Amino Acids | 6 |
| Molecular Weight | 873.03 g/mol |
| Molecular Formula | C₄₆H₅₆N₁₂O₆ |
| Receptor Targets | GHS-R1a (primary) + CD36 (secondary) |
| Purity | >99% (HPLC verified) |
| Form | Lyophilised powder |
| Storage | Store dry at -20°C; protect from light |
| Solubility | Bacteriostatic water, sterile water, or suitable laboratory solvents |
GHRP-6 Research Applications
GHRP-6 peptide UK is supplied strictly for the following in vitro and pre-clinical research uses:
- GHS-R1a receptor binding, phospholipase C/calcium signalling, and GH vesicle exocytosis studies
- GH and IGF-1 axis stimulation, GHRH co-dependency pharmacology, and HPA axis interaction research
- ACTH and cortisol co-stimulation — hypothalamic-pituitary-adrenal axis interaction with ghrelin receptor
- CD36 scavenger receptor binding, PI-3K/AKT1 prosurvival pathway activation studies
- Cardiac protection — ischaemia/reperfusion injury, dilated cardiomyopathy, post-MI and doxorubicin models
- Wound healing — closure kinetics, inflammatory cytokine suppression, hypertrophic scar prevention
- Anti-fibrotic pathway research — PPARγ upregulation, TGF-β1 and CTGF transcriptional suppression
- NPY neuron activation, arcuate nucleus IGF-1 mRNA upregulation, and hypothalamic Akt signalling
- GI motility research — GHS-R1a and motilin receptor co-stimulation in gastric tissue models
- Atherosclerosis and macrophage biology — CD36 azapeptide scaffold SAR investigations
- GHRP class reference compound — comparative pharmacology with Ipamorelin, GHRP-2, and Hexarelin
Why Buy GHRP-6 from Peptides Lab UK?
Peptides Lab UK is a trusted UK peptides supplier, providing research-grade compounds verified by independent HPLC testing. When you buy GHRP-6 in the UK from us, you receive:
- >99% purity, HPLC and MS verified, third-party tested
- Full COA documentation per batch
- Fast same-day UK dispatch with tracked delivery
- Competitive pricing with bulk research discounts available
- Trusted by researchers across the UK and Europe
Whether you’re searching for GHRP-6 peptide UK, buy GHRP-6 UK, growth hormone releasing peptide-6 UK, GHS-R1a agonist UK, ghrelin receptor peptide UK, CD36 peptide UK, UK peptides, peptides UK, research peptides UK, buy GHRP peptide UK, or growth hormone secretagogue UK, Peptides Lab UK is your dedicated UK-based supplier for laboratory-grade research peptides.
Research Disclaimer All products supplied by Peptides Lab UK are intended strictly for in vitro laboratory research and scientific study use only. They are not intended for human consumption, veterinary use, or any medical or therapeutic application. GHRP-6 is not a licensed medicine or drug and has not been approved by the MHRA, FDA, or any regulatory authority for use in humans or animals. GHRP-6, as a growth hormone secretagogue, is classified as a prohibited substance under WADA regulations and is not approved for use in sport or competition. All research citations on this page relate to pre-clinical studies and peer-reviewed pharmacological research and do not constitute a claim of safety or therapeutic efficacy. Peptides Lab UK accepts no liability for any misuse of research compounds. By purchasing, you confirm that you are a qualified researcher and that the product will be used solely within a controlled laboratory environment in compliance with all applicable UK laws, regulations, and institutional guidelines.









