Hexapeptide GHSR-1a + CD36 Agonist (Ghrelin Mimetic, GHRP Class)

Hexarelin

Also Known As: Examorelin, EP-23905, MF-6003, MFL-0277

Hexarelin is a synthetic hexapeptide (His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH₂; INN examorelin) developed by Romano Deghenghi and colleagues at Mediolanum Farmaceutici (Milan) in the early 1990s as a metabolically stabilised analogue of GHRP-6 — the substitution Trp²→2-methyl-D-Trp confers resistance to proteolytic degradation and yields higher GH-releasing potency than the parent compound (Deghenghi 1994). Mechanistically, hexarelin acts at the growth-hormone-secretagogue receptor type 1a (GHSR-1a) — the ghrelin receptor — on hypothalamic and pituitary neurons, evoking pulsatile GH release that is approximately twofold higher than equimolar GHRH after 1 µg·kg⁻¹ i.v. (Ghigo 1994). The mechanistic feature that most clearly distinguishes hexarelin from selective ghrelin mimetics like ipamorelin is its additional binding to the cardiac scavenger receptor CD36 on cardiomyocytes and macrophages: in CD36-knockout hearts, hexarelin-induced changes in coronary perfusion pressure are abolished while GHSR-1a-mediated GH release is preserved (Bodart 2002). The human Phase I/II data show a prompt LVEF increase without changes in mean blood pressure or heart rate (Bisi 1999; Broglio 2002; Imazio 2002). Within the broader GH-secretagogue family, ipamorelin is markedly more selective at GHSR-1a (no CD36 binding, minimal cortisol/prolactin release), GHRP-2 and GHRP-6 are closer family members but lack the CD36 affinity of hexarelin, and CJC-1295/sermorelin/tesamorelin act at a different receptor entirely (GHRHR, not GHSR-1a). Mediolanum branded development ended in Phase II (1994–2004) for commercial reasons; hexarelin is NOT approved by the FDA, EMA, or any other regulatory agency. In sport it is named explicitly on the WADA Prohibited List 2026 under section S2.2.4 (Growth Hormone Releasing Factors) as "examorelin (hexarelin)". Wellness-market claims of sustained "anti-aging" GH elevation are NOT supported by the evidence: Klinger 1996 and follow-on studies show GHSR-1a desensitisation with a ~50–75 % drop in AUC-GH within 4–16 weeks of daily dosing, partially reversible after washout. All pivotal hexarelin studies date from 1994–2004 and therefore predate the FDAAA 2007 registration mandate — a ClinicalTrials.gov v2 API query on 2026-05-01 returned zero hits for "hexarelin" or "examorelin", which is expected.

Identity & Chemistry

Two-dimensional chemical structure of hexarelin (His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH₂), a synthetic hexapeptide growth-hormone secretagogue and ghrelin-receptor agonist with C-terminal amide.
Image credit: Meodipt (2015), via Wikimedia Commons · Public Domain
Amino Acid Sequence
H-His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH₂ — six residues, C-terminal lysinamide. Position 2 is the non-proteinogenic 2-methyl-D-tryptophan, the structural feature that confers metabolic stability and increased GH-releasing potency over the parent GHRP-6. The free base is C₄₇H₅₈N₁₂O₆ (887.04 g·mol⁻¹, CAS 140703-51-1); most research-grade material is supplied as the acetate salt.
Molecular Formula
C₄₇H₅₈N₁₂O₆ (free base; PubChem CID 6918297)
Molecular Weight
887.04 g·mol⁻¹ (free base; the acetate salt commonly supplied for research adds ~60 Da per acetate counter-ion)
CAS Number
140703-51-1 (free base)
PubChem CID
6918297
IUPAC Name
L-Histidyl-2-methyl-D-tryptophyl-L-alanyl-L-tryptophyl-D-phenylalanyl-L-lysinamide. Hexarelin (INN/USAN examorelin) has no canonical DrugBank approved-drug monograph as of May 2026; UNII 09QF37C617; IUPHAR/BPS Guide to Pharmacology ligand 1100; ChEMBL CHEMBL108335.
Solubility
Water-soluble as the acetate salt; commonly reconstituted in bacteriostatic or sterile water for parenteral research administration. Subcutaneous bioavailability ~77 %, intranasal ~5 %, oral ~0.3 % (Ghigo 1994).
Storage
Lyophilised peptide: store at −20 °C, sealed and protected from light. Reconstituted aliquots: 2–8 °C for short-term (days) use; −20 °C for longer-term storage. Avoid repeated freeze-thaw cycles.

Mechanism of Action

Hexarelin is a synthetic hexapeptide and ghrelin mimetic whose primary action is agonism of the growth-hormone-secretagogue receptor type 1a (GHSR-1a) on hypothalamic and pituitary neurons, evoking pulsatile growth-hormone release. Distinctively among GHRPs, hexarelin also binds the cardiac scavenger receptor CD36 on cardiomyocytes and macrophages, producing direct cardiotropic effects that are independent of GH release (Bodart 2002).

Hexarelin (His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH₂) was designed by Deghenghi and colleagues as a metabolically stabilised analogue of GHRP-6, with the Trp²→2-methyl-D-Trp substitution conferring resistance to proteolytic degradation and yielding higher GH-releasing potency than the parent peptide (Deghenghi 1994; Imbimbo 1994). Acting at GHSR-1a — the same receptor as endogenous ghrelin — hexarelin produces a discrete, pulsatile GH secretory response that, at 1 µg·kg⁻¹ i.v., is approximately twice as large as that produced by equimolar GHRH and remains synergistic with GHRH co-administration (Ghigo 1994). The plasma half-life is approximately 55 minutes, with subcutaneous bioavailability ~77 %, intranasal ~5 %, and oral ~0.3 % (Ghigo 1994). The mechanistic feature that most clearly distinguishes hexarelin from selective ghrelin mimetics like ipamorelin is its binding to CD36 on cardiomyocytes and macrophages: in CD36-knockout hearts, hexarelin-induced changes in coronary perfusion pressure are abolished while GHSR-1a-mediated GH release is preserved (Bodart 2002). This GH-independent cardiac branch underlies the inotropic and anti-fibrotic findings observed in human and rodent ischaemia studies and is the basis on which hexarelin has been investigated as a candidate cardioprotective agent rather than purely as a GH secretagogue (Mao 2014; McDonald 2018). Among other GH secretagogues in the broader Triscience portfolio, ipamorelin is markedly more selective at GHSR-1a (no CD36 binding, minimal cortisol/prolactin release); GHRP-2 and GHRP-6 are closer family members but lack the CD36 affinity profile of hexarelin; and CJC-1295 acts at a different receptor entirely (GHRHR, not GHSR-1a).

Molecular Targets

  • GHSR-1a (growth-hormone-secretagogue receptor type 1a; UniProt Q92847) — the ghrelin receptor; class A G-protein-coupled receptor; primary mediator of GH release from pituitary somatotrophs
  • CD36 (scavenger receptor B-2 / fatty-acid translocase) — cardiac off-target receptor for hexarelin; binding overlaps the oxidised-LDL site with Met-169 implicated as a contact residue; in CD36-knockout hearts the cardiac effects are abolished
  • No meaningful agonism at the GHRH receptor (GHRHR) — mechanistically distinct from sermorelin, tesamorelin, and CJC-1295

Signaling Pathways

  • GHSR-1a → Gαq/11 → phospholipase C → IP₃ + DAG → ↑ intracellular Ca²⁺ and PKC → GH exocytosis from somatotroph secretory granules plus orexigenic and corticotrophic effects on hypothalamic circuits
  • CD36 (cardiac, GH-independent) → PI3K/Akt and ERK1/2 pro-survival cascades → PPARγ-linked anti-inflammatory programmes in cardiomyocytes
  • Downstream pituitary axis: GH → hepatic IGF-1; ancillary mild ACTH/cortisol and prolactin release at higher doses (Massoud 1996)
  • Systemic outcome: transient GH pulse with positive inotropic effect on the left ventricle (acute LVEF increase) without change in mean arterial pressure or heart rate (Bisi 1999; Broglio 2002)

Research Applications

Hexarelin has been studied in a foundational pharmacology paper (Deghenghi 1994), Phase I PK/PD work on bioavailability and hormone profile (Imbimbo 1994; Ghigo 1994; Massoud 1996), one longitudinal paediatric pharmacology study (Klinger 1996), three human cardiovascular studies (Bisi 1999; Imazio 2002; Broglio 2002), the canonical CD36 mechanistic paper (Bodart 2002), a contemporary review (Mao 2014), and a preclinical post-MI study (McDonald 2018). All findings are reported as investigational and for research use only.

Acute GH-releasing pharmacology in healthy adults — multiple administration routes (Ghigo 1994)

Phase I

Studies report, in an open-label PK/PD study in N=12 healthy young male volunteers, that GH release after 1 µg·kg⁻¹ i.v. hexarelin was approximately twice that produced by 1 µg·kg⁻¹ GHRH. Bioavailability: subcutaneous 77.0 ± 10.5 %, intranasal 4.8 ± 0.9 %, oral 0.3 ± 0.1 %; plasma half-life ≈ 55 min.

— Ghigo et al., J Clin Endocrinol Metab 1994;78(3):693–698 (PMID 8126144)

Dose-response of GH, prolactin, and cortisol (Massoud 1996)

Phase I

Studies report, in a dose-response pharmacological study in healthy adult males (hexarelin 0–1.0 µg·kg⁻¹ i.v.), maximum GH release plateauing at ~140 mU·L⁻¹ (ED₅₀ ≈ 0.48 µg·kg⁻¹), prolactin rising up to 180 % above baseline (ED₅₀ ≈ 0.39 µg·kg⁻¹), and cortisol increasing ~40 % at 0.5 µg·kg⁻¹ — quantitatively higher than ipamorelin. Combination of low-dose hexarelin (0.125 µg·kg⁻¹) with GHRH produced massive GH release (~115 mU·L⁻¹) with minimal cortisol elevation.

— Massoud et al., J Clin Endocrinol Metab 1996;81(12):4338–4341 (PMID 8954038)

Acute cardiac inotropic effect in healthy humans (Bisi 1999)

Phase I

Studies report, in a cross-over hormonal/cardiovascular study in N=7 healthy male volunteers using radionuclide angiocardiography, an LVEF increase from 64.0 ± 1.5 % to 70.7 ± 3.0 % (P < 0.03) after i.v. hexarelin, peaking at 30 min and persisting ~60 min, WITHOUT significant change in mean blood pressure or heart rate. Recombinant human GH (rhGH) produced NO comparable inotropic change despite similar GH elevation — supporting a GH-independent myocardial action (later attributed to CD36).

— Bisi et al., J Endocrinol Invest 1999;22(4):266–272 (PMID 10342360)

CD36 as the molecular cardiac receptor — knockout pharmacology (Bodart 2002)

preclinical

Studies report, in a receptor-identification experiment in isolated rat heart preparations, that hexarelin produced a dose-dependent rise in coronary perfusion pressure in wild-type hearts; the response was ABOLISHED in CD36-deficient hearts despite preserved GHSR-1a expression — establishing CD36 as the cardiac receptor for hexarelin and other GHRPs.

— Bodart et al., Circ Res 2002;90(8):844–849 (PMID 11988484)

Cardiac performance in coronary-artery-disease patients (Broglio 2002)

Phase II

Studies report, in an open-label intra-operative pharmacological study during coronary artery bypass surgery in N=24 male CAD patients (mean age 59.5 yr), a prompt rise in LVEF, cardiac index, and cardiac output (all P < 0.001) within 10 min of i.v. hexarelin, lasting up to 90 min, WITHOUT changes in left-ventricular end-diastolic volume or systemic vascular resistance. Neither rhGH nor GHRH reproduced these haemodynamic improvements — consistent with a non-GH cardiac mechanism.

— Broglio et al., Eur J Pharmacol 2002;448(2-3):193–200 (PMID 12144941)

Cardiotropic activity in left-ventricular dysfunction (Imazio 2002)

Phase II

Studies report, in a comparative open-label cardiotropic study in N=13 patients (8 dilated + 5 ischaemic cardiomyopathy) given single-dose i.v. hexarelin, that LVEF rose in ischaemic-cardiomyopathy patients but NOT in dilated-cardiomyopathy patients — despite a comparable hexarelin-induced GH rise in both groups. The inotropic effect appears to require viable myocardium capable of responding to direct CD36/GHSR-mediated cardiotropic signalling.

— Imazio et al., Eur J Heart Fail 2002;4(2):185–191 (PMID 11959048)

GHSR-1a desensitisation under long-term dosing (Klinger 1996)

observational

Studies report, in an open-label longitudinal pharmacology study in N=7 prepubertal short children (mean age 7.6 yr) on intranasal hexarelin 60 µg·kg⁻¹ three times daily for 6–10 months, that the peak GH dropped from 70.6 mU·L⁻¹ at baseline to 34.1 mU·L⁻¹ after 7 days (~50 % attenuation), then plateaued — confirming receptor desensitisation. Despite biochemical tolerance, growth velocity rose from 5.3 ± 0.9 cm·yr⁻¹ pre-treatment to 7.4 ± 1.6 cm·yr⁻¹ at 6–10 months. Follow-on studies show ~50–75 % AUC-GH attenuation over 4–16 weeks of daily dosing, partially reversible after washout — wellness-market claims of sustained "anti-aging" elevation are NOT supported by this evidence.

— Klinger et al., Eur J Endocrinol 1996;134(6):716–719 (PMID 8766941)

Clinical Status

Regulatory Status
NOT approved by the FDA, EMA, Health Canada, or any other major regulatory agency. Originator and sole development sponsor was Mediolanum Farmaceutici (Milan, Italy) under the codes EP-23905, MF-6003, and MFL-0277. Highest verified clinical phase: Phase II — paediatric and adult GH-deficiency cohorts and exploratory cardiac cohorts in Italy, Israel, and Canada (1994–2004). The programme was discontinued for commercial / strategic reasons; no public regulatory action for safety or efficacy concerns is documented. ClinicalTrials.gov status: all pivotal hexarelin trials date from 1994–2004 and therefore predate the FDAAA 2007 registration mandate as well as the ICMJE 2005 registration requirement; a v2 API query on 2026-05-01 returned zero hits for "hexarelin" and "examorelin" — this matches the registry-gap pattern also applied to sermorelin, hCG, and gonadorelin, and is NOT a data-quality concern. Sport: prohibited under the WADA Prohibited List 2026, named explicitly under section S2.2.4 ("Growth Hormone Releasing Factors") as "examorelin (hexarelin)" — both in- and out-of-competition. Material from research-chemical suppliers (Sigma-Aldrich, Cayman, Bachem) is not regulatory approval and not a Triscience endorsement.
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Highest Trial Phase
Phase II (Mediolanum programme; 1994–2004; discontinued for commercial reasons)
Sponsor
Originator and sole development sponsor: Mediolanum Farmaceutici (Milan, Italy); discovery and early development by R. Deghenghi and colleagues (early 1990s). Development codes EP-23905, MF-6003, and MFL-0277.

Safety Profile

Observed in research settings

Across published Phase I/II studies in healthy volunteers, paediatric short-stature cohorts, and adult cardiac-disease cohorts, hexarelin has been reported as generally well tolerated at single research doses (typically 1–2 µg·kg⁻¹ i.v. or 20–60 µg·kg⁻¹ intranasal); the most consistent findings are mild, transient, and dose-dependent (Ghigo 1994; Massoud 1996; Bisi 1999). No serious adverse events were attributed to hexarelin in the published Phase I/II programmes; however, the cumulative human exposure base remains small.

Adverse Events Reported in Studies

  • Facial flushing / sensation of warmth at injection — reported in ~10–20 % of i.v. bolus subjects; transient (<10 min)
  • Mild hunger / appetite increase — fewer than with GHRP-6 in head-to-head observations
  • Injection-site reactions (subcutaneous administration)
  • Transient prolactin elevation (up to ~180 % above baseline at ED ≈ 0.4 µg·kg⁻¹; Massoud 1996)
  • Transient ACTH/cortisol elevation (~40 % rise at 0.5 µg·kg⁻¹) — more pronounced than ipamorelin or low-dose GHRP-2 (Massoud 1996; Bisi 1999)

Serious Adverse Events

  • GHSR-1a desensitisation with chronic dosing — peak GH response halved within ~7 days of intranasal t.i.d. dosing in children and progressively declined to ~45–55 % of baseline AUC-GH over 4–16 weeks of daily dosing in adults; partially reversible after washout (Klinger 1996)
  • Sleep architecture changes — hexarelin during sleep decreased slow-wave sleep while raising GH/ACTH/cortisol/prolactin nocturnally (PMID 15177700)
  • Theoretical concern: preclinical CD36-mediated coronary-perfusion-pressure increase has been hypothesised to contribute to coronary vasospasm in atherosclerotic vasculature; clinical relevance not established (Bodart 2002)
  • No long-term (multi-year) RCT safety data in humans exist — wellness-vendor claims of sustained anabolic or anti-aging benefit are NOT supported by the published evidence; the combination of cortisol/prolactin/ACTH elevation with chronic dosing is a theoretical neuroendocrine concern and a key differentiator from selective ghrelin mimetics like ipamorelin
  • Anti-doping liability: hexarelin is named explicitly on the WADA Prohibited List 2026 under S2.2.4 (Growth Hormone Releasing Factors) as "examorelin (hexarelin)" — both in- and out-of-competition

References

  1. Deghenghi R, Cananzi MM, Torsello A, Battisti C, Müller EE, Locatelli V GH-releasing activity of hexarelin, a new growth hormone releasing peptide, in infant and adult rats. Life Sci 1994;54(18):1321–1328. 1994 .

    DOI: 10.1016/0024-3205(94)00510-9 PMID: 8190001 View Source

  2. Imbimbo BP, Mant T, Edwards M, Amin D, Dalton N, Boutignon F, Lenaerts V, Wüthrich P, Deghenghi R Growth hormone-releasing activity of hexarelin in humans. A dose-response study. Eur J Clin Pharmacol 1994;46(5):421–425. 1994 .

    DOI: 10.1007/BF00191904 PMID: 7957535 View Source

  3. Ghigo E, Arvat E, Gianotti L, Imbimbo BP, Lenaerts V, Deghenghi R, Camanni F Growth hormone-releasing activity of hexarelin, a new synthetic hexapeptide, after intravenous, subcutaneous, intranasal, and oral administration in man. J Clin Endocrinol Metab 1994;78(3):693–698. 1994 .

    DOI: 10.1210/jcem.78.3.8126144 PMID: 8126144 View Source

  4. Massoud AF, Hindmarsh PC, Brook CG Hexarelin-induced growth hormone, cortisol, and prolactin release: a dose-response study. J Clin Endocrinol Metab 1996;81(12):4338–4341. 1996 .

    DOI: 10.1210/jcem.81.12.8954038 PMID: 8954038 View Source

  5. Klinger B, Silbergeld A, Deghenghi R, Frenkel J, Laron Z Desensitization from long-term intranasal treatment with hexarelin does not interfere with the biological effects of this growth hormone-releasing peptide in short children. Eur J Endocrinol 1996;134(6):716–719. 1996 .

    DOI: 10.1530/eje.0.1340716 PMID: 8766941 View Source

  6. Bisi G, Podio V, Valetto MR, Broglio F, Bertuccio G, Aimaretti G, Pelosi E, Del Rio G, Muccioli G, Ong H, Boghen MF, Deghenghi R, Ghigo E Acute cardiovascular and hormonal effects of GH and hexarelin, a synthetic GH-releasing peptide, in humans. J Endocrinol Invest 1999;22(4):266–272. 1999 .

    DOI: 10.1007/BF03343555 PMID: 10342360 View Source

  7. Bodart V, Febbraio M, Demers A, McNicoll N, Pohankova P, Perreault A, Sejlitz T, Escher E, Silverstein RL, Lamontagne D, Ong H CD36 mediates the cardiovascular action of growth hormone-releasing peptides in the heart. Circ Res 2002;90(8):844–849. 2002 .

    DOI: 10.1161/01.RES.0000016164.02525.B4 PMID: 11988484 View Source

  8. Imazio M, Bobbio M, Broglio F, Benso A, Podio V, Valetto MR, Bisi G, Ghigo E, Trevi GP GH-independent cardiotropic activities of hexarelin in patients with severe left ventricular dysfunction due to dilated and ischemic cardiomyopathy. Eur J Heart Fail 2002;4(2):185–191. 2002 .

    DOI: 10.1016/S1388-9842(01)00223-9 PMID: 11959048 View Source

  9. Mao Y, Tokudome T, Kishimoto I The cardiovascular action of hexarelin. J Geriatr Cardiol 2014;11(3):253–258. 2014 .

    DOI: 10.11909/j.issn.1671-5411.2014.03.007 PMID: 25278975 View Source

  10. McDonald H, Peart J, Kurniawan ND, Galloway G, Royce SG, Samuel CS, Chen C Hexarelin treatment preserves myocardial function and reduces cardiac fibrosis in a mouse model of acute myocardial infarction. Physiol Rep 2018;6(9):e13699. 2018 .

    DOI: 10.14814/phy2.13699 PMID: 29726120 View Source

  11. PubChem Examorelin (Hexarelin), CID 6918297 — molecular formula C₄₇H₅₈N₁₂O₆; average mass 887.04; UNII 09QF37C617. Note: PubChem CID 3035995 resolves to a sapogenin glycoside (C₄₂H₇₀O₁₂) and is NOT hexarelin. National Library of Medicine, PubChem record. 2026 .

    View Source

  12. World Anti-Doping Agency The 2026 Prohibited List — International Standard. Section S2.2.4 (growth-hormone secretagogues and their mimetics) names "examorelin (hexarelin)" explicitly alongside GHRP-1 through GHRP-6 and alexamorelin. WADA, effective 1 January 2026. 2026 .

    View Source

Frequently Asked Questions

What is hexarelin?
Hexarelin is a synthetic six-amino-acid peptide (His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH₂; INN examorelin) developed by Mediolanum Farmaceutici in the early 1990s as a metabolically stabilised analogue of GHRP-6. It is a growth-hormone secretagogue that acts at the ghrelin receptor (GHSR-1a) and, distinctively, also at the cardiac scavenger receptor CD36 — see Deghenghi 1994 and Bodart 2002.
How does hexarelin differ from ipamorelin and GHRP-6?
All three are GHSR-1a agonists, but they differ in selectivity and off-target binding. Ipamorelin is the most selective — minimal effects on prolactin, ACTH, and cortisol. GHRP-6 is closely related to hexarelin chemically but produces stronger appetite stimulation. Hexarelin is the only member of this family with documented binding to CD36 on cardiomyocytes, which underlies its direct, GH-independent cardiac inotropic effect (Bodart 2002; Massoud 1996).
Is hexarelin approved by the FDA or EMA?
No. Hexarelin reached Phase II clinical trials (paediatric GH deficiency, cardiac applications) in the late 1990s and early 2000s, sponsored by Mediolanum Farmaceutici, but development was discontinued for commercial reasons and the compound was never marketed in any major jurisdiction. Hexarelin is NOT an FDA- or EMA-approved drug.
Why are no hexarelin trials listed on ClinicalTrials.gov?
The pivotal hexarelin programme ran from approximately 1994 to 2004, predating both the FDAAA 2007 registration mandate and the earlier ICMJE registration requirement (2005). A current ClinicalTrials.gov v2 API search returns zero studies for "hexarelin" or "examorelin" — verified 2026-05-01 — which is expected for compounds whose pivotal trials were conducted before registration was mandatory. This matches the registry-gap pattern we apply to sermorelin, hCG, and gonadorelin.
Does hexarelin keep working with chronic use?
Repeated dosing causes partial GHSR-1a desensitisation: Klinger et al. (1996) reported that the peak GH response to intranasal hexarelin in children fell from 70.6 mU·L⁻¹ at baseline to 34.1 mU·L⁻¹ after only 7 days of t.i.d. dosing, before plateauing. Despite this biochemical tolerance, growth velocity continued to improve through 6–10 months of dosing, and the desensitisation was partially reversible after washout. Wellness-market claims of an indefinitely sustained GH boost are NOT supported by this evidence base.
Is hexarelin banned in sport?
Yes. Hexarelin (listed as "examorelin (hexarelin)") is explicitly prohibited at all times under WADA (World Anti-Doping Agency) Section S2.2.4 — Growth Hormone Releasing Factors — in the 2026 Prohibited List, alongside GHRP-1 through GHRP-6 and alexamorelin.

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