GHRP-6

GHRP-6 is the original growth hormone releaser, the compound later GHRPs like GHRP-2 and hexarelin were derived from. It prompts the pituitary gland to release growth hormone by acting on the ghrelin (hunger hormone) receptor, and it's also notable for strongly stimulating appetite through a separate pathway. It's substantially less potent at raising growth hormone than the newer compounds it inspired, which is why development moved on to those instead. It's not FDA-approved, there are no brand-name products, it's sold only as a research peptide, and it's banned in drug-tested sport.

GHRP-6 has been studied to raise growth hormone and IGF-1, with slight increases in cortisol and prolactin, and it also stimulates appetite through a separate mechanism. It is substantially less potent at releasing growth hormone than GHRP-2, which is why later development focused on newer compounds. No large clinical trials support the body-composition uses people pursue. Its only late-stage trial to date is a 2026 Cuban Phase III study testing it combined with epidermal growth factor for acute ischemic stroke — a nerve-protection question, not a growth-hormone one — which did not meet its primary endpoint.

Not FDA-approved for any indication. GHRP-6 was advanced through Phase I/II clinical evaluation in the early 1990s in multiple jurisdictions but clinical development was abandoned in favor of GHRP-2 and hexarelin — both of which are substantially more potent at GH stimulation per the Adams 1996 *Molecular Endocrinology* head-to-head pharmacology data.[⁵] Available exclusively as a research peptide through unregulated research-peptide supply chains. Not DEA-scheduled. WADA-banned in regulated sport — explicitly named under Section S2.2.4 (Growth Hormone Releasing Factors → GH-releasing peptides subsection) of the 2026 Prohibited List as "GHRP-6" alongside alexamorelin, examorelin (hexarelin), GHRP-1, GHRP-2 (pralmorelin), GHRP-3, GHRP-4, and GHRP-5.[⁶]

GHRP-6 is not FDA-approved and is banned in regulated sport (WADA). VialWise is a research and educational reference, not medical advice — consult a licensed professional.

⚠️ For research and educational purposes only. GHRP-6 is not approved by the FDA for any indication. Clinical development was abandoned in favor of GHRP-2 and hexarelin; per Adams 1996, GHRP-2 was considerably more potent than GHRP-6 at GH stimulation.[⁵] GHRP-6 is available exclusively as a research peptide through unregulated supply chains. Information in this entry is informational, not medical advice. Always confirm dose calculations with the in-app calculator and consult appropriate professional guidance before any protocol decisions.

⚠️ Precision matters at low doses. GHRP-6 is dosed in micrograms (mcg), not milligrams. Typical research-community doses ( per dose) at typical reconstitution concentrations ( vial / 2.5 mL BAC water = =) produce small draws in the range on a U-100 syringe. Lower-concentration setups ( / 5 mL =) produce draws — generally easier precision. Always verify draws against the in-app calculator. Same precision concern as Ipamorelin, Hexarelin, GHRP-2, and the other GHS-class peptides.

⚠️ GHRP-6 is the *least* potent of the actively-used GHRPs but is *most* notable for its appetite-stimulation effect — the "hunger peptide" framing. Two load-bearing pharmacological distinctions place GHRP-6 specifically in the GHS-axis cluster: - Substantially less potent than GHRP-2 and hexarelin at GH stimulation. The Adams 1996 head-to-head human-pituitary-somatotropinoma cell-culture study established that "GHRP-2 was considerably more potent than GHRP-6"[⁵] — the foundational finding that anchored the clinical-development choice of GHRP-2 (Wyeth-Ayerst pediatric short-stature program; Kaken Pharmaceutical Japanese diagnostic approval) over GHRP-6 for the GHRP class. Hexarelin was independently derived from GHRP-6 by Mediolanum with the 2-methyl-Trp substitution that conferred greater potency; per the hexarelin development history (see [hexarelin.md](./hexarelin.md)), hexarelin is also more potent than GHRP-6 at GH stimulation. - Notable acute appetite-stimulation effect. The Locke 1995 intracerebroventricular study in rats demonstrated dose-dependent eating stimulation (0–1000 pmol ICV bolus) with linear dose-response (p<0.01) — but plasma GH response was not dose-related at the doses studied.[⁴] This established that GHRP-6's central appetite-stimulation effect operates through a mechanism distinct from its peripheral GH-releasing effect — the foundation of the "hunger peptide" framing that persists in research-community use today. The appetite effect is mediated by ghrelin-receptor activation in hypothalamic feeding centers; GHRP-6 is the GHRP with the most prominent central appetite effect. The clinical-development consequence: GHRP-6 was the original GHRP class member but the modern research-community use of the GHRP class is concentrated on GHRP-2 (the most potent acute GH stimulator of the class per Adams 1996[⁵], and the only GHRP with an approved national-regulator indication) and hexarelin (Mediolanum-developed second-generation derivative). GHRP-6 use is concentrated in researchers specifically seeking the appetite-stimulation effect — or as a less-expensive GHRP option in the research-peptide supply chain.

⚠️ GHRP-6 vs the rest of the GHS-axis cluster — explicit cluster context for navigating the library. The library now has multiple ghrelin-receptor-agonist entries with substantially different pharmacology: - Ipamorelin — pentapeptide; the cleanest GHRP for sustained use; minimal cortisol/prolactin elevation at any dose; minimal tachyphylaxis. The default research-community choice for sustained GH-axis stimulation. - Hexarelin — hexapeptide; high acute GH-stimulating potency; dose-dependent cortisol/prolactin elevation; meaningful tachyphylaxis; derived from GHRP-6 by Mediolanum with 2-methyl-Trp substitution. - GHRP-2 / Pralmorelin — hexapeptide; near-maximal acute GH response at low IV doses; the only GHRP with an approved national-regulator indication (Japan diagnostic). - GHRP-6 (this entry) — hexapeptide; the original Bowers/Momany GHRP — the foundational compound of the entire GHRP class; substantially less potent than GHRP-2 or hexarelin per Adams 1996;[⁵] notable for the central appetite-stimulation effect ("hunger peptide" framing) per Locke 1995;[⁴] limited modern clinical-development presence outside research-peptide use. - MK-677 / Ibutamoren — non-peptide oral small-molecule ghrelin agonist; very long half-life (~24 hours); CHF-safety-signal concern in elderly populations (Adunsky 2011 phase 2b DSMB termination); active phase 3 program at Lumos Pharma. Historical context: GHRP-1, GHRP-2, GHRP-3, GHRP-4, GHRP-5, and GHRP-6 were all developed in the Bowers/Momany research program at Tulane University in the 1980s as the original GHRP class. Hexarelin/examorelin emerged later from Mediolanum (Italy). Ipamorelin emerged still later from Novo Nordisk (Denmark) as a pentapeptide with substantially improved selectivity. Today's research-community use is concentrated on GHRP-2, hexarelin, and ipamorelin from this lineage; GHRP-6 is used specifically for its appetite-stimulation effect or as a lower-cost option; the other older GHRPs (GHRP-1, -3, -4, -5) are essentially absent from modern use.

⚠️ WADA-banned — explicitly named under Section S2.2.4 (Growth Hormone Releasing Factors → GHRP subsection) as "GHRP-6". The 2026 WADA Prohibited List Section S2.2.4 names *"GH-releasing peptides (GHRPs) [e.g. alexamorelin, examorelin (hexarelin), GHRP-1, GHRP-2 (pralmorelin), GHRP-3, GHRP-4, GHRP-5 and GHRP-6]"*.[⁶] Same WADA subsection (S2.2.4) as Ipamorelin, Hexarelin, GHRP-2, CJC-1295, Sermorelin, Tesamorelin, and MK-677. Prohibited at all times.

According to PubMed-indexed research, GHRP-6 is a synthetic hexapeptide growth hormone-releasing peptide (GHRP) with the sequence His-D-Trp-Ala-Trp-D-Phe-Lys-NH2.[³] The compound was developed in the Bowers/Momany research program at Tulane University in the late 1980s as the original GHRP class compound — the foundational hexapeptide from which the entire GHRP class is derived.[¹] Both GHRP-2 (Bowers/Momany second-generation derivative with D-β-naphthyl-alanine substitution; see [ghrp-2.md](./ghrp-2.md)) and hexarelin (Mediolanum-developed derivative with 2-methyl-Trp substitution; see [hexarelin.md](./hexarelin.md)) emerged structurally from GHRP-6 as more-potent analogs. GHRP-6 itself was advanced through Phase I/II clinical evaluation in the early 1990s but GH-directed clinical development was abandoned in favor of the more potent derivatives — no Phase II or III trial of GHRP-6 for GH stimulation or body composition has ever been published. GHRP-6 did later reach Phase III in an unrelated indication: the Cuban COURAGE-2 trial tested an EGF + GHRP-6 combination for neuroprotection in acute ischemic stroke and missed its primary endpoint.[⁷]

Mechanism. Based on articles retrieved from PubMed, GHRP-6 acts as an agonist at the ghrelin receptor (GHS-R1a) at both pituitary and hypothalamic levels to stimulate GH release.[³][⁵] The mechanism is shared with all GHRP-class peptides plus the non-peptide ghrelin-mimetic MK-677. The Adams 1996 study established that GHRP-6 acts via protein kinase C-dependent phosphatidylinositol hydrolysis at the human pituitary somatotroph[⁵] — the same mechanism as GHRP-2, with substantially less potency at the receptor. The "hunger peptide" effect of GHRP-6 operates through hypothalamic ghrelin-receptor activation at central feeding centers — established by the Locke 1995 intracerebroventricular study in rats that demonstrated dose-dependent eating stimulation independent of peripheral GH response.[⁴]

Bowers 1991 normal-adult-men intranasal study (Hayashi 1991 Endocrinologia Japonica). The Hayashi 1991 study in 6 healthy adult men established the foundational human pharmacology of GHRP-6.[³] An IV bolus produced a robust GH peak of 54.9 ± 4.2 µg/L. Intranasal administration produced dose-related GH response: peak of 39.6 ± 15.3 µg/L, 14.1 ± 5.0 µg/L, and 7.5 ± 5.7 µg/L. Plasma prolactin and cortisol levels were slightly but significantly increased after IV administration but GHRP-6 did not affect plasma TSH, LH, FSH, insulin, blood sugar, or GHRH-LI levels — establishing the GH/PRL/cortisol-selective hormonal profile that distinguishes GHRPs from the gonadotropin axis. Seven consecutive intranasal doses ( every 8 hours) over 56 hours did not produce GH-response desensitization and IGF-1 rose from 94.5 ± 5.8 µg/L before GHRP to 125.8 ± 6.0 µg/L after repeated GHRP administration. The Hayashi study is the foundational adult-human GHRP-6 pharmacology citation — Cyril Y. Bowers (Tulane) was a co-author, anchoring the entry to the foundational Bowers research program.

Bitar 1991 dual-receptor pharmacology. The Bitar 1991 *Biochemical and Biophysical Research Communications* study established that GHRP and GHRH act through distinct receptors using a panel of substance P/bombesin antagonists.[²] The GHRP-6 sequence (His-D-Trp-Ala-Trp-D-Phe-LysNH2) was the GHRP used in this study. Substance P/bombesin antagonists (P-7482, P-7483, P-7492) dose-dependently inhibited GHRP-6-induced GH release (IC50 = 0.2 µM, 0.85 µM, and 6 µM respectively) but had only 10–15% inhibitory effect on GHRH-stimulated GH release. Conversely, the GHRH antagonist DC21-366 inhibited GHRH-induced GH release (IC50 = 0.16 µM) but did not inhibit GHRP-6-induced GH release. Established the dual-receptor model that is the basis for the synergistic-GHRP-plus-GHRH-analog combination protocol used across the GHS-axis library.

The "hunger peptide" thread (Locke 1995 ICV eating-stimulation study).[⁴] The Locke 1995 *Life Sciences* study in adult male Sprague-Dawley rats characterized the central appetite-stimulation effect of GHRP-6. Intracerebroventricular GHRP-6 (0–1000 pmol in 5 µL saline) was injected into lateral ventricles of sated rats; for 1 hour after injection, occurrence of eating was noted and arterial blood was collected for plasma GH measurement at 0/15/30/60 minutes. A nearly linear, statistically significant (p<0.01) dose-response relationship between GHRP-6 dose and incidence of eating was observed. Mean change from baseline of plasma GH during the 60 minutes after injection was not dose-related (p>0.2 at 15 min; p>0.1 at 30 and 60 min). The authors concluded that GHRP-6 administered ICV to sated adult male Sprague-Dawley rats stimulates eating "by some mechanism that is independent of its GH-releasing property." This is the foundational citation for the "hunger peptide" framing of GHRP-6 — the central appetite effect operates through hypothalamic ghrelin-receptor activation at feeding centers, distinct from the pituitary ghrelin-receptor activation that produces GH release.

Adams 1996 head-to-head potency comparison (GHRP-2 > GHRP-6).[⁵] The Adams 1996 *Molecular Endocrinology* study in human pituitary somatotropinoma cell cultures established that GHRP-2 was considerably more potent than GHRP-6 at GH stimulation, despite shared mechanism. This is the load-bearing pharmacology finding for the relative-potency framing in this entry: GHRP-6 is the original GHRP but is substantially less potent than its derivatives (GHRP-2 second-generation Bowers/Momany derivative; hexarelin Mediolanum-developed derivative). The Adams 1996 finding explains why modern clinical-development resources concentrated on GHRP-2 and hexarelin rather than GHRP-6.

COURAGE-2 (2026) — the only published late-stage GHRP-6 trial, and it is not a GH-stimulation trial.[⁷] The Hernández-Bernal 2026 *Journal of Clinical Neuroscience* report describes COURAGE-2, a multicenter, randomized, open-label Phase III trial run by the Cuban CIGB program in acute ischemic stroke (n=188). Participants received IV epidermal growth factor plus GHRP-6 twice daily for 7 days versus standard care. The trial missed its primary endpoint — no intention-to-treat difference in modified Rankin Scale, Barthel Index, or survival; the authors report that a severe-stroke subgroup (NIHSS ≥ 15, n=27) showed reduced disability and mortality, which is a subgroup finding and not a primary result. Three things matter for reading this entry correctly: (1) GHRP-6 was given here as a cytoprotective/neuroprotective agent, not as a GH secretagogue, so the trial says nothing about GH stimulation, IGF-1, or body composition; (2) it was tested as a combination with EGF, so no GHRP-6-alone effect can be separated out; (3) the headline result was negative. COURAGE-2 does mean the older blanket statement that "no Phase II or III trial of GHRP-6 has been published" is no longer accurate — the accurate scoping is that no Phase II/III trial of GHRP-6 for GH stimulation or body composition has been published. A companion preclinical mouse study from the same cigb egf+GHRP-6 neuroprotection program was also published in 2026.

Regulatory status (US — current). GHRP-6 is not FDA-approved for any indication. GHRP-6 clinical development was abandoned in the 1990s in favor of GHRP-2 and hexarelin. The compound is available exclusively as a research peptide through unregulated research-peptide supply chains; not legally compoundable through US 503A pharmacies (the compound is not on the 503A bulks list, and per the broader peptide-bulks-list regulatory situation as of 2024, is not approved for compounding). Not DEA-scheduled.

Regulatory status (sport — WADA). GHRP-6 is WADA-banned under Section S2.2.4 (Growth Hormone Releasing Factors → GHRP subsection) of the 2026 Prohibited List, named explicitly as "GHRP-6" alongside alexamorelin, examorelin (hexarelin), GHRP-1, GHRP-2 (pralmorelin), GHRP-3, GHRP-4, and GHRP-5.[⁶] Same WADA subsection as Ipamorelin, Hexarelin, GHRP-2, CJC-1295, Sermorelin, Tesamorelin, and MK-677. Prohibited at all times.

Common research interests. GHRP-6 is used in research-community contexts for: - Acute GH stimulation for body composition and recovery, with deliberate use of the appetite-stimulation effect — the dominant research-community use case. Researchers who specifically want the appetite effect (e.g. during bulking phases) choose GHRP-6 over GHRP-2 or ipamorelin; researchers who specifically want to avoid the appetite effect choose GHRP-2 or ipamorelin instead. - Combined with low-dose GHRH analog (CJC-1295 no-DAC, sermorelin, tesamorelin) — the same synergistic-GHRP-plus-GHRH-analog framework described for GHRP-2 and hexarelin, with the dual-receptor pharmacology established by Bitar 1991.[²] - Lower-cost GHRP option in the research-peptide supply chain — GHRP-6 is typically priced lower than GHRP-2 or hexarelin in research-peptide supply chains, making it a budget-conscious option for the GHRP class. - Preclinical and translational research on central appetite regulation — the Locke 1995 ICV-eating finding[⁴] anchors a substantial preclinical literature on GHRP-6 as a tool for studying hypothalamic feeding regulation, distinct from the clinical/therapeutic-development thread.

Commonly reported

• Pronounced appetite increase / hunger — the signature GHRP-6 effect per Locke 1995; substantially more prominent than for GHRP-2 or ipamorelin
• Mild cortisol elevation — per Hayashi 1991, slight but statistically significant after IV administration; less pronounced than for hexarelin or GHRP-2 at equivalent µg/kg doses
• Mild prolactin elevation — per Hayashi 1991, slight but statistically significant after IV administration
• Tachyphylaxis (GH-response decline with sustained use) — characterized in adult chronic-administration contexts for the GHRP class; Hayashi 1991 specifically did not see desensitization over 7 doses across 56 hours,[³] but longer-duration intervals are less well-characterized
• Injection site reactions — typical of subcutaneous peptide injection
• Water retention / fluid retention — common; same as other GHS-class compounds
• Tingling or numbness in extremities — uncommon; suggests carpal-tunnel-syndrome-like effect; warrants dose reduction
• Joint stiffness — uncommon
• Sleep changes (typically improved sleep quality at modest doses; sleep disturbance at high doses) — mixed reports
• Long-term safety in adults using GHRP-6 off-label is not well characterized in published literature. The longest published human exposures are short: the Hayashi 1991 study dosed 7 intranasal doses across 56 hours,[³] and the COURAGE-2 Phase III dosed IV GHRP-6 (with EGF) twice daily for 7 days in a stroke population whose baseline risk profile has nothing in common with research-community use.[⁷] Multi-year off-label use in the research community remains uncharacterized. A 2026 case report of a ~20-year recreational GH/secretagogue user — whose regimen included a sermorelin/GHRP-6 combination — describes anterior cervical osteophyte-related dysphagia and hypothesizes a contribution from chronic GH-axis stimulation; the case is confounded by concurrent somatropin use and is a single report, not evidence of causation.[⁹]
• CHF-related concerns — the Adunsky 2011 MK-677 phase 2b DSMB termination for CHF safety signal applies mechanism-wise to the entire ghrelin-receptor agonist class; whether the same concern applies to GHRP-6 is theoretical but mechanistically plausible. See [mk-677.md](./mk-677.md).
• Appetite-stimulation effect creates clinical risk in disordered-eating populations — researchers with active or remote history of binge eating disorder, bulimia, or other disordered-eating presentations should consider GHRP-6's appetite-stimulation effect as a specific contraindication.

Serious

• Severe headache with visual changes — could suggest acute intracranial pressure elevation or pituitary pathology; rare but warrants immediate medical evaluation
• New-onset glucose dysregulation with symptoms (polyuria, polydipsia, blurred vision) — GH-axis activation can worsen insulin resistance; new-onset diabetic symptoms warrant immediate medical evaluation
• Severe or persistent injection-site reaction (induration, abscess, signs of infection) — warrants medical evaluation
• Severe disordered-eating presentation in context of GHRP-6's appetite-stimulation effect — if appetite-stimulation effect drives binge-eating-disorder symptoms or other disordered-eating presentation, immediate discontinuation and mental-health evaluation warranted
• Allergic reaction (hives, swelling, difficulty breathing) — extremely rare but warrants immediate medical evaluation

Active malignancy or known IGF-1R-positive tumors — GH/IGF-1 axis activation is contraindicated

Active hyperprolactinemia or prolactinoma — additive concerns

Active hypercortisolism or Cushing's syndrome — additive concerns

Active eating disorder or binge-eating disorder — GHRP-6's appetite-stimulation effect is contraindicated

Pregnancy and lactation — no human data; default to contraindicated

Pediatric use — no FDA-approved indication; no pediatric clinical development program (unlike GHRP-2's Wyeth-Ayerst Phase II/III program)

Concurrent corticosteroid therapy — additive cortisol effects (mild)

Active diabetes / impaired glucose tolerance — caution; GH-axis stimulation may worsen insulin resistance

Regulatory note (US): GHRP-6 is not FDA-approved for any indication and is not legally compoundable through US 503A pharmacies.

Regulatory note (sport): WADA-banned in regulated sport — explicitly named under Section S2.2.4 of the 2026 Prohibited List as "GHRP-6".[⁶]

Not DEA-scheduled.

Peptide

A short chain of amino acids, the building blocks of proteins. Many compounds in this library are peptides.

Growth hormone secretagogue

A compound that signals the body to release its own growth hormone, rather than supplying growth hormone directly.

Ghrelin receptor

a receptor that, when activated, triggers growth hormone release and hunger.

Preclinical

Research done in cells or animals, before human clinical trials. Promising preclinical results don't always hold up in people.

WADA Prohibited List

The list of substances banned in regulated sport by the World Anti-Doping Agency.

1. Bowers CY, Momany F, Reynolds GA, et al. Discovery and characterization of growth hormone-releasing peptides (GHRP class), Tulane University development program, 1977–1991. Foundational discovery work establishing the GHRP class — GHRP-6 was the original GHRP from which the entire class is derived (GHRP-1 through GHRP-5 are structural variants from the same Bowers/Momany research program; GHRP-2 was the second-generation derivative with D-β-naphthyl-alanine substitution; hexarelin was the Mediolanum-developed derivative with 2-methyl-Trp substitution). Source for: GHRP class discovery history; GHRP-6 as the foundational class member; the structural relationships between GHRP-6 and GHRP-2 / hexarelin; the regulatory framework for current research-peptide-only availability.
2. Bitar KG, Bowers CY, Coy DH. (1991). Effect of substance P/bombesin antagonists on the release of growth hormone by GHRP and GHRH. Biochemical and Biophysical Research Communications, 180(1):156–161 (October 15, 1991).(PMID 1718273)
3. Hayashi S, Okimura Y, Yagi H, Uchiyama T, Takeshima Y, Shakutsui S, Oohashi S, Bowers CY, Chihara K. (1991). Intranasal administration of His-D-Trp-Ala-Trp-D-Phe-LysNH2 (growth hormone releasing peptide) increased plasma growth hormone and insulin-like growth factor-I levels in normal men. Endocrinologia Japonica, 38(1):15–21 (February 1991).(PMID 1915110)
4. Locke W, Kirgis HD, Bowers CY, Abdoh AA. (1995). Intracerebroventricular growth-hormone-releasing peptide-6 stimulates eating without affecting plasma growth hormone responses in rats. Life Sciences, 56(16):1347–1352 (March 10, 1995).(PMID 8614257)
5. Adams EF, Lei T, Buchfelder M, Bowers CY, Fahlbusch R. (1996). Protein kinase C-dependent growth hormone releasing peptides stimulate cyclic adenosine 3',5'-monophosphate production by human pituitary somatotropinomas expressing gsp oncogenes: evidence for crosstalk between transduction pathways. Molecular Endocrinology, 10(4):432–438 (April 1996).(PMID 8721987)
6. World Anti-Doping Agency. The 2026 Prohibited List, International Standard (effective 1 January 2026). Canonical PDF: wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf (linked from the WADA landing page; local archival copy in `docs/legal/wada-2026-prohibited-list.pdf`). GHRP-6 is named explicitly under Section S2.2.4 (Growth Hormone Releasing Factors → GHRP subsection) — page 8 of the canonical PDF — as "GHRP-6". Verbatim from the canonical PDF: under S2.2.4 ("Growth hormone releasing factors, including, but not limited to:"), the GHRP bullet reads "GH-releasing peptides (GHRPs) [e.g. alexamorelin, examorelin (hexarelin), GHRP-1, GHRP-2 (pralmorelin), GHRP-3, GHRP-4, GHRP-5 and GHRP-6]". Same S2.2.4 subsection as Ipamorelin, Hexarelin, GHRP-2, CJC-1295, Sermorelin, Tesamorelin, and MK-677. Prohibited at all times.
7. Hernández-Bernal F, et al. (2026). Phase III Open-Label, Randomized Clinical Trial of Epidermal Growth Factor and Growth Hormone Releasing Hexapeptide in Acute Ischemic Stroke. Journal of Clinical Neuroscience, 152:112195 (published 16 July 2026).(PMID 42462342)
8. Dominikowski A, et al. (2026). The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration. Frontiers in Endocrinology (Lausanne), 17:1822475 (published 18 June 2026).(PMID 42395176)
9. Perez SL, et al. (2026). Anterior cervical osteophyte-related dysphagia in a long-term growth hormone user: a case report. Frontiers in Surgery, 13:1859548 (published 3 July 2026).(PMID 42465868)

• MK-677 (Ibutamoren) — discussed together in this entry's stacks section
• Testosterone — discussed together in this entry's stacks section
• IGF-1 LR3 — discussed together in this entry's stacks section
• CJC-1295 / Ipamorelin Blend — same mechanism class
• CJC-1295 — same mechanism class
• GHRP-2 — same mechanism class