PerformanceGrowth Hormone-Releasing Peptide-6His-D-Trp-Ala-Trp-D-Phe-Lys-NH₂

GHRP-6

Growth-hormone-releasing peptide · ghrelin-receptor (GHS-R1a) agonist

GHRP-6 is a synthetic hexapeptide growth-hormone secretagogue — first synthesized and characterized by Cyril Bowers and Frank Momany in 1984 as a peptide that acts on the pituitary to release growth hormone through a mechanism entirely distinct from GHRH. It is an agonist at the growth-hormone-secretagogue receptor GHS-R1a, the receptor later shown to be the ghrelin receptor, which makes GHRP-6 historically the tool compound that predated and helped reveal ghrelin biology. Its human evidence base is old and small — predominantly acute GH-provocation studies in healthy men — and it is approved nowhere as a drug. Two honest caveats define it: alongside growth hormone it also raises cortisol, ACTH, and prolactin, and as a ghrelin-receptor agonist it stimulates appetite. It is prohibited in sport at all times.

The short version

GHRP-6 is a small lab-made peptide (six amino acids) that tells the pituitary gland to release growth hormone — but through a different doorway than the body's own growth-hormone-releasing hormone.

That doorway turned out to be the receptor for ghrelin, the 'hunger hormone,' which GHRP-6 was actually used to discover. So beyond raising growth hormone, GHRP-6 also tends to make you hungry, and it nudges up stress-related hormones like cortisol.

Almost all the human research on GHRP-6 is decades old and consists of short tests measuring a growth-hormone spike — not long-term studies of benefit or safety. It is not an approved medicine anywhere, and it is banned in competitive sport.

Molecular identity

Specs

Molecular weight: 873.0 g/mol
Molecular formula: C46H56N12O6
Monoisotopic mass: 872.44 Da

Sequence (6 AA): His-D-Trp-Ala-Trp-D-Phe-Lys-NH₂Bowers et al. (PMID 2108187)
Structure / class: Synthetic GHRP-class hexapeptide (GHS-R1a agonist)PMID 2108187
CAS number: 87616-84-0Widely cited (not registry-verified)
Molecular target: GHS-R1a (ghrelin receptor); hypothalamus + pituitaryPMID 2108187
Half-life: ~7.6 min dist · ~2.5 h elim (human IV)PMID 23099431Half-life curve →
Regulatory status: Not approved any country (research chemical) · WADA S2 prohibitedResearch literature / WADA

Plain English

Mechanism

GHRP-6 is an agonist (a molecule that switches a receptor on) at the growth-hormone-secretagogue receptor GHS-R1a — a G-protein-coupled receptor (a common type of cell-surface switch that relays an outside signal into the cell) found on the anterior pituitary (the hormone-control gland at the base of the brain) and the hypothalamus (the brain region just above it that directs the pituitary). That receptor was cloned (isolated and identified) using GHRP-class secretagogues — compounds that prompt a gland to secrete a hormone — as the search molecules, and was subsequently shown to be the receptor for ghrelin, the body's 'hunger hormone.' Because GHRP-6 acts on this receptor rather than the GHRH receptor, its growth-hormone-releasing mechanism is entirely distinct from that of GHRH analogs (lab-made copies of the body's own growth-hormone-releasing hormone) such as sermorelin or CJC-1295 — which is precisely why the two classes synergize (work together to produce more than the sum of their parts).

Although GHRP-6 acts at both the pituitary and the hypothalamus, the hypothalamus is the dominant site in the intact organism (the living body with its signaling pathways unbroken): in patients with hypothalamo-pituitary disconnection (where the link between those two brain structures has been surgically or medically severed), both the growth-hormone (GH) response to GHRP-6 and its synergy with GHRH are abolished. GHRP-6 also requires the body's own hypothalamic GHRH to be present for maximal growth-hormone stimulation.

Beyond growth hormone, GHRP-6 stimulates the release of ACTH (adrenocorticotropic hormone — the pituitary signal that tells the adrenal glands to make cortisol, the body's main stress hormone) and prolactin (the hormone best known for driving milk production); this co-release is dose-dependent (bigger at higher doses) and emerges above the dose that already saturates — fully maxes out — the growth-hormone response. As a ghrelin-receptor agonist it also drives appetite: central administration (dosing directly into the brain) in rats activates hypothalamic feeding centers and induces eating, an effect blocked by a neuropeptide-Y receptor antagonist (a molecule that switches off the brain's main hunger-signaling receptor). The quantified human food-intake data, however, exists for ghrelin itself, not for GHRP-6 specifically.

Sources:PMID 2108187 PMID 7883854 JCEM 83(4):1186 PMID 10336729 PMID 11751604 PMID 11739476

Why people reach for it

Potential benefits

GHRP-6 is the original GH-releasing peptide — the tool compound that helped reveal ghrelin biology. Here's what draws people to it.

Raise your own growth hormone, not inject it — Its core action: it fires the body's own GH pulse through the ghrelin receptor, so the natural feedback and rhythm stay in the loop rather than being overridden by outside hormone.
A strong appetite drive for a bulk — Its most distinctive effect: as a ghrelin-receptor agonist it's the hungriest of the GHRPs, with a clear hunger surge ~20–30 min after a dose — deliberately used to eat enough during a weight-gain phase (and the main reason people avoid it when cutting).
Synergizes with a GHRH analog — Because it works the ghrelin receptor, it stacks with a GHRH peptide for a combined pulse bigger than either alone — most commonly CJC-1295 or Sermorelin.
Body-composition and recovery support — The GH/IGF-1 rise is what people reach for it for alongside the appetite drive — bulking and recovery contexts where eating enough and an anabolic backdrop are both wanted.
A long history as the reference GHRP — First characterized in 1984 and used to clone the ghrelin receptor, it's the compound much of the GH-secretagogue field was built on.

Sources:PMID 2108187 PMID 7883854 PMID 10336729

What people reach for GHRP-6 for, drawn from what the research reports (old, mostly acute human data) and how it's used — not proven outcomes or medical claims. Note it also raises cortisol, ACTH, and prolactin as a class effect.

Implied timing

Best time to dose

Implied best time

Bedtime (empty stomach)

Most people inject GHRP-6 at bedtime on an empty stomach, with extra fasted doses (morning or pre-workout) optional through the day.

GHRP-6 amplifies the body's own GH release, and the single largest natural GH pulse fires in early slow-wave (deep) sleep — a bedtime dose stacks the peptide's pulse on top of that nocturnal surge.
Food is the reason for the empty stomach: a meal raises insulin and somatostatin (GH's off-switch), both of which blunt the pulse — even a small carb or fat load can cut the response, so the dose goes ~2 hours clear of eating (and hold food 30–60 min after).
It can be split — e.g. morning + bedtime — to hit two GH-pulse windows a day, but the bedtime dose is the anchor.
Expect a pronounced hunger surge ~20–30 minutes after a dose; if fat loss is the goal, timing the injection where that appetite is manageable matters more here than with the cleaner GHRPs.

No study establishes an ideal time of day for GHRP-6 — this is reasoned from its GH-secretagogue mechanism and how it's used. As a rule of thumb peptide dosing lands in the midday-to-evening window; for GHRP-6 the lean is bedtime, fasted.

Sources:PMID 10336729

How to run it

Dosing & protocol

GHRP-6 is injected subcutaneously — the form sold as a research peptide, the route the calculator is built for. The defining timing rule for this whole GH-secretagogue class: inject on an EMPTY stomach. Food — especially fat and carbohydrate — triggers insulin and raises somatostatin, the body's GH off-switch, and both blunt the GH pulse. Allow roughly a 2-hour window with no food around each dose. GHRP-6's unique wrinkle: expect a notable hunger surge ~20–30 minutes after dosing — the strongest appetite effect in the GHRP family.

Community and practitioner convention, not a validated wellness trial: GHRP-6's human data is old (1988–1999) and narrow — acute GH-provocation studies, not long-term efficacy or safety RCTs. It is approved nowhere and is WADA S2 prohibited. Every number here is a usage pattern drawn from that evidence base, not a prescription.

Tiered dose ranges

Community convention anchored to the human GH-saturation data: more dose past the plateau adds cortisol/prolactin, not more GH.

Low / conservative:: 100 mcg per injection — a good starting dose for a new user to assess the appetite response and tolerance before escalating.
Standard:: 100–200 mcg per injection, 1–2× daily — the typical working range for GH-pulse goals. Covers the sub-saturation zone where GH is rising and cortisol/prolactin co-release is modest.
High (appetite / bulk phase):: 200–300 mcg per injection, up to 3× daily — used deliberately when the appetite drive is the point (weight-gain phase). Above ~1 µg/kg body weight the GH plateau is reached; additional dose primarily amplifies cortisol, ACTH, and prolactin, so 300 mcg is a practical ceiling for most adults.

Subcutaneous administration

Inject into subcutaneous fat; the GHRP-6-specific timing insight is the empty-stomach requirement.

Injection site:: The abdomen (2+ inches from the navel), the love-handle area, or the outer thigh. Rotate sites between doses to prevent lipohypertrophy (fatty lumps from repeated injection into one spot).
Measuring the dose:: Using a standard 5 mg vial + 2 mL bacteriostatic water: the reconstituted solution is 2,500 mcg per mL. On a U-100 insulin syringe: 100 mcg = 4 IU · 150 mcg = 6 IU · 200 mcg = 8 IU · 300 mcg = 12 IU. The calculator adjusts this for any vial size.
Time of day:: Most common windows: (1) bedtime, fasted (rides the body's own largest overnight GH surge in slow-wave sleep); (2) fasted morning on waking; (3) pre-workout fasted. Split doses — e.g. morning + bedtime — are used to hit two GH-pulse windows per day. Separate each injection from the previous meal by ~2 hours, and hold food for at least 30–60 minutes after dosing.
The hunger surge:: Expect a clear appetite increase ~20–30 minutes post-injection — a direct ghrelin-receptor effect. Plan a protein-forward meal for that window if you are in a growth phase; or dose at a time where the hunger is manageable if fat loss is the goal.

Cycle & washout

GH secretagogues are typically pulsed in cycles to prevent receptor desensitization.

Standard cycle:: 8–12 weeks of daily use, then evaluate. Many practitioners run 5-days-on / 2-days-off rather than continuous daily to reduce tachyphylaxis (diminishing response from constant receptor stimulation).
Washout:: 4 weeks off between cycles. IGF-1 (growth hormone's downstream messenger) can be measured mid-cycle and post-washout to gauge response — a pragmatic marker since GH itself pulses unpredictably.
Appetite note:: The hunger drive typically fades over the first 1–2 weeks as the novelty of ghrelin-receptor stimulation settles. If appetite suppression becomes the goal instead, GHRP-2 or ipamorelin (cleaner GH profile, less appetite) are the usual alternatives.

Reconstitution at a glance

The on-page calculator does this live; quick reference for the default 5 mg vial:

Mixing:: 5 mg vial + 2 mL bacteriostatic water = 2,500 mcg per mL. On a 100-unit (1 mL) insulin syringe: 100 mcg = 4 IU · 150 mcg = 6 IU · 200 mcg = 8 IU · 250 mcg = 10 IU · 300 mcg = 12 IU.

Sources:PMID 2108187 PMID 23099431 PMID 10336729 PMID 7883854

Substrate the signal needs

Nutritional cofactor precision

GHRP-6's cofactor logic runs through three questions. AMPLIFY the pulse: what nutrients relieve somatostatin (GH's off-switch) or directly prime the pituitary? MITIGATE the cost: GHRP-6's defining side effect is intense appetite and a cortisol/prolactin nudge — what blunts those? SUPPLY the substrate: the GH/IGF-1 signal drives protein synthesis, so the raw material has to be there.

Reasoned from GH/IGF-1 physiology and ghrelin-receptor biology — not a GHRP-6 cofactor study. Supplement doses are common community ranges applied to the mechanism, not GHRP-6-specific findings.

AMPLIFY — L-arginine + Alpha-GPC (relieve the brake)

Somatostatin is GH's off-switch. L-arginine suppresses somatostatin tone; Alpha-GPC primes the cholinergic GH-release pathway.

L-arginine:: 3–6 g taken 30–60 minutes before the GHRP-6 injection, on an empty stomach. Suppresses hypothalamic somatostatin release, letting the GHRP-6-triggered pulse reach a higher ceiling. Most effective at the bedtime or fasted-AM dose.
Alpha-GPC:: 300–600 mg taken 30–60 minutes before dosing. Raises acetylcholine, which stimulates the pituitary's cholinergic GH-release pathway — a complementary amplifier to GHRP-6's ghrelin-receptor route. The 600 mg dose is associated with the largest pre-exercise GH augmentation in the supplement literature.

MITIGATE — Appetite management + cortisol buffer

GHRP-6's defining cost: a strong hunger surge ~20–30 min post-dose (the most pronounced in the GHRP family) plus a cortisol/prolactin nudge above the GH-saturation dose.

Protein-first meal planning:: The appetite surge is real and difficult to suppress — work with it rather than against it. Have a protein-forward meal (30–50 g protein, low-glycemic carbohydrate) ready for the hunger window. In a growth phase this is a feature; in a cut it is the primary reason users switch to ipamorelin or GHRP-2 instead.
Berberine 500 mg:: With the post-dose meal, especially relevant on GHRP-6 because its appetite drive tends to push caloric intake up. Berberine activates AMPK and improves insulin sensitivity, helping prevent the GH-driven glucose drift from landing in fat storage.
Alpha-lipoic acid (ALA) 300–600 mg:: Antioxidant cofactor that supports insulin sensitivity. Pair with the post-dose meal, particularly if dosing GHRP-6 multiple times daily. Mitigates the blood-sugar excursions that recurrent GH pulses can cause.
Cortisol — keep dose in range:: Cortisol/prolactin co-release is dose-dependent and emerges above the GH-plateau dose (~1 µg/kg IV; roughly ~200 mcg SC). The most actionable mitigation is not overshooting the dose — there is nothing to gain hormonally above the plateau, and the cortisol/prolactin cost rises. Phosphatidylserine 400 mg is a common cortisol-buffering supplement used by practitioners running GH secretagogues; evidence base is modest but the risk is negligible.

SUPPLY — Protein + ZMA (give the signal its substrate)

GH releases; IGF-1 is the downstream messenger that drives protein synthesis. The signal is useless if the building material isn't there.

Protein 1.6–2.0 g/kg/day:: The minimum effective protein intake for an anabolic goal. GHRP-6's appetite drive typically makes hitting this easy — the discipline is steering the calories toward protein and complex carbs rather than letting hunger run into empty calories. Leucine-rich sources (whey, eggs, meat) maximize the mTOR signal that IGF-1 triggers.
ZMA before bed:: Zinc 30 mg + magnesium glycinate 400 mg + B6 10 mg, taken 30–60 minutes before the bedtime GHRP-6 dose. Zinc is required for IGF-1 synthesis (low zinc → lower IGF-1); magnesium supports deep slow-wave sleep — the window where GH peaks naturally and GHRP-6's bedtime dose piggybacks. A sleep-quality cofactor and a GH-axis substrate in one.
Vitamin D3 2,000–5,000 IU/day:: Vitamin D deficiency is associated with blunted GH-axis function. A pragmatic background supplement given how common insufficiency is — not a GHRP-6-specific mechanism, but a dependency the axis has regardless of the secretagogue used.

Combinations + timing

Stacking notes + timing windows

GHRP-6 covers the ghrelin-receptor arm of GH release. The classic pairing is the other arm: a GHRH analog. The synergy is genuine human pharmacology, not convention — submaximal GHRP-6 + submaximal GHRH produces greater-than-additive GH in the published studies. One critical stacking rule for this class: pairing two GHRPs (Ipamorelin, GHRP-2, Hexarelin) is redundant — they hit the same receptor; you get no additional GH and double the off-target effects.

Cross-class GHRH+GHRP synergy is human-pharmacology-grounded (Bowers 1990, Popovic 1995). Specific branded pairings and cycle conventions are practitioner convention, not head-to-head RCTs. WADA S2 applies to the whole stack.

GHRP-6 + CJC-1295 (the canonical GH stack)

CJC-1295 supplies the GHRH-receptor arm; GHRP-6 supplies the ghrelin-receptor arm — two independent inputs into one synergistic GH pulse.

Why it works:: CJC-1295 (a long-acting GHRH analog) occupies the GHRH receptor on the pituitary; GHRP-6 simultaneously activates the GHS-R1a (ghrelin) receptor. Because the two pathways converge on the pituitary somatotroph from different angles, together they produce a GH pulse greater than either alone — established in the Bowers 1990 human pharmacology. CJC-1295's long half-life also sustains background GHRH tone between GHRP-6 doses.
The protocol:: GHRP-6 100–200 mcg subcutaneous + CJC-1295 (without DAC) 100 mcg subcutaneous, co-injected at the same time in the same or adjacent sites. Typical windows: fasted AM and/or bedtime. CJC-1295 with DAC (the depot form) is dosed less frequently — 2 mg once or twice weekly — and is typically not co-injected but timed to maintain background GHRH.
Outcome:: The combination users reach for when the goal is maximal GH-pulse amplitude with a clean profile. Note: GHRP-6's appetite effect is fully present in this stack — if hunger is not wanted, Ipamorelin is the cleaner GHRP-side substitute.

GHRP-6 + Sermorelin (the gentler GHRH partner)

Sermorelin is a shorter-acting GHRH-receptor agonist — the same synergy with a softer hormonal footprint.

Why it works:: Sermorelin acts on the GHRH receptor; GHRP-6 acts on GHS-R1a — the same complementary-receptor synergy as the CJC-1295 stack. Sermorelin's shorter half-life means the GHRH input is more tightly timed to the injection rather than providing sustained background tone, which some practitioners prefer for a more physiologically pulsatile pattern.
The protocol:: GHRP-6 100–200 mcg + sermorelin 100–200 mcg, co-injected subcutaneously. Bedtime is the favored window; the two clear quickly, allowing the body's own GH rhythm to dominate off-cycle hours.
Outcome:: Commonly used when a gentler or more cycling-friendly GH protocol is preferred, or as an introduction to the GHRH+GHRP class before committing to a longer-acting analog.

GHRP-6 alone — appetite/bulk phase (no GHRH partner)

When the appetite drive IS the goal — a deliberate weight-gain or eating phase — GHRP-6 is used as a standalone to leverage the hunger surge rather than pair it with anything.

Why it works:: GHRP-6 is the ghrelin-receptor agonist with the strongest appetite signal of the GHRP family. Used solo, the hunger effect is fully expressed without needing to manage a GHRH partner. This is not a 'stack' in the synergy sense — it is a deliberate use of GHRP-6's defining side effect as a feature.
The protocol:: GHRP-6 100–300 mcg subcutaneous, 1–3× daily. Time doses before meals to align the hunger surge with planned eating windows. Higher-end doses (200–300 mcg) are used when appetite stimulation is the primary objective, not GH optimization.
Outcome:: Used in bulking or appetite-support contexts where eating enough is the constraint. Not recommended when fat loss is the goal — the hunger drive works against a deficit.

Redundant pairings to avoid

Two GHRPs together push the same receptor twice — the GH response does not compound, but the side effects do.

GHRP-6 + ipamorelin / GHRP-2 / Hexarelin:: All four are GHS-R1a agonists. Combining any two of them saturates the same receptor without producing additive GH — you get doubled cortisol/prolactin/appetite exposure for no additional GH benefit. If you want the cleaner GHRP profile alongside GHRP-6's appetite drive, switch entirely to Ipamorelin or GHRP-2 instead; don't run both.

Sources:PMID 2108187 PMID 7883854 JCEM 83(4):1186

Reconstitution math

Reconstitution calculator

Calculated for a 1 mL U-100 insulin syringe (100 units/mL).

Peptide per vial

BAC water added

Desired dose

Units per dose

Draw to this mark on a U-100 syringe

Volume per dose: 0.04 mL
Doses per vial: 50
Concentration: 2.5 mg/mL

One vial lasts

Daily: 50 days
Every other day: 100 days
5×/week: 70 days

Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.

From the studies

Side effects from research

The two characteristic off-target signals are hormonal and orexigenic. Above the dose that saturates the growth-hormone response, GHRP-6 increases ACTH and cortisol and raises prolactin; this is an intrinsic property of the GHRP class rather than an impurity effect.

As a ghrelin-receptor agonist, GHRP-6 stimulates appetite. This is firmly established mechanistically and in animal feeding studies; a precise, quantified human food-intake figure for GHRP-6 itself is not available in the primary literature (the well-known +28% food-intake figure is for ghrelin, the receptor's natural ligand).

GHRP-6 is not an approved drug in any country and has no modern clinical safety dataset for wellness use; commonly repeated claims such as water retention are not backed by a located GHRP-6-specific primary safety study and are therefore not asserted here.

Sources:PMID 10336729 PMID 11751604 PMID 11739476

As reported in literature

Research dosing ranges

These are the doses actually used in the published studies — the evidence the practical figures above lean on, shown separately so research data is never mistaken for a recommended human dose. GHRP-6's human data is research-grade and old: chiefly acute growth-hormone-provocation studies (single doses given to measure the GH spike) in healthy men, plus one modern pharmacokinetic study (which tracks how the drug moves through and clears the body). These are not endorsed protocols. Doses are reported per kilogram of body weight (1 µg/kg = one microgram per kilogram; 1 kg ≈ 2.2 lb). Note the wide gap between the GH-provocation doses (around 1 µg/kg) and the much larger doses used in the pharmacokinetic study (100–400 µg/kg), which were chosen to let the drug be measured in the blood rather than as therapeutic doses.

Dose	Route	Model	Outcome	Sources:
0.1, 0.3, 1.0 µg/kg	IV bolus	Human (normal men)	Dose-dependent GH release; submaximal doses synergize with 1 µg/kg GHRH	PMID 2108187
1 µg/kg (+ GHRH 1 µg/kg)	IV	Human (hypothalamo-pituitary disconnection)	GH response and GHRH synergy abolished → hypothalamic site of action	PMID 7883854
100, 200, 400 µg/kg	IV bolus	Human (9 healthy men)	Pharmacokinetic characterization (dose-proportional AUC)	PMID 23099431
30 µg/kg intranasal; 300 µg/kg oral	Intranasal / oral	Human (normal young men)	Intranasal raised nocturnal GH; oral negligible; ACTH trended up	PMID 10336729
Central (icv)	Intracerebroventricular	Rat	Induced feeding; blocked by a neuropeptide-Y (Y1) receptor antagonist	PMID 11751604

Quick answers

Frequently asked

Does GHRP-6 make you hungry?

Mechanistically yes — it is an agonist at the ghrelin receptor (GHS-R1a), and in animal studies central GHRP-6 drives feeding through hypothalamic neuropeptide-Y signaling. The quantified human appetite data, however, comes from ghrelin itself rather than from GHRP-6 directly, so the exact human magnitude for GHRP-6 is not established.

How is GHRP-6 different from GHRP-2?

Both are hexapeptide agonists at the same ghrelin receptor (GHS-R1a). GHRP-2 is commonly reported as the stronger growth-hormone releaser per microgram, while GHRP-6 is associated with a more prominent appetite-stimulating signal. Both also raise cortisol and prolactin.

How does GHRP-6 differ from sermorelin or CJC-1295?

Sermorelin and CJC-1295 are GHRH-receptor agonists; GHRP-6 acts on a different receptor — the ghrelin receptor (GHS-R1a). Because they work through independent pathways, combining a GHRP with a GHRH analog produces synergistic growth-hormone release.

Is GHRP-6 FDA-approved?

No. GHRP-6 is not approved as a drug in any country; it is a research chemical with no modern efficacy or safety approval.

Is GHRP-6 banned in sport?

Yes. Growth-hormone secretagogues including GHRP-6 are named on the WADA Prohibited List under Section S2 and are prohibited at all times, in and out of competition.

What is GHRP-6's half-life?

In the one modern human intravenous pharmacokinetic study, disposition was bi-exponential: a distribution half-life of about 7.6 minutes and an elimination half-life of about 2.5 hours.

Primary sources

References

PubChem CID 4345065PubChem — GHRP-6 (CID 4345065)
PMID 2108187Bowers et al. 1990 — GHRP-6 GH release and GHRH synergy in normal men (JCEM)
PMID 23099431Cabrales et al. 2013 — human IV pharmacokinetics of GHRP-6 (Eur J Pharm Sci)
PMID 10336729Frieboes et al. 1999 — nocturnal GH/ACTH, route comparison (J Neuroendocrinol)
PMID 7883854Popovic et al. 1995 — GHRP-6 GH secretion abolished in hypothalamo-pituitary disconnection (JCEM 80(3))
JCEM 83(4):1186GHRP-6 requires endogenous hypothalamic GHRH for maximal GH stimulation (JCEM 1998)
PMID 11751604Lawrence et al. 2002 — central ghrelin/GHRP-6 induce feeding via NPY (rat, Endocrinology)
PMID 11739476Wren et al. 2001 — ghrelin increases food intake in humans (+28%) (JCEM)
WADA Prohibited List S2WADA Prohibited List — S2 Peptide Hormones / GH secretagogues (GHRP-6 named)

Research use only · Not medical advice · Updated 2026-06-01