Mechanism

How it works

GHRP-4 acts as an agonist at the growth hormone secretagogue receptor type 1a (GHS-R1a), a G-protein coupled receptor predominantly expressed on somatotroph cells in the anterior pituitary. Binding to GHS-R1a triggers a Gq/11-mediated intracellular signaling cascade that elevates intracellular calcium via phospholipase C and IP3, ultimately causing pulsatile release of endogenous growth hormone. This mechanism is distinct from GHRH, allowing synergistic GH stimulation when both pathways are activated simultaneously.

Reported in research

Benefits

Stimulates pulsatile endogenous growth hormone release from the anterior pituitary
May support lean muscle mass accrual and body composition improvements over time
Potential enhancement of recovery from exercise and soft tissue stress
May contribute to improved sleep quality due to GH's role in restorative sleep phases

Context, not a prescription

Dosing

Typical range: 100-300 mcg per injection, 1-3 times daily (Subcutaneous, Intramuscular)
Cycle length: 8-12 weeks
Half-life: ~15-30 minutes

Safety

Side effects & contraindications

Possible side effects

Increased appetite (ghrelin-mediated, though potentially less pronounced than GHRP-6)
Transient water retention due to elevated GH and downstream IGF-1
Tingling or numbness at injection site
Elevated cortisol and prolactin with higher doses
Mild fatigue or lethargy shortly post-injection

Contraindications

Active or history of hormone-sensitive malignancies (e.g., pituitary tumors, GH-dependent cancers)
Pregnancy or breastfeeding due to unknown fetal safety profile
Severe hypopituitarism without physician supervision
Diabetic patients or those with insulin resistance, given GH's counter-insulin effects

Research information, not medical advice. Always consult a licensed clinician before considering any peptide.

In depth

Full profile

What it does

Users may notice improved sleep quality, faster recovery from workouts, subtle improvements in skin texture, and over weeks, gradual changes in body composition (more muscle, less fat).

How it works

Imagine your pituitary gland is a vending machine for growth hormone. Normally, your body inserts a certain number of coins each day. GHRP-4 is like an extra coin that gets inserted several times a day, causing the machine to dispense more growth hormone than it normally would.

After injection, GHRP-4 travels through your bloodstream and docks onto a specific receptor in your pituitary gland. This docking event triggers a short, sharp pulse of growth hormone release — similar to the natural pulses your body produces during deep sleep. The elevated GH then signals the liver to produce IGF-1, which is responsible for many of the downstream tissue-building effects.

What to expect

GH pulse begins within 15-30 minutes of injection. Noticeable physical changes (body composition, recovery) typically emerge after 4-6 weeks of consistent use.

Week 1: Body adjusts to increased GH pulses. You may notice improved sleep depth and mild appetite increases around injection times. No dramatic physical changes yet.
Weeks 2-4: Recovery from exercise begins to feel noticeably faster. Some users report better skin hydration and slightly improved energy levels. Mild water retention may be visible.
Weeks 4-8: Gradual improvements in body composition become apparent — lean muscle may increase slightly while body fat begins to reduce, particularly with consistent training and nutrition.

Good to know

Start with the lowest effective dose (100 mcg) to assess individual tolerance before increasing
Inject on an empty stomach or away from high-carbohydrate meals to maximize GH pulse amplitude

Staying safe

Increased hunger, especially in the hour after injection
Mild water retention or puffiness, particularly in hands and feet
Brief fatigue or a 'heavy' feeling shortly after dosing

Avoid if you have:

Anyone with a history of cancer, especially hormone-sensitive types
Pregnant or breastfeeding individuals
People with poorly controlled diabetes

Overview

Physiological changes include elevated 24-hour integrated GH secretion, rising serum IGF-1 over weeks, enhanced nitrogen retention, increased lipolysis (particularly visceral adipose tissue), and improved extracellular matrix turnover. In sleep architecture studies with related GHRPs, slow-wave (stage 3/4) sleep duration has been shown to increase, correlating with nocturnal GH secretion. Modest water retention from GH-mediated renal sodium reabsorption is expected, particularly early in the cycle.

How it works

GHS-R1a can be conceptualized as a lock with two complementary keys — endogenous ghrelin and synthetic GHRPs. GHRP-4 acts as a master key engineered to fit this lock with high affinity, triggering the same intracellular cascade but potentially with a modified pharmacological profile, analogous to a selective beta-agonist designed to activate bronchodilation with reduced cardiac side effects compared to a non-selective agonist.

GHRP-4 has a very short plasma half-life of approximately 15-30 minutes due to rapid proteolytic degradation. Peak GH secretion is observed within 15-30 minutes post-injection. The pulsatile nature of induced GH secretion mimics endogenous physiological patterns, preserving pituitary feedback sensitivity and avoiding the downregulation associated with continuous GH infusion. At the tissue level, elevated GH increases lipolysis via hormone-sensitive lipase activation and upregulates IGF-1 receptor signaling in skeletal muscle, promoting nitrogen retention and satellite cell proliferation. Concurrent cortisol and prolactin elevation — mediated by GHS-R1a expression on corticotrophs and lactotrophs — represent key off-target effects that may attenuate the anabolic benefit at supraphysiological doses.

Onset & timeline

GH pulse is detectable by serum GH assay within 15 minutes of subcutaneous injection, peaking at 30-45 minutes and returning to baseline within 2-3 hours. IGF-1 elevation is a slower process, typically measurable after 2-4 weeks of consistent multi-dose daily regimens. Subjective effects (sleep quality, recovery) may precede measurable IGF-1 changes due to direct GH action on target tissues.

Days 1-3: GH pulse pharmacokinetics established. Serum GH spikes 15-30 minutes post-injection with each dose. Mild appetite stimulation and possible transient lethargy post-injection as GH exerts counter-regulatory effects. No measurable IGF-1 change at this stage.
Weeks 1-2: Cumulative GH pulsatility begins to elevate 24-hour integrated GH area under the curve. Early improvements in sleep architecture (increased slow-wave sleep) may become subjectively apparent. Mild edema possible. IGF-1 may begin rising modestly by end of week 2.
Weeks 2-8: Progressive IGF-1 elevation supports enhanced protein synthesis, nitrogen retention, and lipolysis. Body composition changes become measurable — reduced skinfold thickness, potential lean mass accretion in training individuals. Monitoring for cortisol/prolactin elevation recommended if dosing exceeds 300 mcg per injection three times daily.

Getting the most from it

Dose at least 90 minutes post-meal and 30 minutes pre-meal to avoid blunting of GH pulse by somatostatin-inducing postprandial hyperglycemia and free fatty acids
Cycle with a minimum 4-week off period to prevent GHS-R1a desensitization and preserve hypothalamic-pituitary axis responsiveness
Monitor fasting glucose and IGF-1 levels every 4 weeks during extended cycles to ensure IGF-1 remains within age-appropriate physiological range
Consider co-administration with a GHRH analog (e.g., Mod-GRF 1-29/CJC-1295) for synergistic GH pulse amplification via dual-pathway stimulation

Common side effects

Orexigenic effect mediated by GHS-R1a activation in the hypothalamic arcuate nucleus (NPY/AgRP neurons); may be less pronounced than GHRP-6 depending on structural modifications
Transient hypercortisolemia and hyperprolactinemia at doses above 300 mcg per injection, potentially blunting anabolic response
Peripheral edema secondary to GH-induced anti-natriuretic effect on the kidney

Mechanism of action

GHRP-4 is a synthetic hexapeptide GHS-R1a agonist structurally related to GHRP-2 and GHRP-6. Upon binding to GHS-R1a — a 7-transmembrane Gq/11-coupled receptor expressed on anterior pituitary somatotrophs and hypothalamic neurons — GHRP-4 activates phospholipase C-beta, generating inositol-1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3-mediated calcium release from the endoplasmic reticulum, combined with DAG-activated protein kinase C, depolarizes the somatotroph cell membrane and triggers exocytosis of GH-containing secretory granules. Simultaneously, GHS-R1a signaling in the hypothalamus may suppress somatostatin tone, further amplifying the net GH pulse. Downstream, elevated GH triggers hepatic IGF-1 synthesis via JAK2-STAT5b signaling, mediating anabolic and lipolytic effects in peripheral tissues.

GHRP-4 has a very short plasma half-life of approximately 15-30 minutes due to rapid proteolytic degradation. Peak GH secretion is observed within 15-30 minutes post-injection. The pulsatile nature of induced GH secretion mimics endogenous physiological patterns, preserving pituitary feedback sensitivity and avoiding the downregulation associated with continuous GH infusion. At the tissue level, elevated GH increases lipolysis via hormone-sensitive lipase activation and upregulates IGF-1 receptor signaling in skeletal muscle, promoting nitrogen retention and satellite cell proliferation. Concurrent cortisol and prolactin elevation — mediated by GHS-R1a expression on corticotrophs and lactotrophs — represent key off-target effects that may attenuate the anabolic benefit at supraphysiological doses.

Pharmacodynamics

GH pulse is detectable by serum GH assay within 15 minutes of subcutaneous injection, peaking at 30-45 minutes and returning to baseline within 2-3 hours. IGF-1 elevation is a slower process, typically measurable after 2-4 weeks of consistent multi-dose daily regimens. Subjective effects (sleep quality, recovery) may precede measurable IGF-1 changes due to direct GH action on target tissues.

Physiological changes include elevated 24-hour integrated GH secretion, rising serum IGF-1 over weeks, enhanced nitrogen retention, increased lipolysis (particularly visceral adipose tissue), and improved extracellular matrix turnover. In sleep architecture studies with related GHRPs, slow-wave (stage 3/4) sleep duration has been shown to increase, correlating with nocturnal GH secretion. Modest water retention from GH-mediated renal sodium reabsorption is expected, particularly early in the cycle.

Timeline

Days 1-3: GH pulse pharmacokinetics established. Serum GH spikes 15-30 minutes post-injection with each dose. Mild appetite stimulation and possible transient lethargy post-injection as GH exerts counter-regulatory effects. No measurable IGF-1 change at this stage.
Weeks 1-2: Cumulative GH pulsatility begins to elevate 24-hour integrated GH area under the curve. Early improvements in sleep architecture (increased slow-wave sleep) may become subjectively apparent. Mild edema possible. IGF-1 may begin rising modestly by end of week 2.
Weeks 2-8: Progressive IGF-1 elevation supports enhanced protein synthesis, nitrogen retention, and lipolysis. Body composition changes become measurable — reduced skinfold thickness, potential lean mass accretion in training individuals. Monitoring for cortisol/prolactin elevation recommended if dosing exceeds 300 mcg per injection three times daily.

Comparisons

GHRP-4 — effectiveness Moderate, safety Moderate, cost $$, Medium to use
GHRP-2 — effectiveness High, safety Good, cost $$, Medium to use
Mod-GRF 1-29 + GHRP-4 Stack — effectiveness High, safety Moderate, cost $$$, High to use

Adverse effects

Common:

Orexigenic effect mediated by GHS-R1a activation in the hypothalamic arcuate nucleus (NPY/AgRP neurons); may be less pronounced than GHRP-6 depending on structural modifications
Transient hypercortisolemia and hyperprolactinemia at doses above 300 mcg per injection, potentially blunting anabolic response
Peripheral edema secondary to GH-induced anti-natriuretic effect on the kidney

Rare:

Carpal tunnel syndrome-like symptoms from GH-mediated fluid accumulation in synovial sheaths (incidence <5% in GHRP class studies)
Transient dysglycemia in insulin-resistant individuals due to GH counter-regulatory effects on glucose metabolism

Contraindications & risk mitigation

Contraindicated in:

Patients with active acromegaly or GH hypersecretion syndromes
Individuals with known GH-dependent neoplasia (e.g., GH receptor-positive breast cancer, colonic polyps)
Patients on glucocorticoid therapy (potential synergistic HPA axis disruption)
Type 1 or Type 2 diabetics with poor glycemic control

Dose at least 90 minutes post-meal and 30 minutes pre-meal to avoid blunting of GH pulse by somatostatin-inducing postprandial hyperglycemia and free fatty acids
Cycle with a minimum 4-week off period to prevent GHS-R1a desensitization and preserve hypothalamic-pituitary axis responsiveness
Monitor fasting glucose and IGF-1 levels every 4 weeks during extended cycles to ensure IGF-1 remains within age-appropriate physiological range
Consider co-administration with a GHRH analog (e.g., Mod-GRF 1-29/CJC-1295) for synergistic GH pulse amplification via dual-pathway stimulation

Qué hace

Users may notice improved sleep quality, faster recovery from workouts, subtle improvements in skin texture, and over weeks, gradual changes in body composition (more muscle, less fat).

Cómo funciona

Imagine your pituitary gland is a vending machine for growth hormone. Normally, your body inserts a certain number of coins each day. GHRP-4 is like an extra coin that gets inserted several times a day, causing the machine to dispense more growth hormone than it normally would.

After injection, GHRP-4 travels through your bloodstream and docks onto a specific receptor in your pituitary gland. This docking event triggers a short, sharp pulse of growth hormone release — similar to the natural pulses your body produces during deep sleep. The elevated GH then signals the liver to produce IGF-1, which is responsible for many of the downstream tissue-building effects.

Qué esperar

GH pulse begins within 15-30 minutes of injection. Noticeable physical changes (body composition, recovery) typically emerge after 4-6 weeks of consistent use.

Week 1: Body adjusts to increased GH pulses. You may notice improved sleep depth and mild appetite increases around injection times. No dramatic physical changes yet.
Weeks 2-4: Recovery from exercise begins to feel noticeably faster. Some users report better skin hydration and slightly improved energy levels. Mild water retention may be visible.
Weeks 4-8: Gradual improvements in body composition become apparent — lean muscle may increase slightly while body fat begins to reduce, particularly with consistent training and nutrition.

Bueno saber

Start with the lowest effective dose (100 mcg) to assess individual tolerance before increasing
Inject on an empty stomach or away from high-carbohydrate meals to maximize GH pulse amplitude

Manteniéndose seguro

Increased hunger, especially in the hour after injection
Mild water retention or puffiness, particularly in hands and feet
Brief fatigue or a 'heavy' feeling shortly after dosing

Evitar si tienes:

Anyone with a history of cancer, especially hormone-sensitive types
Pregnant or breastfeeding individuals
People with poorly controlled diabetes

Descripción general

Physiological changes include elevated 24-hour integrated GH secretion, rising serum IGF-1 over weeks, enhanced nitrogen retention, increased lipolysis (particularly visceral adipose tissue), and improved extracellular matrix turnover. In sleep architecture studies with related GHRPs, slow-wave (stage 3/4) sleep duration has been shown to increase, correlating with nocturnal GH secretion. Modest water retention from GH-mediated renal sodium reabsorption is expected, particularly early in the cycle.

Cómo funciona

GHS-R1a can be conceptualized as a lock with two complementary keys — endogenous ghrelin and synthetic GHRPs. GHRP-4 acts as a master key engineered to fit this lock with high affinity, triggering the same intracellular cascade but potentially with a modified pharmacological profile, analogous to a selective beta-agonist designed to activate bronchodilation with reduced cardiac side effects compared to a non-selective agonist.

GHRP-4 has a very short plasma half-life of approximately 15-30 minutes due to rapid proteolytic degradation. Peak GH secretion is observed within 15-30 minutes post-injection. The pulsatile nature of induced GH secretion mimics endogenous physiological patterns, preserving pituitary feedback sensitivity and avoiding the downregulation associated with continuous GH infusion. At the tissue level, elevated GH increases lipolysis via hormone-sensitive lipase activation and upregulates IGF-1 receptor signaling in skeletal muscle, promoting nitrogen retention and satellite cell proliferation. Concurrent cortisol and prolactin elevation — mediated by GHS-R1a expression on corticotrophs and lactotrophs — represent key off-target effects that may attenuate the anabolic benefit at supraphysiological doses.

Inicio y cronología

GH pulse is detectable by serum GH assay within 15 minutes of subcutaneous injection, peaking at 30-45 minutes and returning to baseline within 2-3 hours. IGF-1 elevation is a slower process, typically measurable after 2-4 weeks of consistent multi-dose daily regimens. Subjective effects (sleep quality, recovery) may precede measurable IGF-1 changes due to direct GH action on target tissues.

Days 1-3: GH pulse pharmacokinetics established. Serum GH spikes 15-30 minutes post-injection with each dose. Mild appetite stimulation and possible transient lethargy post-injection as GH exerts counter-regulatory effects. No measurable IGF-1 change at this stage.
Weeks 1-2: Cumulative GH pulsatility begins to elevate 24-hour integrated GH area under the curve. Early improvements in sleep architecture (increased slow-wave sleep) may become subjectively apparent. Mild edema possible. IGF-1 may begin rising modestly by end of week 2.
Weeks 2-8: Progressive IGF-1 elevation supports enhanced protein synthesis, nitrogen retention, and lipolysis. Body composition changes become measurable — reduced skinfold thickness, potential lean mass accretion in training individuals. Monitoring for cortisol/prolactin elevation recommended if dosing exceeds 300 mcg per injection three times daily.

Cómo aprovecharlo al máximo

Dose at least 90 minutes post-meal and 30 minutes pre-meal to avoid blunting of GH pulse by somatostatin-inducing postprandial hyperglycemia and free fatty acids
Cycle with a minimum 4-week off period to prevent GHS-R1a desensitization and preserve hypothalamic-pituitary axis responsiveness
Monitor fasting glucose and IGF-1 levels every 4 weeks during extended cycles to ensure IGF-1 remains within age-appropriate physiological range
Consider co-administration with a GHRH analog (e.g., Mod-GRF 1-29/CJC-1295) for synergistic GH pulse amplification via dual-pathway stimulation

Efectos secundarios comunes

Orexigenic effect mediated by GHS-R1a activation in the hypothalamic arcuate nucleus (NPY/AgRP neurons); may be less pronounced than GHRP-6 depending on structural modifications
Transient hypercortisolemia and hyperprolactinemia at doses above 300 mcg per injection, potentially blunting anabolic response
Peripheral edema secondary to GH-induced anti-natriuretic effect on the kidney

Mecanismo de acción

GHRP-4 is a synthetic hexapeptide GHS-R1a agonist structurally related to GHRP-2 and GHRP-6. Upon binding to GHS-R1a — a 7-transmembrane Gq/11-coupled receptor expressed on anterior pituitary somatotrophs and hypothalamic neurons — GHRP-4 activates phospholipase C-beta, generating inositol-1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3-mediated calcium release from the endoplasmic reticulum, combined with DAG-activated protein kinase C, depolarizes the somatotroph cell membrane and triggers exocytosis of GH-containing secretory granules. Simultaneously, GHS-R1a signaling in the hypothalamus may suppress somatostatin tone, further amplifying the net GH pulse. Downstream, elevated GH triggers hepatic IGF-1 synthesis via JAK2-STAT5b signaling, mediating anabolic and lipolytic effects in peripheral tissues.

GHRP-4 has a very short plasma half-life of approximately 15-30 minutes due to rapid proteolytic degradation. Peak GH secretion is observed within 15-30 minutes post-injection. The pulsatile nature of induced GH secretion mimics endogenous physiological patterns, preserving pituitary feedback sensitivity and avoiding the downregulation associated with continuous GH infusion. At the tissue level, elevated GH increases lipolysis via hormone-sensitive lipase activation and upregulates IGF-1 receptor signaling in skeletal muscle, promoting nitrogen retention and satellite cell proliferation. Concurrent cortisol and prolactin elevation — mediated by GHS-R1a expression on corticotrophs and lactotrophs — represent key off-target effects that may attenuate the anabolic benefit at supraphysiological doses.

Farmacodinamia

GH pulse is detectable by serum GH assay within 15 minutes of subcutaneous injection, peaking at 30-45 minutes and returning to baseline within 2-3 hours. IGF-1 elevation is a slower process, typically measurable after 2-4 weeks of consistent multi-dose daily regimens. Subjective effects (sleep quality, recovery) may precede measurable IGF-1 changes due to direct GH action on target tissues.

Physiological changes include elevated 24-hour integrated GH secretion, rising serum IGF-1 over weeks, enhanced nitrogen retention, increased lipolysis (particularly visceral adipose tissue), and improved extracellular matrix turnover. In sleep architecture studies with related GHRPs, slow-wave (stage 3/4) sleep duration has been shown to increase, correlating with nocturnal GH secretion. Modest water retention from GH-mediated renal sodium reabsorption is expected, particularly early in the cycle.

Cronología

Days 1-3: GH pulse pharmacokinetics established. Serum GH spikes 15-30 minutes post-injection with each dose. Mild appetite stimulation and possible transient lethargy post-injection as GH exerts counter-regulatory effects. No measurable IGF-1 change at this stage.
Weeks 1-2: Cumulative GH pulsatility begins to elevate 24-hour integrated GH area under the curve. Early improvements in sleep architecture (increased slow-wave sleep) may become subjectively apparent. Mild edema possible. IGF-1 may begin rising modestly by end of week 2.
Weeks 2-8: Progressive IGF-1 elevation supports enhanced protein synthesis, nitrogen retention, and lipolysis. Body composition changes become measurable — reduced skinfold thickness, potential lean mass accretion in training individuals. Monitoring for cortisol/prolactin elevation recommended if dosing exceeds 300 mcg per injection three times daily.

Comparaciones

GHRP-4 — efectividad Moderate, seguridad Moderate, costo $$, Medium de usar
GHRP-2 — efectividad High, seguridad Good, costo $$, Medium de usar
Mod-GRF 1-29 + GHRP-4 Stack — efectividad High, seguridad Moderate, costo $$$, High de usar

Efectos adversos

Comunes:

Orexigenic effect mediated by GHS-R1a activation in the hypothalamic arcuate nucleus (NPY/AgRP neurons); may be less pronounced than GHRP-6 depending on structural modifications
Transient hypercortisolemia and hyperprolactinemia at doses above 300 mcg per injection, potentially blunting anabolic response
Peripheral edema secondary to GH-induced anti-natriuretic effect on the kidney

Raros:

Carpal tunnel syndrome-like symptoms from GH-mediated fluid accumulation in synovial sheaths (incidence <5% in GHRP class studies)
Transient dysglycemia in insulin-resistant individuals due to GH counter-regulatory effects on glucose metabolism

Contraindicaciones y mitigación de riesgos

Contraindicado en:

Patients with active acromegaly or GH hypersecretion syndromes
Individuals with known GH-dependent neoplasia (e.g., GH receptor-positive breast cancer, colonic polyps)
Patients on glucocorticoid therapy (potential synergistic HPA axis disruption)
Type 1 or Type 2 diabetics with poor glycemic control

Dose at least 90 minutes post-meal and 30 minutes pre-meal to avoid blunting of GH pulse by somatostatin-inducing postprandial hyperglycemia and free fatty acids
Cycle with a minimum 4-week off period to prevent GHS-R1a desensitization and preserve hypothalamic-pituitary axis responsiveness
Monitor fasting glucose and IGF-1 levels every 4 weeks during extended cycles to ensure IGF-1 remains within age-appropriate physiological range
Consider co-administration with a GHRH analog (e.g., Mod-GRF 1-29/CJC-1295) for synergistic GH pulse amplification via dual-pathway stimulation

Reference data

Specifications

Half-life: ~15-30 minutes
Route: Subcutaneous, Intramuscular
Cycle length: 8-12 weeks
Storage: Store lyophilized powder at -20°C for long-term stability (up to 24 months). After reconstitution with bacteriostatic water, store at 2-8°C (refrigerated) and use within 28 days. Protect from light and repeated freeze-thaw cycles.
Legal status: Research chemical; not approved for human therapeutic use by FDA, EMA, or equivalent agencies. Legal to purchase for research purposes in many jurisdictions. Not approved as a drug or dietary supplement.

FAQ

Common questions

How does GHRP-4 differ pharmacologically from GHRP-2 and GHRP-6?

GHRP-2, GHRP-6, and GHRP-4 are all GHS-R1a agonists derived from the same hexapeptide scaffold originally developed by Cyril Bowers' group. GHRP-6 (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) has the most potent appetite-stimulant profile due to strong hypothalamic NPY/AgRP activation. GHRP-2 tends to produce higher cortisol and prolactin co-secretion. GHRP-4 is a less characterized structural analog with limited published preclinical data; it is hypothesized to have an intermediate or modified receptor binding profile, but direct head-to-head pharmacological comparison studies are not publicly available for this specific analog.

Does GHRP-4 cause pituitary desensitization?

Continuous or very high-frequency GHRP dosing can lead to GHS-R1a downregulation and reduced pituitary responsiveness over time. This is why pulsatile dosing protocols (mimicking endogenous GH secretory patterns) and periodic cycle breaks are recommended. Animal studies with related GHRPs suggest receptor resensitization occurs within 2-4 weeks of cessation.

What is the evidence level?

This compound is classified as Anecdotal. Evidence relies primarily on self-reported user experiences. Controlled studies are lacking.

Research

Research & sources

Anecdotal

Current evidence for GHRP-4 is rated as Anecdotal. No controlled clinical research is available.

1. Synthetic peptides as growth hormone secretagogues (1996) — Endocrine Reviews, Bowers CY
2. Ghrelin: a growth-hormone-releasing acylated peptide from stomach (1999) — Nature, Kojima M et al., doi:10.1038/45230
3. The growth hormone secretagogue receptor (2007) — Vitamins and Hormones, Chollet C et al.
4. Growth hormone secretagogues: mechanisms of action and use in clinical practice (2010) — Reviews in Endocrine and Metabolic Disorders

Explore

Often discussed alongside

GHRP-2 · growth GHRP-6 · growth CJC-1295 · growth BPC-157 · healing TB-500 · healing