Ipamorelin is a small lab-made peptide that nudges the pituitary gland to release more growth hormone. It's popular because it does this cleanly, without raising stress hormones like cortisol. It's often paired with CJC-1295, but it isn't FDA-approved and its long-term benefits for anti-aging or performance have never been proven in people.
What is Ipamorelin?
Ipamorelin is a pentapeptide (five amino acids) that selectively stimulates growth hormone release from the pituitary gland. What makes it notable is its selectivity — in the original animal studies it released GH without raising ACTH or cortisol, unlike GHRP-6 and GHRP-2. This selectivity is why it is considered one of the most well-tolerated peptides in the growth hormone category.
What Ipamorelin Is Investigated For
Ipamorelin is investigated for GH-mediated body composition improvement, sleep quality, and recovery, and is often discussed in the context of the CJC-1295 + ipamorelin stack that dual-activates the GHRH and ghrelin receptor pathways. The strongest evidence is for its defining selectivity profile, and it comes from animal work: in swine, Raun et al. (1998) found that GHRP-6 and GHRP-2 raised ACTH and cortisol along with GH while ipamorelin did not, even at doses more than 200-fold above its effective GH-releasing dose. None of the secretagogues in that study changed prolactin, so it does not show prolactin selectivity. Human data are limited to pharmacokinetic work showing a single, dose-proportional GH pulse. Two Phase 2 efficacy trials were completed in postoperative ileus, and between them they are the whole of ipamorelin's efficacy record. The published one found no significant difference from placebo (time to first tolerated meal 25.3 vs 32.6 hours, p=0.15). The second, NCT01280344, was nearly three times larger at 320 patients, finished in May 2014, and has never posted results or appeared in the literature — so the only efficacy data the public can read are negative, and the larger dataset that might have changed that picture was never released. The program did not advance, and ipamorelin is not FDA-approved for any indication. Downstream outcomes — body composition, lean-mass gain, sleep improvement, recovery — are plausible from GH/IGF-1 pharmacology but have never been tested in long-duration human endpoint trials. The best honest framing is 'cleanest of the GHRPs on side-effect profile, but without definitive clinical efficacy data for anti-aging or performance use.'
History & Discovery
Ipamorelin was developed at Novo Nordisk in the late 1990s and first reported in the peer-reviewed literature in 1998 (Raun et al., European Journal of Endocrinology). It emerged from a medicinal-chemistry program aimed at improving on the earlier growth hormone-releasing peptides (GHRP-6, GHRP-2, hexarelin) by stripping away the off-target hormonal effects — particularly cortisol, ACTH, and prolactin elevation — that limited the older compounds. Novo Nordisk screened a series of pentapeptides and identified the Aib-His-D-2-Nal-D-Phe-Lys-NH2 sequence as retaining potent ghrelin-receptor agonism while demonstrating remarkable selectivity: in the original swine studies, even at doses more than 200-fold above the effective GH-releasing dose, it did not significantly raise ACTH or cortisol (prolactin did not change with any of the secretagogues tested). Novo Nordisk progressed ipamorelin into early human trials but ultimately did not advance it toward an approved indication; the compound was later licensed to Helsinn Therapeutics, which ran a Phase 2 proof-of-concept trial of intravenous ipamorelin in postoperative ileus (published 2014). It found no significant difference from placebo (time to first tolerated meal 25.3 vs 32.6 hours, p=0.15), and the program did not move to Phase III. No approved therapeutic indication has materialized. Like CJC-1295, ipamorelin migrated into the research-chemical and compounding-pharmacy channel during the 2010s, where it became one of the most commonly discussed peptides in the GH-optimization space — largely on the strength of its selectivity profile and the 'cleanest of the GHRPs' reputation it earned in the preclinical literature.
How It Works
Ipamorelin works by mimicking ghrelin, a natural hunger hormone that also triggers growth hormone release. However, it is designed to be very selective — it tells the pituitary to release GH without triggering other hormonal responses that could cause unwanted side effects.
Ipamorelin is a pentapeptide ghrelin mimetic that binds to the GHS-R1a (growth hormone secretagogue receptor) in the pituitary gland. Unlike GHRP-6 and GHRP-2, it released GH without increasing ACTH or cortisol in swine studies, even at doses far above its GH-releasing dose. It acts synergistically with GHRH, which is why it is commonly paired with CJC-1295. GH release follows a saturating dose-response curve — Raun's swine work fitted an ED50 of 2.3 nmol/kg against a ceiling response, and the human PK/PD study fitted a half-maximal concentration of 214 nmol/L across a 33-fold dose range without a downturn — and it preserves the natural pulsatile pattern of GH secretion. The synergy with GHRH that underpins every stacking protocol was demonstrated for GHRP-6, not for ipamorelin: Bowers and colleagues showed in 1990 that submaximal GHRP-6 plus GHRH released GH synergistically in normal men. No published study has co-administered ipamorelin with a GHRH analog in humans, so the stack is a class extrapolation.
Evidence Snapshot
Human Clinical Evidence
Limited, and thinner than the peptide's popularity suggests. One Phase 1 PK/PD study in healthy men established that a single intravenous dose produces a single GH pulse, with dose-proportional ipamorelin kinetics. Beyond that, the human record is two completed Phase 2 trials in postoperative ileus run by the same sponsor: the published 117-patient trial missed its endpoint, and the 320-patient trial has never reported. No human study has measured IGF-1, ACTH or cortisol on ipamorelin, so the selectivity that defines the molecule rests entirely on animal data.
Animal / Preclinical
Strong. Well-characterized selectivity profile in multiple animal models.
Mechanistic Rationale
Strong. GHS-R1a receptor pharmacology is well understood.
Research Gaps & Open Questions
What the current literature has not yet settled about Ipamorelin:
- 01Long-term (>12 month) human safety and efficacy data in healthy adults is absent — ipamorelin has no completed late-stage human program at any indication.
- 02Whether the superior selectivity profile observed preclinically (no ACTH or cortisol elevation in swine) translates into a meaningfully better long-term human safety margin vs. older GHRPs has not been directly tested in long-duration trials.
- 03Head-to-head clinical comparison of ipamorelin monotherapy vs. ipamorelin + GHRH-analog stacks — the stacking argument is pharmacological rather than outcome-validated in controlled human endpoint data.
- 04Optimal cycling cadence vs. continuous dosing has not been studied; tachyphylaxis risk at the ghrelin receptor with chronic exposure is theoretical rather than quantified.
- 05IGF-1 elevation magnitude and downstream cancer-promotion risk specific to ipamorelin has not been characterized in long-term human pharmacovigilance.
- 06No indication has Phase 3 data: the postoperative ileus program produced a negative Phase 2 trial, and cachexia data are preclinical (a ferret cisplatin model, co-authored with the sponsor of the ipamorelin trials).
- 07A second, larger Phase 2 trial has never reported. NCT01280344 randomised 320 bowel-resection patients across three ipamorelin dose arms and placebo, completed in May 2014, and has posted no results and generated no publication in more than a decade. Until it does, the public efficacy record for ipamorelin is one negative trial a third its size.
- 08Whether ipamorelin's cortisol and ACTH selectivity holds in humans. The claim rests entirely on swine; no human study has measured either hormone on ipamorelin, and a 2024 fish study found luteinizing hormone and 11-ketotestosterone rose with dosing, which is not what the swine data would predict.
Forms & Administration
Ipamorelin is administered via subcutaneous injection, typically in the evening before bed to align with natural GH release patterns. Protocols should be determined by a qualified clinician.
Dosing & Protocols
The ranges below reflect protocols commonly discussed in the literature and by clinicians — not a prescription. Actual dosing for any individual should be determined by a qualified healthcare provider who knows the patient.
Typical Range
Protocols commonly discussed for ipamorelin run 200–300 mcg per dose, administered 1–3 times daily. The most conservative protocols use 200 mcg once daily at bedtime; more aggressive body-composition protocols use 300 mcg three times daily (morning, pre-workout or midday, bedtime). Total daily doses above roughly 1 mg produce diminishing returns because the GH response saturates: both the swine and the human dose-response data fit a ceiling, so higher single doses do not produce proportionally greater GH release. The widely repeated claim that the curve is bell-shaped, with high doses actively suppressing the response, has no published support for ipamorelin.
Frequency
Ipamorelin is short-acting (serum half-life ~2 hours), so frequent dosing produces multiple discrete GH pulses per day. The standard stacking rationale with a GHRH analog like CJC-1295 or sermorelin rests on two distinct receptor pathways: ipamorelin acts at the ghrelin/GHS-R1a receptor on somatotrophs, while GHRH analogs act at the GHRH receptor. In the GHRP class this combination produces a GH pulse substantially greater than either component alone — a synergistic rather than additive effect, because the GHRH component increases somatotroph readiness while the GHRP component triggers release. It is worth being precise about where that evidence comes from: the human demonstration is Bowers 1990, using GHRP-6, and no published human study has given ipamorelin together with a GHRH analog. The dual-pathway rationale behind nearly every ipamorelin + CJC protocol in circulation is sound pharmacology extrapolated across the class, not a measured result for this peptide.
Timing Considerations
Time of day
Bedtime is the most common window, aligned with the natural nocturnal GH pulse; multi-dose protocols typically add a mid-morning fasted dose and a pre-workout dose.
Relative to meals
Fasted — at least 30 minutes before food and 2+ hours after a meal. Elevated insulin and circulating amino acids substantially blunt GH release, so meal timing directly affects pulse amplitude.
Relative to exercise
Independent of training, though some users add a pre-workout dose on training days for an additional GH pulse around exercise.
Cycle Length
Commonly discussed protocols run 8–12 weeks on, followed by a 4-week off period. Continuous use is also discussed in wellness contexts; pituitary desensitization is usually described as purely theoretical, which overstates the case. In the one chronic-dosing study on this page, adult female rats given ipamorelin three times daily for 15 days showed a marginally reduced GH response to a provocative dose at the end (P<0.03), while the response to GHRH was unchanged and pituitary GH content was unaffected — a small, receptor-specific blunting rather than a collapse. Nothing equivalent has been measured in humans, and no trial has compared continuous against cycled dosing.
Protocol Notes
Ipamorelin is supplied as a lyophilized powder — typically 2 mg or 5 mg per vial — reconstituted in bacteriostatic water. A 5 mg vial in 2 mL of BAC water yields 2,500 mcg/mL, making 250 mcg roughly 0.1 mL or 10 units on an insulin syringe. Subcutaneous injection into the abdominal fat pad is the standard route. Because ipamorelin acts at the ghrelin receptor, dosing on a relatively empty stomach matters: circulating amino acids and elevated insulin blunt GH release, so most protocols call for injection at least 30 minutes before eating or 2+ hours after a meal. Bedtime dosing is popular because it aligns with the natural nocturnal GH pulse and can enhance slow-wave sleep in users. When stacked with CJC-1295 no-DAC or sermorelin, both peptides are typically drawn into the same syringe and injected together at each dosing window.
Ipamorelin is not FDA-approved for any indication. The numbers above describe commonly-referenced protocols, not a prescription. Use should be supervised by a qualified clinician with appropriate IGF-1 and metabolic monitoring.
Timeline of Effects
Onset
Sleep-quality improvements — particularly deeper and more restorative slow-wave sleep — are the most commonly reported early signal, often within the first 1–2 weeks of bedtime dosing. Subjective recovery benefits (less post-workout soreness, faster return to training) follow in a similar window. Body-composition changes — modest fat mass reduction, lean mass preservation or gain — typically require 4–8+ weeks of consistent use before becoming visible.
Peak Effect
Serum IGF-1 is the marker everyone tracks, but it is worth knowing that no human ipamorelin study has ever measured it — the human PK/PD trial assayed only ipamorelin and GH — and the one chronic animal study on this page found no change in total IGF-1, IGFBPs or bone-turnover markers after 15 days. The expectation that IGF-1 rises progressively over the first month and then plateaus is inferred from GH physiology and from better-studied secretagogues, not demonstrated for this peptide. GH pulse amplitude is elevated from the first dose; any downstream IGF-1 accumulation would take weeks. Subjective benefits most commonly plateau around the 3-month mark. Ipamorelin's effect size on IGF-1 is typically modest compared to MK-677 or high-dose CJC-1295 DAC — it is characterized more by its clean side-effect profile than by maximum IGF-1 elevation.
After Discontinuation
Short half-life and no suppression of endogenous GHRH mean endogenous pulsatile GH secretion returns to baseline within days of discontinuation. IGF-1 drifts back to pre-treatment levels over 2–4 weeks. Any accumulated body-composition or sleep benefits wane over weeks to months depending on the underlying reason for the benefit (e.g., sleep improvement tends to regress faster than lean-mass gains). No post-cycle therapy is required, as ipamorelin does not suppress the HPG axis.
Monitoring & Measurement
Bloodwork & Labs
- •IGF-1 (serum) — the primary response marker; the GH pulse itself is too short to catch reliably in routine labs, so IGF-1 is the practical proxy
- •Fasting glucose and HbA1c — GH secretagogues can mildly raise both
- •Lipid panel — visceral-fat-driven changes show here first
- •Cortisol and prolactin — cortisol is expected to stay flat on ipamorelin (it did not raise ACTH or cortisol in animal studies); a clear rise in either suggests a non-selective or contaminated batch
Functional & Performance Tests
- •DEXA scan — lean mass and visceral fat are the endpoints that matter
- •Waist circumference
- •Grip strength (dynamometer)
- •Overnight sleep quality via wearable (Oura, Whoop, Apple Watch) — sleep depth is a frequently reported effect
When to Test
Baseline, 6 weeks, and 12 weeks on-cycle.
Interpretation & Notes
Treat IGF-1 as the practical response marker while recognising that no published human ipamorelin study has measured it, so there is no validated responder threshold — any specific percentage you see quoted for ipamorelin is extrapolated from other secretagogues. Fasting glucose may drift up 5–15 mg/dL — tolerable, but if it crosses 100 mg/dL or HbA1c reaches 5.7, pull the dose back. Ipamorelin's defining feature is selectivity: unlike GHRP-6 or hexarelin, it should not move cortisol. A marked cortisol or prolactin rise on ipamorelin suggests either a dose too high, a non-selective contaminant, or a mislabeled vial — a useful quality signal for unregulated market sourcing. Standard IGF-1 and metabolic panels are direct-to-consumer via LabCorp, Quest, Marek Health, and Ulta Lab Tests; interpret with a clinician.
Common Questions
Why is Ipamorelin considered 'cleaner' than other GH peptides?
In the original swine studies, ipamorelin released GH without raising ACTH or cortisol, whereas GHRP-6 and GHRP-2 raised both. This selectivity may reduce side effects, though it has not been confirmed in long-term human studies.
Is it often combined with CJC-1295?
Yes. The CJC-1295/Ipamorelin combination is one of the most commonly discussed peptide pairings. CJC-1295 amplifies the GHRH signal while Ipamorelin provides the GH secretagogue stimulus. The synergy itself is well documented in humans — but for GHRP-6, in a 1990 study. No published human trial has given ipamorelin alongside a GHRH analog, so the specific pairing is a reasonable class extrapolation rather than a measured result.
Did the October 2026 HHS policy make ipamorelin legal to compound?
No. On 28 October 2026 HHS announced it would not take enforcement action against pharmacies compounding six named peptide bulk substances — BPC-157, TB-500, epitalon, KPV, MOTS-c and semax. Ipamorelin is not among them. Its position is unchanged: nominations for both the acetate and the free base were withdrawn in September 2024, FDA's advisory committee voted 0-12 against adding either form to the 503A Bulks List the following month, and ipamorelin acetate remains in 503B Category 2.
Does ipamorelin raise cortisol in humans?
Nobody has measured it. The selectivity that defines ipamorelin — GH release without the ACTH and cortisol rise seen with GHRP-6 and GHRP-2 — comes from swine studies, where it held even at doses more than 200-fold above the GH-releasing dose. The one human pharmacology study assayed only ipamorelin and growth hormone. The animal result is strong and consistent; it has simply never been confirmed in people, which is a different claim from the one usually made for this peptide.
Who Ipamorelin Is NOT For
- •Active or recent-history cancer — GH and IGF-1 elevation may accelerate proliferation of existing malignancies; clinicians exclude active cancer from secretagogue protocols.
- •Pregnancy — no human pregnancy safety data; reproductive-toxicology characterization is absent.
- •Breastfeeding — no data on transfer into breast milk or effects on nursing infants.
- •Diabetes or uncontrolled insulin resistance — GH opposes insulin action; ipamorelin's GH effect is milder than MK-677's but glycemic monitoring remains prudent.
- •Pediatric use outside a diagnosed GH deficiency — development-related endocrine effects from unmonitored secretagogue use are a concern.
- •Active acromegaly or pituitary adenoma — further stimulation of GH-producing cells is contraindicated.
- •Uncontrolled hypertension or moderate-to-severe sleep apnea — GH elevation can worsen fluid retention and upper-airway edema, though ipamorelin's milder water-retention profile makes this less prominent than with rhGH.
- •Known hypersensitivity to peptide therapeutics or to excipients in compounded preparations.
Drug & Supplement Interactions
Documented clinical drug interactions for ipamorelin are sparse, as no post-marketing surveillance exists. Theoretical concerns track the GH-secretagogue class. Glucose-regulating medications: insulin, sulfonylureas, and GLP-1 agonists may require dose adjustment as GH/IGF-1 rise, because GH opposes insulin action. Ipamorelin's effect is milder than MK-677's but is not zero over weeks of use. Corticosteroids (prednisone, dexamethasone) blunt somatotroph responsiveness and can attenuate ipamorelin's GH-releasing effect at the pituitary level. Thyroid hormone status matters — uncorrected hypothyroidism reduces GH response. Somatostatin analogs (octreotide, lanreotide) directly antagonize GH release and will pharmacologically oppose ipamorelin. Opioids have complex interactions with the ghrelin/GHS-R axis — chronic opioid use can alter ghrelin tone and potentially modulate ipamorelin response, though this is not well characterized in humans. Oral estrogens reduce hepatic IGF-1 generation and can affect interpretation of IGF-1 labs. SSRIs and other serotonergic agents have been implicated in ghrelin-pathway modulation in some preclinical work, but clinical significance for ipamorelin specifically is unclear. Disclose all concurrent medications to the prescribing clinician.
Safety Profile
Common Side Effects
Cautions
- • Not FDA-approved
- • Should be monitored with blood work
- • Not appropriate for those with active malignancies
What We Don't Know
Long-term safety data from large clinical trials is not available. Optimal cycle length and long-term effects are not well established.
Legal Status
United States
Ipamorelin is not FDA-approved for any medical indication, and it is not on the 503A Bulks List or in 503A Category 1. FDA placed ipamorelin acetate in 503B Category 2 (bulk drug substances that may present significant safety risks) on September 29, 2023, citing immunogenicity risk from aggregation and peptide-related impurities, unnatural amino acids that complicate characterization, and serious adverse events, including deaths of unclear causality, in the published intravenous postoperative-ileus trial. Ipamorelin acetate was also in 503A Category 2. The 503A nominations for ipamorelin acetate and ipamorelin free base were withdrawn by their nominators on September 19, 2024, but FDA still presented its evaluation to the Pharmacy Compounding Advisory Committee (PCAC) on October 29, 2024, and the committee voted 0–12 (one abstention) against adding each form to the 503A Bulks List, citing a lack of safety and efficacy data for GH deficiency and postoperative ileus. FDA subsequently removed ipamorelin acetate from 503A Category 2 following those withdrawals, and it now appears on FDA's list of 17 substances nominated but withdrawn; removal from Category 2 is not authorization to compound, and ipamorelin acetate remains in 503B Category 2. Ipamorelin was not on the July 23–24, 2026 PCAC docket, and it was not among the six peptide bulk drug substances — BPC-157, TB-500, epitalon, KPV, MOTS-c and semax — covered by the HHS 503A enforcement discretion policy announced on 28 October 2026. That policy is the most common current source of confusion about whether these peptides can now be compounded: for ipamorelin the answer is no, nothing changed. Research-chemical vendors continue to sell ipamorelin labeled 'not for human consumption,' which is not an authorized channel for human use. Practitioners should verify current compounding status before prescribing.
International
The European Medicines Agency and UK MHRA have not authorized ipamorelin as a medicine. Australia's TGA classifies GH secretagogues as Schedule 4 prescription-only substances. Canada treats it as an unapproved investigational agent.
Sports & Competition
Ipamorelin is explicitly prohibited under WADA's S2.2.4 (growth hormone releasing factors), which names ipamorelin among the growth hormone secretagogues — prohibited at all times, both in and out of competition. Detection assays for ipamorelin and its metabolites in urine (via LC-MS/MS) are well-established. Athletes subject to WADA, USADA, UKAD, or equivalent bodies must avoid it.
Regulatory status changes over time. Verify current local rules with a qualified professional.
Myths & Misconceptions
Myth
Ipamorelin is completely side-effect free because it's selective.
Reality
The selectivity profile (no significant ACTH or cortisol elevation in the original swine studies) is real and documented in preclinical work — that's what distinguishes it from GHRP-6 and GHRP-2. But it still raises IGF-1, still causes mild water retention and appetite increase in some users, and still carries the theoretical IGF-1-mediated concerns about cancer promotion. 'Clean relative to other GHRPs' is not 'clean absolutely.'
Myth
Ipamorelin is FDA-approved for anti-aging.
Reality
Ipamorelin is not FDA-approved for any indication. Its one Phase 2 efficacy trial (intravenous ipamorelin for postoperative ileus) found no significant benefit over placebo, and cachexia data are preclinical. PCAC voted 0–12 against adding it to the 503A Bulks List in October 2024. FDA later removed ipamorelin acetate from 503A Category 2 after its nominations were withdrawn, but that is not authorization to compound, and it remains in 503B Category 2. It was not on the July 2026 PCAC docket, and it was not one of the six peptides granted enforcement discretion by HHS in October 2026.
Myth
The CJC-1295 + ipamorelin stack is a substitute for HGH that avoids its risks.
Reality
The stack preserves physiological pulsatility better than flat exogenous rhGH dosing, which does plausibly attenuate some side effects like edema and carpal tunnel symptoms. But the downstream effector — IGF-1 — is the same pathway, and the theoretical long-term concerns that attach to sustained IGF-1 elevation attach to the stack too. It is 'HGH-like effects via a different mechanism,' not a fundamentally different risk category.
Myth
Ipamorelin won't show up on a drug test.
Reality
WADA-accredited labs have LC-MS/MS methods for detecting ipamorelin and its metabolites in urine, and the metabolite work is published — ipamorelin (1-4) free acid is still detectable after the parent compound has cleared. It is explicitly named under S2.2.4 and prohibited at all times, as a non-Specified Substance, which carries the longer default sanction. Athletes have in fact been sanctioned: USADA announced a three-year period of ineligibility for a weightlifter in February 2026 after a December 2025 sample returned ipamorelin, its M16 metabolite and ibutamoren, and a UFC fighter accepted a two-year sanction for an ipamorelin positive from an out-of-competition sample in 2019.
Myth
Ipamorelin works regardless of when you dose it — meals don't matter.
Reality
Ipamorelin acts at the ghrelin receptor, and GH response is substantially blunted by elevated insulin and circulating amino acids. Dosing on a relatively empty stomach (≥30 min before eating, or 2+ hours after a meal) meaningfully affects the size of the GH pulse. This is why bedtime dosing is so common — it aligns with both the fasted state and the natural nocturnal GH pulse.
Published Research
16 studiesInjectable Peptides in Sports Medicine: A Structured Narrative Review of Evidence, Safety, and Antidoping Implications (JBJS Rev, 2026)
The growth hormone secretagogue receptor 1a agonists, anamorelin and ipamorelin, inhibit cisplatin-induced weight loss in ferrets: Anamorelin also exhibits anti-emetic effects via a central mechanism
The influence of ghrelin agonist ipamorelin acetate on the hypothalamic-pituitary-testicular axis in a cichlid fish, Oreochromis mossambicus
Determination of growth hormone releasing peptides metabolites in human urine after nasal administration of GHRP-1, GHRP-2, GHRP-6, Hexarelin, and Ipamorelin
The primary support for the page's detection claim, and a human study rather than a preclinical one. Volunteers received each secretagogue intranasally and urine was analysed by LC-MS/MS. Ipamorelin was metabolised extensively, and the ipamorelin (1-4) free acid metabolite remained detectable in urine after the parent compound had cleared — which is why a short half-life offers no protection in anti-doping testing.
Prospective, randomized, controlled, proof-of-concept study of the Ghrelin mimetic ipamorelin for the management of postoperative ileus in bowel resection patients
Phase 2 proof-of-concept RCT (Beck et al., 2014) of intravenous ipamorelin in 117 bowel-resection patients. Time to first tolerated meal was 25.3 vs 32.6 hours with placebo (p=0.15), and there were no significant differences on key or secondary efficacy endpoints. It is the only one of ipamorelin's two completed Phase 2 trials to have been published; the larger 320-patient trial has not reported.
Efficacy of ipamorelin, a novel ghrelin mimetic, in a rodent model of postoperative ileus
Mechanism of ipamorelin-evoked insulin release from the pancreas of normal and diabetic rats
Influence of chronic treatment with the growth hormone secretagogue Ipamorelin, in young female rats: somatotroph response in vitro
The growth hormone secretagogue ipamorelin counteracts glucocorticoid-induced decrease in bone formation of adult rats
The GH secretagogues ipamorelin and GH-releasing peptide-6 increase bone mineral content in adult female rats
Pharmacokinetic-pharmacodynamic modeling of ipamorelin, a growth hormone releasing peptide, in human volunteers
Key human PK/PD study (Gobburu et al., 1999): healthy men received 15-minute IV infusions at five dose levels. Ipamorelin showed dose-proportional kinetics and a terminal half-life of about 2 hours, and each dose produced a single GH pulse peaking at about 0.67 hours. Only ipamorelin and GH were measured, so the study does not address selectivity.
Ipamorelin, a new growth-hormone-releasing peptide, induces longitudinal bone growth in rats
Pharmacokinetic evaluation of ipamorelin and other peptidyl growth hormone secretagogues with emphasis on nasal absorption
Ipamorelin, the first selective growth hormone secretagogue
Foundational Novo Nordisk paper (Raun et al., 1998). In swine, GHRP-6 and GHRP-2 raised ACTH and cortisol along with GH, while ipamorelin did not, even at doses more than 200-fold above its GH-releasing ED50. None of the secretagogues tested changed FSH, LH, prolactin or TSH, so the study shows ACTH/cortisol selectivity, not prolactin selectivity.
A new series of highly potent growth hormone-releasing peptides derived from ipamorelin
Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone
Bowers et al., JCEM 1990 — the human study every GHRP-plus-GHRH stacking protocol ultimately rests on. In 18 normal men, submaximal doses of GHRP (0.1 and 0.3 mcg/kg) combined with 1 mcg/kg GHRH released GH synergistically rather than additively. The peptide used was His-DTrp-Ala-Trp-DPhe-Lys-NH2, which is GHRP-6, not ipamorelin — the synergy is a class finding that has never been reproduced with ipamorelin in humans. The same study found prolactin and cortisol roughly doubled at the highest GHRP-6 dose.
Popular Stacks Including Ipamorelin
CJC-1295 + Ipamorelin (The GH Secretagogue Stack)
The classic growth hormone secretagogue stack — often called the GH stack or sleep stack. Combines GHRH signaling (CJC-1295) with selective ghrelin receptor activation (ipamorelin) to amplify the body's natural nighttime growth hormone pulse.
Tesamorelin + Ipamorelin (FDA-Backed GHRH Analog + Selective Ghrelin-Mimetic)
A growth hormone secretagogue stack that pairs the only FDA-approved GHRH analog (tesamorelin) with the cleanest ghrelin-receptor trigger (ipamorelin). Delivers the same GHRH + ghrelin dual-pathway synergy as CJC-1295 + ipamorelin, with tesamorelin's Phase III evidence base standing in for the compounded GHRH leg.
Sermorelin + Ipamorelin (Compounded GH Blend)
The default growth hormone blend at many anti-aging, men's health, and telehealth clinics. It pairs sermorelin, a GHRH fragment once FDA-approved as Geref, with ipamorelin, the most selective ghrelin-receptor agonist. The GHRH-plus-ghrelin-mimetic synergy is real human physiology, but no trial has tested this pair, and the two halves have very different US compounding status.
Quick Facts
- Class
- Growth Hormone Secretagogue
- Tier
- C
- Evidence
- Moderate
- Safety
- Moderate Data
- Updated
- Nov 2026
- Citations
- 16PubMed
Also known as
Tags
Peptide Families
Related Goals
Conditions Discussed
Evidence Score
Clinical Trials
View Clinical TrialsLinks to ClinicalTrials.gov for reference. Listing does not imply endorsement.