Ipamorelin
Research PeptideAlso known as: NNC 26-0161 · NNC26-0161
Preliminary Human
Ipamorelin has one published human pharmacokinetic study (Gobburu 1999, n=40, Novo Nordisk–affiliated) confirming GH release after IV infusion, and one published human efficacy RCT (Beck 2014, n=114 postoperative ileus) which FAILED its primary endpoint (p=0.15). No further human efficacy trials have been published; no human data exists for the body-composition, anti-aging, sleep, or wound-healing claims that drive off-label demand. Compounding the evidence gap, the most commonly cited "preserves pulsatile GH release" reference (Ionescu & Frohman 2006, JCEM) is a CJC-1295 study, not an ipamorelin study — a misattribution routinely propagated in vendor marketing.
The "preserves pulsatility" source is a CJC-1295 paper
The paper most often cited online to support the claim that ipamorelin "preserves natural GH pulsatility" — Ionescu M & Frohman LA, JCEM 2006 (PMID 17018654) — is a study of CJC-1295, not ipamorelin. The misattribution is pervasive in vendor marketing and clinic blogs. No ipamorelin-specific human pulsatility study has been published. The underlying mechanism (GHS release is somatostatin-feedback-governed, unlike exogenous rhGH) is sound, but claims that ipamorelin specifically "preserves pulsatility in humans" are extrapolations, not findings.
The only human efficacy RCT for ipamorelin failed its primary endpoint
Beck DE, Sweeney WB, McCarter MD (2014) — a multicenter, double-blind, placebo-controlled Phase II trial in 114 bowel-resection patients sponsored by Rhythm Pharmaceuticals — tested ipamorelin for postoperative ileus. Median time to first tolerated meal was 25.3 h (ipamorelin) vs 32.6 h (placebo), p=0.15. The primary endpoint was NOT met. No further clinical development has been publicly announced. This is the entire published human efficacy database for ipamorelin — a single trial that failed. Every marketing claim not directly validated by this trial rests on animal data or extrapolation.
Research use only. Not approved for human consumption in any jurisdiction listed here unless the Regulatory Status table below explicitly states otherwise.
Evidence Tier
Preliminary Human
Human Studies
2
FDA Status
Not Nominated
WADA Status
Prohibited (S2)
Mol. Weight
711.85 Da
Last Reviewed
Apr 21, 2026
Claimed benefits by evidence tier
Column header colour matches the tier
Preliminary Human2
- Stimulates GH secretion in humans
- Accelerates GI recovery after bowel surgery
Animal Only7
- Selective for GH (does not raise cortisol/ACTH)
- Increases lean body mass / muscle
- Reduces body fat
- Increases bone mineral density / content
- Counteracts steroid/glucocorticoid-induced muscle & bone loss
- Preserves natural pulsatile GH pattern vs exogenous GH
- Treatment of GH deficiency
Anecdotal3
- Anti-aging / longevity effects
- Improves sleep quality
- Accelerates wound healing or recovery
Regulatory watch
FDA 503A Categories Update finalization — following the October 29, 2024 PCAC recommendation that ipamorelin acetate NOT be included on the 503A Bulks List, the formal outcome should appear in the 503A Categories Update document. If finalized, 503A compounding pharmacies cannot lawfully compound ipamorelin as a bulk drug substance for office use.
Would formally close the compounded ipamorelin pathway under 503A in the US. 503B outsourcing facilities operate under different regulations. Nominators could resubmit with new clinical evidence but have not publicly done so.
Docket FDA-2024-N-4188 · FDA-2024-N-4188FDA
WADA 2027 Prohibited List review — annual publication (typically late September/early October) of the following year's list.
No reclassification of ipamorelin is anticipated; GHS-class listing is stable. Included as a routine watch item because any change to S2 framing would affect TUE availability and anti-doping sanctions.
Expected 2026-10-01 · WADA
Vendors selling Ipamorelin
Found 14 vendors currently offering Ipamorelin in their catalog.
🇪🇺Particle Peptides
Slovakia
COA Coverage
25/25
100%
✓ HPLC✓ MS✓ Endo✓ Ster✓ Metals
Verified Peptides
COA Coverage
138/138
100%
✓ HPLC✓ MS✓ Endo✓ Ster— Metals
🇺🇸Soma Chems
USA
COA Coverage
60/64
94%
✓ HPLC✓ MS✓ Endo— Ster— Metals
🇺🇸Sports Technology Labs
USA
COA Coverage
57/61
93%
✓ HPLC✓ MS— Endo— Ster— Metals
Vida Labz
COA Coverage
48/49
98%
✓ HPLC— MS— Endo— Ster— Metals
Panda Peptides
COA Coverage
33/37
89%
✓ HPLC— MS— Endo— Ster— Metals
Peptide Partners
COA Coverage
29/35
83%
✓ HPLC— MS✓ Endo✓ Ster✓ Metals
🇺🇸BioLongevityLabs
USA
COA Coverage
43/89
48%
✓ HPLC✓ MS✓ Endo✓ Ster— Metals
SwissChems
COA Coverage
23/52
44%
✓ HPLC✓ MS— Endo— Ster— Metals
🇺🇸Core Peptides
USA
COA Coverage
18/103
17%
✓ HPLC✓ MS— Endo— Ster— Metals
Pulse Peptides
COA Coverage
1/17
6%
✓ HPLC— MS— Endo— Ster— Metals
BioEdge Research Labs
No verified COAs
COA Coverage
0/20
0%
— HPLC— MS— Endo— Ster— Metals
Research Peptides Europe
No verified COAs
COA Coverage
0/36
0%
— HPLC— MS— Endo— Ster— Metals
Blue Sky Peptide
No verified COAs
COA Coverage
0/45
0%
— HPLC— MS— Endo— Ster— Metals
All Ipamorelin products
Every Ipamorelin product across 14 verified vendors — sorted by vendor trust tier, then by COA purity (quantified reports beat unquantified), then by most recent COA date.
About this peptide
Plain English
Ipamorelin is an injectable research peptide developed in the 1990s by Novo Nordisk. It works by signaling the pituitary gland — the brain's master hormone regulator — to release a pulse of growth hormone. Unlike older peptides with a similar mechanism, ipamorelin appears to do this without substantially raising stress hormones like cortisol, which was considered an improvement when it was first described. It has never been approved as a medicine anywhere in the world. In humans, it has been studied in only two published contexts: a pharmacokinetic study in volunteers confirming it reaches the bloodstream and causes GH release, and a randomized trial in post-surgery patients where it failed to outperform placebo. The many claims made about it online — fat loss, muscle gain, anti-aging, sleep improvement — are either extrapolated from animal studies or have no formal research behind them at all.
Technical
Ipamorelin is a synthetic pentapeptide growth hormone secretagogue (GHS) that acts as a selective agonist at the ghrelin receptor (GHS-R1a, also called the growth hormone secretagogue receptor). Upon binding GHS-R1a in pituitary somatotroph cells, it activates G-protein signaling pathways that elevate intracellular Ca²⁺ and cAMP, triggering pulsatile GH secretion. Its defining pharmacological characteristic relative to its predecessors (GHRP-2, GHRP-6) is its selectivity: at doses exceeding 200-fold the GH-release ED₅₀, ipamorelin does not stimulate significant release of adrenocorticotropic hormone (ACTH), cortisol, prolactin, FSH, LH, or TSH — in animal studies. The non-standard residues in its sequence (Aib, D-2-Nal, D-Phe) confer metabolic stability against peptidase degradation and constrain the bioactive conformation. Its pharmacokinetic profile in humans shows a short terminal half-life (~2 hours) and is known only from a single IV-infusion PK/PD study; subcutaneous bioavailability in humans is unpublished. GH-mediated downstream effects (hepatic IGF-1 production, anabolic signaling) are the proposed basis for claimed metabolic benefits, but the one human efficacy RCT (Beck 2014 postoperative ileus, n=114) failed its primary endpoint.
Mechanism of action
GHS-R1a agonism → pulsatile GH secretion
Ipamorelin binds and activates GHS-R1a on pituitary somatotroph cells. Receptor activation couples to Gαq proteins, elevating intracellular IP₃ and Ca²⁺, which triggers exocytosis of stored GH. The result is a discrete pulse of GH release subject to normal somatostatin-mediated negative feedback — theoretically preserving pulsatility, unlike exogenous recombinant GH which produces sustained non-physiologic serum levels.
Selectivity for GH — absence of ACTH/cortisol stimulation
In rats, pigs, and dogs, GHRP-2 and GHRP-6 at GH-stimulating doses also produced significant ACTH and cortisol elevations. Ipamorelin, even at doses 200-fold above its GH-release ED₅₀, did not raise ACTH or cortisol above levels seen with GHRH alone. The structural basis is attributed to the D-2-Nal substitution and C-terminal amide. CRITICAL CAVEAT: this has not been formally replicated in a controlled human cortisol/ACTH challenge study.
GH → IGF-1 → downstream anabolic effects
GH released by ipamorelin acts on hepatic GH receptors to induce IGF-1 production, which mediates most of the classically "anabolic" effects attributed to GH (protein synthesis, lipolysis, nitrogen retention, bone turnover). The magnitude and duration of IGF-1 elevation following ipamorelin dosing in humans is NOT characterised in published literature beyond the acute PK window.
GI motility (ghrelin-mimetic peripheral effect)
Ghrelin receptors are expressed in the gastrointestinal tract where ghrelin promotes gastric motility. As a ghrelin mimetic, ipamorelin was hypothesized to accelerate gastric emptying and GI transit — the mechanistic rationale for the Beck 2014 postoperative ileus RCT. That RCT failed its primary endpoint.
All mechanistic characterization of ipamorelin — including its defining cortisol-selectivity claim — was performed in rats, pigs, and dogs. The human PK/PD study (Gobburu 1999) confirmed GH release but was not designed to test downstream efficacy outcomes or the cortisol-selectivity claim in humans. Receptor pharmacology is largely conserved across species for GHS-R1a, but dose-response relationships, receptor density, and feedback dynamics differ. The failure of ipamorelin in the postoperative ileus RCT (Beck 2014) is a concrete example of why animal findings cannot be assumed to translate. All post-2001 mechanistic discussion in review articles is derivative of the original Novo Nordisk-authored papers; there is no independent mechanistic replication outside the GHS class literature.
Key studies
Ipamorelin, the first selective growth hormone secretagogue (1998)
Raun K, Hansen BS, Johansen NL, Thøgersen H, Madsen K, Ankersen M, Andersen PH · European Journal of Endocrinology 139(5):552–561
- Participants
- Rats (Sprague-Dawley), pigs, dogs; in vitro pituitary cells. No human subjects.
- Methodology
- In vitro receptor binding and pituitary cell GH release; in vivo IV/SC dose-response in rodents and large animals; comparison to GHRH, GHRP-2, GHRP-6 for GH, ACTH, and cortisol release.
- Result
- Ipamorelin was highly potent for GH release and, uniquely among GHRPs tested, did not raise ACTH or cortisol above GHRH baseline even at doses 200× the GH-release ED₅₀.
Honest read
All authors are employees of Novo Nordisk A/S, the developer of ipamorelin — a clear conflict of interest. This is an animal study; the cortisol-selectivity finding, which became the cornerstone of ipamorelin's marketing, has not been replicated in a human cortisol challenge study. The study established ipamorelin's GH selectivity profile in animals but cannot be extrapolated to human safety or efficacy. This paper has been cited extensively in clinic marketing materials without disclosing that it is entirely animal work from the peptide's manufacturer.
Pharmacokinetic-Pharmacodynamic Modeling of Ipamorelin, a Growth Hormone Releasing Peptide, in Human Volunteers (1999)
Gobburu JVS, Agersø H, Jusko WJ, Agerso H · Pharmaceutical Research 16(9):1412–1416
- Participants
- 40 healthy male volunteers (8 per dose group, 5 dose groups: 4.21, 14.02, 42.13, 84.27, and 140.45 nmol/kg over 15-minute IV infusion)
- Methodology
- Dose-escalation IV infusion study; PK/PD modeling of serum ipamorelin concentration and GH response.
- Result
- Terminal half-life ~2 hours; clearance 0.078 L/h/kg; volume of distribution at steady-state 0.22 L/kg. PK dose-proportional. Dose-dependent GH release confirmed in humans.
Honest read
This is the only published human pharmacokinetic study. It confirms ipamorelin reaches systemic circulation and releases GH in humans, but it is a mechanistic PK study, not an efficacy or safety trial. It does not report body composition, bone, or clinical outcome data. The route studied (IV infusion) differs from the subcutaneous injection used in virtually all compounding protocols; SC pharmacokinetics in humans remain unpublished. Author affiliations include Novo Nordisk, representing the same conflict noted in Study 1.
Prospective, randomized, controlled, proof-of-concept study of the ghrelin mimetic ipamorelin for the management of postoperative ileus in bowel resection patients (2014)
Beck DE, Sweeney WB, McCarter MD · International Journal of Colorectal Disease 29(12):1527–1534
- Participants
- 117 enrolled; 114 in safety and modified intent-to-treat population (adults undergoing open or laparoscopic small/large bowel resection)
- Methodology
- Multicenter, double-blind, randomized, placebo-controlled, proof-of-concept Phase II trial (NCT00672074). IV infusion of 0.03 mg/kg ipamorelin vs placebo twice daily from postoperative day 1 through day 7 or discharge. Sponsored by Rhythm Pharmaceuticals.
- Result
- Median time to first tolerated meal: 25.3 h (ipamorelin) vs 32.6 h (placebo), p=0.15. Primary endpoint NOT MET. No significant differences in secondary endpoints. Ipamorelin was well tolerated (TEAE rate 87.5% vs 94.8% placebo, not significantly different).
Honest read
This is the most important study for understanding ipamorelin's clinical potential, because it is the only large human efficacy trial — and it failed. The study was appropriately powered for its indication, multicenter, and double-blind. The fact that no further clinical development was publicly announced following publication suggests the sponsor concluded the signal was insufficient. The ipamorelin dose (0.03 mg/kg IV) was selected from preclinical data; whether SC dosing used in compounding contexts produces equivalent systemic exposure is not established. This failure does not definitively rule out efficacy in other indications, but it substantially lowers the prior probability for unevaluated claims.
The GH secretagogues ipamorelin and GH-releasing peptide-6 increase bone mineral content in adult female rats (2000)
Svensson J, Lall S, Dickson SL, Bengtsson BA, Rømer J, Ahnfelt-Rønne I, Ohlsson C, Jansson JO · Journal of Endocrinology 165(3):569–577
- Participants
- Adult female Sprague-Dawley rats
- Methodology
- SC treatment with ipamorelin or GHRP-6; DXA bone mineral content and density measurements vs controls.
- Result
- Both GHS increased total BMC. Tibial area BMD increased. Total and vertebral BMD unchanged.
Honest read
Rat model, female-only, no comparison to human-relevant doses. Whether this translates to human bone outcomes is unknown. No human bone density data for ipamorelin exists.
The growth hormone secretagogue ipamorelin counteracts glucocorticoid-induced decrease in bone formation of adult rats (2001)
Svensson J, et al. · Journal of Bone and Mineral Research 16(12):2280–2286
- Participants
- Adult rats treated with prednisolone ± ipamorelin
- Methodology
- In vivo treatment; bone formation markers, nitrogen balance, body composition. Followed by Aagaard 2009 which extended to N-balance.
- Result
- Ipamorelin partially counteracted glucocorticoid-induced decreases in bone formation markers. Aagaard 2009 showed partial rescue of nitrogen wasting, though less effectively than exogenous GH.
Honest read
Rat study only. Prednisolone doses appropriate to rat glucocorticoid excess models; translation to human corticosteroid therapy is speculative. No human data exists on ipamorelin in steroid-treated patients. This finding is frequently cited by clinics offering ipamorelin to people on corticosteroids — that extrapolation is not supported by available evidence.
Growth hormone (GH)-independent stimulation of adiposity by GH secretagogues (2001)
Lall S, Tung LY, Ohlsson C, Jansson JO, Dickson SL · Biochemical and Biophysical Research Communications 280(1):132–138
- Participants
- GH-deficient and GH-intact mice
- Methodology
- 9-week SC ipamorelin treatment; DXA body composition; fat pad weights; comparison to GH treatment.
- Result
- In GH-deficient mice, ipamorelin increased body weight by 15.3% vs 95.5% for GH. In GH-intact mice, ipamorelin increased total body fat percentage on DEXA. Relative fat pad weights increased. Weight gain occurred in BOTH GH-deficient and GH-intact mice, suggesting a GH-independent adipogenic component.
Honest read
This finding — that ipamorelin may increase body fat independent of GH action — directly contradicts the popular claim that ipamorelin causes fat loss. It is almost never mentioned in online discussions of ipamorelin. The study was conducted in mice; translation to humans is uncertain, but the finding is mechanistically plausible given ghrelin's known orexigenic and lipogenic effects. This study should be considered in any honest assessment of body composition claims.
Research timeline
- 1997
Novo Nordisk A/S medicinal chemistry program (Måløv, Denmark) identifies ipamorelin within a GHRP-1 analogue series; internal development code NNC 26-0161 assigned.
- 1998
Raun K, Hansen BS, Johansen NL et al. publish the founding characterization paper — "Ipamorelin, the first selective growth hormone secretagogue" — in European Journal of Endocrinology. All seven authors are Novo Nordisk employees. Animal studies only (rats, pigs, dogs).
- 1999
Gobburu JVS et al. publish the only human PK/PD study (n=40 healthy males, IV dose-escalation) in Pharmaceutical Research. Confirms human GH release; no efficacy endpoint. Novo Nordisk / SUNY Buffalo affiliation.
- 2000
Svensson J et al. publish rat BMC data in Journal of Endocrinology, showing ipamorelin increases total bone mineral content in adult female rats.
- 2001
Svensson J et al. publish rat data showing ipamorelin counteracts glucocorticoid-induced bone formation loss (JBMR). Same year, Lall S et al. document GH-INDEPENDENT ADIPOGENIC effects in GH-deficient and GH-intact mice (BBRC) — a countersignal to fat-loss claims.
- 2006
Ionescu M & Frohman LA publish "Pulsatile Secretion of Growth Hormone (GH) Persists during Continuous Stimulation by CJC-1295" in JCEM. This is a CJC-1295 study, not an ipamorelin study — but the paper is frequently misattributed in ipamorelin marketing to support a "preserves natural pulsatility" claim. Recorded here for that reason.
- 2009
Aagaard NK et al. publish prednisolone N-balance rat data (Growth Horm IGF Res), showing ipamorelin counteracts accelerated nitrogen wasting though less efficiently than GH.
- 2012
Greenwood-Van Meerveld B et al. publish rodent postoperative ileus studies providing the preclinical rationale for clinical development in GI motility.
- 2014
Beck DE, Sweeney WB, McCarter MD publish the Phase II RCT (NCT00672074) in International Journal of Colorectal Disease. Primary endpoint (time to first tolerated meal) FAILED at p=0.15. No further clinical development announced. This remains the only human efficacy RCT for ipamorelin.
- 2017
Sigalos JT & Pastuszak AW publish a broad GHS-class safety and efficacy review (Sex Med Rev) from Baylor College of Medicine urology. Limited ipamorelin-specific primary data; useful as class context.
- 2020
Sinha DK et al. publish narrative review on GHS in hypogonadal males (Transl Androl Urol); ipamorelin mentioned but no new primary data.
- 2024
FDA Pharmacy Compounding Advisory Committee meeting (October 29, 2024). FDA proposes ipamorelin acetate NOT be included on the 503A Bulks List, citing absence of USP monograph, absence of FDA approval, insufficient evidence of clinical need and safety for compounding, and nominator data inconsistencies. Docket FDA-2024-N-4188.
- 2026
WADA 2026 Prohibited List enters force (January 1, 2026). Ipamorelin explicitly named in category S2.2.4 — Growth Hormone Secretagogues and their mimetics — prohibited at all times (in- and out-of-competition) with no TUE pathway.
What we don't know
- Human efficacy for any marketed indication — no human trial supports ipamorelin for body composition, GH deficiency treatment, anti-aging, sleep, wound healing, or any of the indications driving off-label demand. The one completed human efficacy RCT (Beck 2014, postoperative ileus) was negative.
- Long-term human safety — the longest human exposure documented in published literature is 7 days (Beck 2014). No published study characterizes safety at the weeks-to-months treatment durations used in compounding.
- Human subcutaneous pharmacokinetics — all published PK data (Gobburu 1999) is IV infusion. SC bioavailability, Tmax, Cmax, and GH response following SC injection (the compounding-clinic route) are unpublished.
- IGF-1 response in humans — whether ipamorelin-stimulated GH pulses produce sustained, clinically meaningful IGF-1 elevation is not established.
- Optimal dose for any human indication — all compounding protocols (typically cited as 200–300 µg/day SC) are extrapolated from animal studies with no published dose-response or dose-optimization in humans.
- Drug interactions — no formal interaction studies. Theoretical interactions with insulin, exogenous GH, somatostatin analogues, glucocorticoids, thyroid hormone, and other GHS-R1a ligands are mechanistically plausible.
- Carcinogenesis risk — chronic IGF-1 elevation is epidemiologically associated with increased cancer risk; no ipamorelin-specific carcinogenicity studies exist.
- Oral / intranasal bioavailability — oral bioavailability is essentially zero (peptide-bond hydrolysis in GI tract). Intranasal delivery was studied preclinically but no human bioavailability data has been published.
- The adipogenic signal from Lall 2001 — whether GH-independent fat gain occurs in humans at clinical doses is unknown. Potentially directly contradicts the fat-loss marketing claim.
- Cortisol selectivity in humans — the cornerstone selectivity claim has been demonstrated in animals only; no human cortisol/ACTH challenge study exists for ipamorelin.
Regulatory status
| Jurisdiction | Status | Details | Last Verified | Source |
|---|---|---|---|---|
| United States (FDA) | Not Nominated | FDA proposed at the October 29, 2024 Pharmacy Compounding Advisory Committee meeting that ipamorelin acetate NOT be included on the 503A Bulk Drug Substances list, citing: absence of USP monograph, absence of FDA approval, insufficient evidence of clinical need and safety for compounding use, and inconsistent nominator data between the acetate and free base forms. Docket FDA-2024-N-4188. As of April 2026, if this recommendation has been formally finalized in the 503A Categories Update, 503A compounding pharmacies cannot lawfully compound ipamorelin as a bulk drug substance. Nominators (Wells Pharmacy Network and LDT Health Solutions) could resubmit with additional clinical evidence but no resubmission has been publicly identified as of this verification date. Ipamorelin has never had FDA approval for any indication. | 2026-04-21 | |
| Canada (Health Canada) | Not Authorized | No Drug Identification Number (DIN). No authorization under the Food and Drugs Act. Not listed in the Natural Health Products Ingredients Database (ipamorelin is a therapeutic peptide, not a natural health product). Health Canada has issued public advisories warning consumers about unauthorized injectable peptides including GHRP-class compounds such as ipamorelin. Compounding by licensed pharmacists for specific patients under the prescription-compounding exemption may be permissible but is not authorized as a general practice. | 2026-04-21 | |
| United Kingdom (MHRA) | Not Authorized | No MHRA marketing authorization. No product licence. Classified as an unlicensed medicinal product (a "special") under the Human Medicines Regulations 2012, Regulation 167. UK prescribers may prescribe unlicensed medicines under their professional responsibility; pharmacists may source from licensed specials manufacturers or import. Online sale without prescription is illegal. | 2026-04-21 | |
| European Union (EMA) | Not Authorized | No EMA central marketing authorization. Not listed in the EU Union Register of medicinal products. Not in the centralized procedure database. Individual EU member states may have national licensing pathways for unlicensed medicines; ipamorelin's status may vary by member state under national law. | 2026-04-21 | |
| Australia (TGA) | Prescription Only | Schedule 4 (Prescription Only Medicine) under the Poisons Standard. Not TGA-registered for any therapeutic indication. Possession without a valid prescription is a criminal offence. Available through compounding pharmacies with a prescription under the extemporaneous compounding exemption (TGA regulation 12). The TGA's 2023 enforcement operation against unregulated peptide vendors targeted non-prescription sales; prescription-based compounding access remains a grey area given the absence of an approved indication. | 2026-04-21 | |
| WADA | Prohibited (S2) | Explicitly named in the 2026 WADA Prohibited List under category S2.2.4 — Growth Hormone Secretagogues (GHS) and their mimetics. Prohibited at all times (in-competition and out-of-competition) with no Therapeutic Use Exemption pathway available. The category explicitly lists ipamorelin alongside anamorelin, capromorelin, ibutamoren (MK-677), lenomorelin (ghrelin), macimorelin, and tabimorelin. This distinguishes ipamorelin from Pinealon (S0 by default) and matches TB-500 (also S2) — it is named by regulation, not captured by default. | 2026-04-21 |
Safety profile
Reported side effects
- From Beck 2014 RCT (n=114, up to 7 days IV): treatment-emergent adverse events occurred in 87.5% of ipamorelin patients vs 94.8% of placebo — a non-significant difference. Most AEs were consistent with post-surgical recovery rather than ipamorelin-specific.
- Nausea, pain, and constipation (most common events in Beck 2014, reflective of postoperative context)
- No ipamorelin-specific serious adverse events were identified that distinguished it from placebo in the only published RCT
- Gobburu 1999 PK/PD study reported no adverse events in accessible summary
- IMPORTANT — there are NO published safety data for subcutaneous injection of ipamorelin in humans. All compounding-clinic SC protocols operate without published human SC safety data.
Theoretical concerns
GH-independent adipogenesis (documented in mice)
Lall 2001 documented that ipamorelin increased body fat percentage and fat pad weights in GH-INTACT mice via a GH-independent mechanism. If this translates to humans, patients using ipamorelin for fat loss may experience the opposite effect. This is a documented animal finding, not pure theory.
Severity: documented
Insulin resistance from chronic GH axis stimulation
Chronic GH elevation is known to cause insulin resistance and glucose intolerance (acromegaly model). Long-term ipamorelin use, if it produces sustained IGF-1/GH elevation, carries this theoretical risk. No human data characterizes this for ipamorelin specifically.
Severity: theoretical
Theoretical cancer growth promotion via chronic IGF-1 elevation
Elevated IGF-1 acts as a growth factor for multiple tumor types; chronic elevation is a class-wide concern for all GH secretagogues. The risk magnitude for ipamorelin at typical compounding doses and treatment durations is uncharacterized.
Severity: theoretical
Acromegalic features with sustained high-dose use
Supraphysiologic sustained GH exposure causes soft tissue hypertrophy, organomegaly, and cardiovascular complications. Clinically relevant risk at typical compounding doses is unknown given absence of long-term human safety data.
Severity: theoretical
Class-level risks of unapproved injectable peptides
Unapproved compounded/imported peptides have been associated at the class level with anaphylaxis, systemic inflammatory response, infection, and local tissue damage per multiple regulatory advisories. Ipamorelin is captured under these class-level risks.
Severity: possible
Contraindications
- Active malignancy or personal/family history of hormone-sensitive cancers (theoretical, mechanism-based — not label-validated)
- Acromegaly or active pituitary tumors (theoretical, mechanism-based)
- Proliferative diabetic retinopathy (theoretical, extrapolated from recombinant GH)
- Pregnancy and breastfeeding (no safety data in any species)
- Known hypersensitivity to ipamorelin or any component
Interactions
- No formal drug-interaction studies in humans have been conducted.
- Somatostatin analogues (octreotide, lanreotide) may blunt or abolish GH response
- Exogenous GH or IGF-1 — redundant stimulation, additive risk of supraphysiologic IGF-1
- Insulin and oral antidiabetics — GH-mediated insulin resistance may require dose adjustment
- Glucocorticoids — antagonistic at the GH/bone level (studied in rats only)
Dosing observed in the literature
No published human subcutaneous dosing studies exist. All SC dosing observed in compounding-clinic contexts (commonly cited 200–300 µg/day SC) is extrapolated from animal research and the single IV human RCT. There is no published human PK or dose-response basis for SC dosing. Ipamorelin is not approved for human use in any jurisdiction documented in this profile. Content is for research reference only and is not medical advice.
| Route | Range | Context | Source |
|---|---|---|---|
| intravenous | 4.21–140.45 nmol/kg over 15-min IV infusion (5 dose levels) | Gobburu 1999 PK/PD study in 40 healthy male volunteers — the only human PK study. | PMID:10496658 |
| intravenous | 0.03 mg/kg IV twice daily, up to 7 days | Beck 2014 Phase II RCT in bowel resection patients (n=114). Primary endpoint failed. | PMID:25331030 |
| subcutaneous | Various doses (rat/mouse; not directly translatable to human) | Raun 1998 founding characterization + Svensson 2000/2001 bone studies + Lall 2001 body-composition study — all animal work. | PMID:9849822 |
Stability & handling
- Lyophilized shelf life
- Up to ~24 months from manufacture at −20°C (vendor-claimed; no peer-reviewed stability study specific to ipamorelin identified)
- Lyophilized storage
- Freeze at −20°C (preferred) or 2–8°C short-term; sealed, desiccated, protected from light and moisture
- Reconstitution diluents
- Bacteriostatic water for injection (benzyl alcohol preserved; standard for multi-dose research vials), Sterile saline (0.9% NaCl), Sterile water for injection (single-use only)
- Reconstituted (refrigerated)
- ~28–40 days at 2–8°C (vendor/manufacturer guidance; no peer-reviewed analytical stability validation)
- Reconstituted (room temp)
- Degrades within hours to days; not recommended — peptide-bond hydrolysis and D-amino acid epimerization risk increases with temperature
- OK to refreeze
- No
- Light sensitive
- Yes — protect from light
Contains two D-amino acid residues (D-2-Nal, D-Phe) critical for receptor binding and metabolic stability; racemization during synthesis or storage reduces potency substantially and is not detectable by standard reverse-phase HPLC (requires chiral HPLC). Commonly sold as the acetate salt — salt counterions add ~60 Da per acetate, so stated mass is not pure peptide content unless a salt-corrected peptide content value is reported. Residual TFA from preparative HPLC mobile phases can be cytotoxic and is under-reported on research-grade COAs. No peer-reviewed stability study specific to ipamorelin has been identified; values above are vendor-derived.
Frequently asked questions
Is ipamorelin the same as CJC-1295, and why are they often sold together?
No, they are mechanistically distinct. Ipamorelin acts on the ghrelin receptor (GHS-R1a) to release GH. CJC-1295 is a GHRH analogue that acts on the GHRH receptor — a different receptor on the same pituitary cells. The rationale for combining them is that they act through complementary pathways and may produce synergistic GH release (the "dual-pulse" or "stack" hypothesis). This synergy has been demonstrated in animal models but has not been confirmed in human efficacy trials for body composition, fat loss, or GH deficiency. The combination has no published human RCT data as a paired regimen. Both share the same regulatory status: not FDA approved, not on the 503A list, WADA-prohibited.
Does ipamorelin raise cortisol?
In animals (rats, pigs, dogs), ipamorelin does not raise ACTH or cortisol at doses up to 200× its GH-release ED₅₀ (Raun 1998). This has not been formally replicated in a human cortisol challenge study. It is reasonable to expect the animal finding directionally holds in humans given conserved GHS-R1a pharmacology, but the absence of human data means the claim should be stated as animal-derived. Clinicians marketing ipamorelin as "cortisol-neutral in humans" are overstating the evidence.
Can I get ipamorelin legally in the United States from a compounding pharmacy?
The FDA's October 2024 PCAC recommendation proposed that ipamorelin acetate should NOT be included on the 503A Bulk Drug Substances list. If this recommendation has been formally finalized — which should be verified against the current 503A Categories Update document — then 503A compounding pharmacies cannot lawfully compound ipamorelin as a bulk drug substance. Access through a compounding pharmacy claiming 503A authorization would be legally questionable. 503B outsourcing facilities operate under different regulations and should be checked independently. This is not legal advice; consult a regulatory attorney or pharmacist for current status.
Does ipamorelin cause fat loss?
The available evidence is mixed and primarily from animals. The popular claim that ipamorelin causes fat loss via GH-stimulated lipolysis is mechanistically plausible but unproven in humans. More importantly, Lall et al. 2001 found that ipamorelin INCREASED total body fat percentage in GH-intact mice — the opposite of the claimed effect — through a GH-independent adipogenic mechanism. No human body composition study with ipamorelin has been published. The evidence does not currently support the fat loss claim.
What is the longest ipamorelin has been studied in humans?
Seven days, by IV infusion in the Beck 2014 postoperative ileus trial. That is the entire published human safety database for ipamorelin. All claims about long-term safety or efficacy with weeks-to-months of daily subcutaneous injection are unsupported by any published human data.
Is ipamorelin detectable in drug testing?
Yes. WADA has detection methods for GHS-class compounds including ipamorelin, and it is explicitly named in the 2026 Prohibited List under S2.2.4 as prohibited in- and out-of-competition. Athletes subject to anti-doping programs face sanctions for ipamorelin use regardless of how it was obtained. Detection windows vary with analytical method (urine vs blood, LC-MS/MS sensitivity).
Is ipamorelin better than sermorelin or tesamorelin?
"Better" depends on the indication and evidence standard. Sermorelin has a longer regulatory history (previously FDA-approved for pediatric GH deficiency diagnostic use, now withdrawn as a branded product but available as compounded). Tesamorelin is FDA-approved for HIV-associated lipodystrophy — the only GH-axis peptide with a current US approval for a specific indication, supported by Phase 3 RCTs. Ipamorelin has no approved indication and one failed efficacy RCT. For indications where sermorelin or tesamorelin have evidence, they represent a stronger evidence basis. For body composition or anti-aging in non-HIV patients, none has strong human evidence.
Does ipamorelin preserve "natural" GH pulsatility unlike exogenous GH injections?
This is a theoretically well-founded claim that is commonly supported by citing Ionescu & Frohman 2006 (JCEM, PMID 17018654) — which is a CJC-1295 study, NOT an ipamorelin study. That misattribution is pervasive in ipamorelin marketing. The mechanistic principle (GHS release is somatostatin-feedback-governed) is sound and animal data on ipamorelin supports the pulsatile pattern, but ipamorelin-specific human pulsatility studies do not exist. Whether preserved-pulsatility translates into better clinical outcomes — fewer side effects, better body composition, lower cancer risk — is untested for ipamorelin. The framing is mechanistically defensible but clinically unvalidated for this compound.
What should I look for on an ipamorelin COA?
Four things, separately reported: (1) salt form — acetate vs free base — with salt-corrected peptide content distinct from HPLC chromatographic purity, because each acetate counterion adds ~60 Da to stated mass; (2) chiral / stereochemistry confirmation (chiral HPLC or amino acid analysis) because the two critical D-amino acid residues (D-2-Nal, D-Phe) cannot be distinguished from L-isomers by standard reverse-phase HPLC; (3) residual TFA content — preparative HPLC leaves TFA as counterion unless converted via ion exchange; TFA is cytotoxic at high residuals; (4) endotoxin (LAL) testing per USP <85> because the product is injectable and bacterial endotoxin contamination causes fever and systemic toxicity at very low concentrations. A COA showing only "HPLC purity ≥98%" without these four items has not actually characterized what's in the vial.
Last researched: Apr 21, 2026