Aib-His-D-2-Nal-D-Phe-Lys-NH₂ · Synthetic pentapeptide GHRP · Not FDA approved
Ipamorelin: Halflife Labs records ~2h (animal estimate; human PK unknown) for SC (research context). Evidence classification: Preclinical, inferred, community, or unresolved source. Source summary: Raun et al., Eur J Endocrinol 1998, PMID 9855420 — animal and in-vitro evidence; human PK unknown.
Limitation: A suitable human or formulation-specific value is unknown or unresolved. Do not treat this record as an established human half-life. Scientific review is documented on this page; the limited reviewer scope is defined on the About page.
Stable record ID: hlc:ipamorelin · Page revision: 2026-06-11 · Open the primary source
Ipamorelin's human half-life is not established by a suitable peer-reviewed human pharmacokinetic study. The commonly repeated approximately two-hour value is an animal-derived estimate. Ipamorelin is not FDA approved, and FDA lists ipamorelin among bulk substances that may present significant safety risks in compounding.
The 1998 Raun study characterizes ipamorelin as a selective growth hormone secretagogue using animal and in-vitro work. It supports mechanistic and preclinical statements about growth-hormone release and selectivity in the studied models. It does not establish an FDA-approved human use, an optimal human schedule, a validated human half-life, or long-term human safety.
| Claim | Classification | Reason |
|---|---|---|
| Human plasma half-life is two hours | Not established | The commonly cited figure is animal-derived |
| Ipamorelin can stimulate GH release in studied models | Supported preclinical mechanism | Primary animal/in-vitro study |
| A specific human dose or frequency is appropriate | Unknown / not recommended here | No FDA-approved instructions or suitable evidence basis |
| Ipamorelin is FDA approved | No | No approved product identified; FDA flags compounding risk |
A repeated amount or schedule in community discussions does not establish absorption, half-life, exposure, efficacy, or safety. It should not be used to reverse-engineer a treatment recommendation. On this page, model math based on the animal estimate is labeled as nonhuman and illustrative only.
A tracker can preserve the event that a user chose to record, along with route, timing, units, source, and notes. It cannot authenticate a research product, determine safety, validate a protocol, or infer an exact human concentration.
| Parameter | Value | Data Source |
|---|---|---|
| Half-life (plasma, t½) | ~2 hours | Animal study (Raun et al. 1998, PMID 9855420) |
| GH pulse duration | ~3–4 hours post-injection | Animal study (Raun et al. 1998) |
| IGF-1 elevation onset | ~6–12 hours post-injection | Inferred from GH → IGF-1 kinetics |
| IGF-1 half-life (IGFBP-3 bound) | ~12–15 hours | Human data — endocrinology literature |
| Route | SC injection (research); IV (animal studies) | — |
| Human dose or schedule | Not established | No FDA-approved instructions or suitable human PK basis |
| 5 half-lives (clearance) | ~10 hours | Calculated from animal t½ |
| Selectivity | GH only — no cortisol, prolactin, or ACTH at maximal GH doses | Animal study (Raun et al. 1998) |
| Data Quality | Animal Study — no published human PK RCT. Treat all PK values as estimates requiring human validation. | |
Ipamorelin (Aib-His-D-2-Nal-D-Phe-Lys-NH₂) is a synthetic pentapeptide growth hormone releasing peptide (GHRP) and selective ghrelin receptor (GHSR-1a) agonist. It was developed by Novo Nordisk in the late 1990s as a research tool to study GH secretagogue receptor pharmacology.[1] Unlike earlier GHRPs (GHRP-2, GHRP-6, hexarelin), ipamorelin was specifically engineered for selectivity: at doses that maximally stimulate GH release in animal models, it does not significantly elevate cortisol, ACTH, or prolactin.[1]
Ipamorelin is not FDA approved for any indication. It is used as a research chemical in animal studies and investigational human protocols. Tesamorelin is the FDA-approved GHRH analogue for HIV-associated lipodystrophy. Neither ipamorelin nor its combination products have received regulatory approval in the US, EU, or major markets.
Ipamorelin's mechanism differs fundamentally from GHRH analogues like sermorelin or CJC-1295: GHRPs act at the ghrelin receptor on pituitary somatotrophs and hypothalamic neurons to amplify GH pulse amplitude, whereas GHRH analogues act at the GHRH receptor to increase the releasable GH pool. Theoretical combination claims do not establish a safe or effective human protocol.
Ipamorelin binds to the growth hormone secretagogue receptor type 1a (GHSR-1a, the ghrelin receptor) expressed on anterior pituitary somatotrophs and hypothalamic neurons. GHSR-1a activation via Gq/11 coupling triggers phospholipase C, producing IP3 and DAG, which mobilizes intracellular calcium and triggers GH granule exocytosis.[1] The resulting GH pulse peaks at approximately 15–30 minutes post-injection in animal models and returns to baseline by approximately 3–4 hours.
The critical pharmacological distinction of ipamorelin is that cortisol, ACTH, and prolactin are not significantly elevated even at doses that maximally stimulate GH, as demonstrated in Raun et al. 1998.[1] GHRP-6 and GHRP-2 activate GHSR-1a but also interact with additional receptor targets and downstream pathways that drive cortisol and prolactin responses. Hexarelin shows even more pronounced cortisol elevation. Ipamorelin's side chain chemistry (D-2-naphthylalanine at position 3 and D-phenylalanine at position 4) appears to confer selectivity for the GH release pathway over these neuroendocrine side effects.
Because ipamorelin acts at the ghrelin receptor, some degree of orexigenic (appetite-stimulating) signaling is expected. However, in animal studies, ipamorelin produces less pronounced appetite stimulation than GHRP-6.[1] The magnitude of hunger increase in humans using ipamorelin has not been established in published clinical trials.
Preserve recorded events and observations while keeping the animal-derived model and its limitations explicit.
Download Free — iOSPlasma half-life, GH pulse duration, and downstream IGF-1 effect operate on completely different timescales. Most sources only report one of these. This is Halflife Labs' three-layer breakdown:
| Layer | Metric | Value | Data Basis |
|---|---|---|---|
| Layer 1 | Plasma half-life (ipamorelin peptide) | ~2 hours | Animal study — Raun et al. 1998 (PMID 9855420) |
| Layer 2 | GH pulse duration | ~3–4 hours post-injection | Animal study — Raun et al. 1998; GH itself t½ ~20–30 min (human) |
| Layer 3 | IGF-1 effect duration | ~12–24 hours (IGF-1 t½ ~12–15 h bound to IGFBP-3) | Human endocrinology literature (not ipamorelin-specific) |
Why does the GH pulse (3–4 h) outlast the plasma half-life (~2 h)? Because receptor activation triggers calcium signaling and granule exocytosis — the GH secretory response continues even after ipamorelin plasma concentrations drop. Additionally, newly secreted GH has its own half-life (~20–30 min), prolonging the measurable GH elevation window. IGF-1, produced in the liver in response to GH, is bound primarily to IGFBP-3 which extends its half-life to 12–15 hours, further separating effect duration from plasma PK.
Using a ~2-hour plasma half-life (animal data; human data not available):
| Time After Injection | Half-lives Elapsed | Approx. % Remaining | Note |
|---|---|---|---|
| 2 hours | 1 | ~50% | GH pulse typically still active |
| 4 hours | 2 | ~25% | GH pulse returning to baseline |
| 6 hours | 3 | ~12.5% | Peptide substantially cleared |
| 8 hours | 4 | ~6% | Near-complete peptide clearance |
| 10 hours | 5 | ~3% | Pharmacologically negligible ipamorelin remaining |
| Route | Published Human Data? | Notes |
|---|---|---|
| Subcutaneous injection (abdomen) | No published human PK studies | Most common research route; SC preferred over IM for peptide GHRPs |
| Intravenous | Animal studies only | Used in original Raun et al. 1998 research; not a clinical route |
| Intranasal | No published data | Not established for ipamorelin |
| Oral | No published data | Peptide degraded by gastrointestinal proteases; not bioavailable orally without special formulation |
The key differentiator between GHRPs is their hormonal side effect profile beyond GH:
| Compound | GH Stimulation | Cortisol Elevation | Prolactin Elevation | Appetite | Data Basis |
|---|---|---|---|---|---|
| Ipamorelin | +++ | No (at max GH dose) | No (at max GH dose) | Mild (animal) | Raun et al. 1998 (PMID 9855420) — animal |
| GHRP-6 | +++ | Yes — dose-dependent | Yes — dose-dependent | Strong (animal & human) | Animal + human data |
| GHRP-2 | +++ | Yes — dose-dependent | Yes — dose-dependent | Moderate (animal) | Animal + limited human data |
| Hexarelin | ++++ | Strong elevation | Strong elevation | Moderate | Animal + human data |
| Compound | Class | Half-life | Mechanism | FDA Status |
|---|---|---|---|---|
| Ipamorelin | GHRP (ghrelin agonist) | ~2 h (animal) | GHSR-1a agonist → GH pulse amplitude ↑ | Not approved |
| CJC-1295 (no DAC) | GHRH analogue | ~30 min | GHRHR agonist → GH pool ↑ (pulsatile) | Not approved |
| CJC-1295 (with DAC) | GHRH analogue | ~8 days (albumin-bound) | GHRHR agonist → sustained GHRH signal | Not approved |
| GHRP-6 | GHRP (ghrelin agonist) | ~15–20 min (animal) | GHSR-1a agonist; cortisol & prolactin co-stimulation | Not approved |
| Sermorelin | GHRH analogue | ~10–20 min | GHRHR agonist; formerly Rx in US | Withdrawn (not currently marketed) |
| Tesamorelin | GHRH analogue | ~8 min (Egrifta SV) / ~11 min (Egrifta WR) | GHRHR agonist; HIV-associated lipodystrophy | FDA approved (Egrifta) |
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Download Free — iOSIpamorelin is not FDA approved and has not undergone large-scale human safety trials. Based on animal studies and small investigational studies, potential concerns include: water retention (from GH-mediated aldosterone effects), transient tingling or flushing (GHRP class effect), potential for IGF-1-mediated proliferative effects with long-term supraphysiologic GH/IGF-1 elevations (theoretical, no long-term human data), and hypoglycemia risk if combined with insulin. The long-term safety profile in humans is unknown. Any use carries substantial individual risk given the absence of regulatory approval and clinical trial data. This is not medical advice. Consult a qualified healthcare provider before using any research chemical.
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