IGF-1 LR3
| Category | Growth Hormone Secretagogues |
| Goals | Muscle & Performance |
| Evidence level | Preclinical (cell/animal; no human efficacy or safety trials) |
| Legal status | Research-only — not approved for human use |
| FDA status | Not approved; sold as a research/cell-culture reagent |
| Half-life | ~20–30 hours (long) |
| Routes | Subcutaneous · Intramuscular (as used non-clinically) |
| CAS / MW / Sequence | 946870-92-4 · ~9118 g/mol · 83-aa IGF-1 analog |
| Last reviewed | 2026-06-05 |
In one line
A long-acting, modified version of insulin-like growth factor 1 (IGF-1) — the hormone through which growth hormone exerts most of its anabolic effects — engineered to resist binding proteins so it stays active far longer than natural IGF-1.
Evidence at a glance
IGF-1 LR3 is primarily a laboratory cell-culture reagent. Its muscle-growth reputation comes from its biology and animal data, not from human clinical trials — there are no controlled human efficacy or safety studies for performance use. Because it activates the same pathways as insulin and IGF-1, it carries real hypoglycemia and growth-signaling risks. See Evidence Grading Explained and the Disclaimer.
Key Takeaways
- A synthetic analog of IGF-1 with 83 amino acids (vs 70 in native IGF-1): a 13-aa N-terminal extension plus arginine replacing glutamate at position 3 (“R3”).
- Those modifications make it evade IGF binding proteins (IGFBPs) — roughly 100× weaker IGFBP-3 binding — so far more stays free and active, giving a much longer half-life (~20–30 h) and ~3× the potency of native IGF-1.
- Sits downstream of the entire GH axis: where Sermorelin/CJC-1295 coax the body to make GH (which then makes IGF-1), this supplies the active growth factor directly.
- Acts on the IGF-1 receptor to drive PI3K/Akt (protein synthesis) and MAPK/ERK (cell proliferation) — the core hypertrophy pathways.
- Marketed for muscle growth, but human evidence is absent; technically sold as a cell-culture reagent.
What Is It
IGF-1 LR3 (“Long R3 IGF-1”) is a recombinant, modified form of human IGF-1. Native IGF-1 is a 70-amino-acid protein that mediates most of growth hormone’s anabolic effects but is tightly regulated in the bloodstream by a family of IGF binding proteins (IGFBPs) that keep most of it inactive.
LR3 is engineered to escape that control in two ways: a 13-residue extension on the N-terminus (“Long”) and an arginine substituted for glutamate at position 3 (“R3”). Together these dramatically reduce IGFBP binding, so a much larger fraction circulates free and active, with a substantially longer half-life and greater potency. It was developed largely as a cell-culture supplement to boost the productivity of cultured cells, and is sold in that context.
Mechanism of Action
- IGF-1 receptor (IGF-1R) agonism (established) — binds the IGF-1R tyrosine kinase on muscle, bone, fat, and many other cells.
- PI3K/Akt/mTOR signaling (established) — drives protein synthesis, satellite-cell activation, and anti-catabolic effects, the basis of muscle-growth interest.
- MAPK/ERK signaling (established) — promotes cell proliferation/differentiation.
- IGFBP evasion (established) — the Arg³ + N-terminal extension cut IGFBP-3 affinity ~100-fold, keeping it free in circulation and prolonging action.
- Insulin-receptor cross-talk (established risk) — at higher exposure it can activate insulin receptors and IGF-1R hybrids, which underlies its hypoglycemia risk.
Limitations
The same pathways that build muscle also drive general cell proliferation, raising theoretical concern about tumor promotion if abnormal cells are present. None of the performance claims are backed by human trials; the molecule was designed for bioreactors, not bodies.
Evidence by Outcome
| Outcome | Evidence | Notes |
|---|---|---|
| Cell proliferation / culture productivity | Established (in vitro) | Its actual validated use — a cell-culture reagent |
| Muscle protein synthesis / hypertrophy | Preclinical | Strong mechanistic + animal rationale; no human RCTs |
| Local muscle growth (site injection) | Anecdotal | Popular bodybuilding claim; no controlled human data |
| Recovery / nutrient partitioning | Anecdotal | Extrapolated from IGF-1 biology |
| Hypoglycemia risk | Established (mechanistic) | Predictable from insulin/IGF-1R cross-activation |
Reported Dosing
Not medical advice
IGF-1 LR3 is not approved for human use and has no established human dose. Figures below are as reported in non-clinical/community sources, documented for education only — not a recommendation. Hypoglycemia is a real risk. See Reconstitution & Dosing Math and Injection Technique.
| Route | Dose (reported) | Frequency | Notes |
|---|---|---|---|
| Subcutaneous | ~20–50 µg/day | Once daily | Anecdotal range; long half-life means once-daily |
| Intramuscular (local) | ~20–50 µg | Per session | ”Site injection” claim; unproven in humans |
Pharmacokinetics
The defining PK feature is its long half-life (~20–30 hours) — far longer than native IGF-1 (~12–15 h) and dramatically longer than free IGF-1’s minutes-long half-life when bound proteins are intact. This is a direct result of IGFBP evasion: with little protein binding to clear or sequester it, the molecule persists and acts systemically. Once-daily dosing is therefore typical in non-clinical use. See Half-Life & Pharmacokinetics.
Side Effects & Risks
- Hypoglycemia — the most immediate hazard; IGF-1/insulin-receptor activity can drop blood sugar, sometimes sharply.
- Growth-signaling concerns — chronic IGF-1R activation drives proliferation; theoretical tumor-promotion risk is the central long-term concern and is not adequately studied in this context.
- Possible organ/tissue growth (including reports of visceral effects with high GH/IGF-1 exposure), water retention, and headaches.
- No human safety data for performance use — “few reported effects” reflects absence of study, not proven safety.
- Sourcing risk — as a research reagent, identity/purity vary widely; mislabeling is common. See Side Effects & Risk Management, Bloodwork & Monitoring, Red Flags & Scams.
Cycling
No evidence-based cycling standard exists. Anecdotal protocols run short blocks (a few weeks) alongside training, citing receptor and growth-signaling concerns for limiting duration — but this is not validated. See Cycling.
Stacks It Appears In
- Sits downstream of GH secretagogues; some non-clinical stacks pair it with GH-axis peptides (CJC-1295 + Ipamorelin, MK-677) on the theory of “GH up top, IGF-1 directly.”
- Often discussed alongside other muscle-targeted compounds like Follistatin (different mechanism: myostatin inhibition).
Comparisons
- vs Sermorelin / CJC-1295 — those stimulate the body’s own GH (and thus IGF-1) with feedback intact; IGF-1 LR3 bypasses the axis and supplies the active growth factor directly, removing that safety buffer.
- vs native IGF-1 — LR3 is longer-acting and more potent because it evades IGFBPs.
- vs Follistatin — both target muscle growth, but Follistatin works by blocking myostatin, not by activating growth-factor receptors.
Sourcing & Quality
IGF-1 LR3 is sold as a research/cell-culture reagent, not a human drug, so identity and purity are not guaranteed for human-use contexts. Recombinant proteins are also prone to mislabeling and degradation. Verify before trusting any product: How to Read a CoA, Third-Party Testing, Red Flags & Scams. Reconstitution and storage (it is sensitive): Reconstitution & Dosing Math, Storage & Handling. No vendors are endorsed here.
Legal & Regulatory Status
(As of 2026-06-05.) IGF-1 LR3 is not FDA-approved for human use; it is sold legally only as a research/laboratory reagent, not for administration to people. IGF-1 and its analogs are explicitly prohibited in sport by WADA. Status varies by country, and human use falls outside approved medical practice. See Regulatory & Legal Status.
FAQ
What does “Long R3” mean? “Long” = a 13-amino-acid N-terminal extension; “R3” = arginine replacing glutamate at position 3. Both reduce binding-protein interference so the molecule stays active longer.
How is it different from taking growth hormone? GH works largely by raising IGF-1. This skips that step and delivers a potent, long-acting IGF-1 directly — bypassing the body’s feedback controls.
Is it dangerous? It carries real risks: hypoglycemia acutely and proliferative/growth-signaling concerns long-term. Human safety for performance use is unstudied.
Is it the same as the IGF-1 your body makes? No — it is a modified analog designed to resist the binding proteins that normally regulate natural IGF-1.
References
- IGF-1 LR3 — Wikipedia (structure: 83 aa, Arg³ substitution, N-terminal extension; potency; half-life).
- Tomas F.M. et al. (1993). “Insulin-like growth factor-I (IGF-I) and especially IGF-I variants are anabolic in dexamethasone-treated rats.” Biochemical Journal — LR3 anabolic data in animals.
- Francis G.L. et al. (1992). “Novel recombinant fusion protein analogues of insulin-like growth factor-I…” — IGFBP-evasion mechanism of Long R3 IGF-I.
- ChemicalBook — IGF-1 LR3, CAS 946870-92-4 (formula/MW).
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