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IGF-1 LR3

Also known as Long R3 IGF-1, LR3-IGF-1, long arginine 3-IGF-1

Cell culture reagent and IGF-1 analogue with a real hypoglycaemia risk; not studied in humans.

preclinical Recovery & tissue research chemical

At a glance

Category
Recovery & tissue
Status
research chemical
Made from
recombinant Recombinant protein expressed in Escherichia coli and sold as a cell culture reagent; the 13-residue N-terminal extension derives from methionyl porcine growth hormone but no porcine material is used in manufacture.
Route
subcutaneous in practice
Half-life
Not established. No human pharmacokinetic study exists. The only published pharmacokinetic study (rat, 1993) shows that LR3-IGF-1 is cleared from plasma roughly ten times faster than native IGF-1, the authors concluding that the binding proteins protect IGF-1 from rapid clearance 1
Onset
unknown
Molecular weight
approximately 9.1 kDa
Sequence
83 amino acids: human IGF-1 with arginine in place of glutamic acid at position 3 and an N-terminal extension of 13 residues. Sources differ over one residue in that extension

Not approved for human use anywhere. Its legitimate commercial application is as a cell culture reagent in biopharmaceutical manufacturing (serum-free media, CHO cell culture), sold with the explicit note 'laboratory research use only'. Even 'GMP-grade' variants are GMP as a raw material for manufacturing, not as an injectable medicine.

Doping status: Prohibited (WADA S2.3, growth factors)

Checked against the WADA 2026 Prohibited List. For a specific product and country, Global DRO is the lookup athletes are expected to use — the List names substances, not brand names.

Mechanism of action

IGF-1 LR3 is an agonist of the IGF-1 receptor and thereby activates the PI3K/Akt/mTOR pathway (protein synthesis, anti-apoptosis) and the Ras/MAPK pathway (cell division).

The two structural changes sharply reduce affinity for the IGF-binding proteins (IGFBPs) while binding to the IGF-1 receptor is retained. This makes an unusually high free fraction available at the receptor: in rats the analogue is roughly three times more potent than native IGF-1.

The peptide also binds the insulin receptor, with appreciable cross-reactivity at supraphysiological concentrations. That is the direct basis of the hypoglycaemia risk.

An important correction to a widespread misconception: escaping the IGFBPs yields more potency, not a longer residence time in plasma. It is precisely binding to the ternary IGFBP-3/ALS complex that gives native IGF-1 its long apparent half-life.

What the research shows

There is no human study of IGF-1 LR3 in any form: no pharmacokinetics, no safety research, no efficacy research. Everything said about effects in humans is extrapolated from mecasermin (native recombinant human IGF-1) — a different molecule, with different binding behaviour. That extrapolation is also not reassuring: the absence of IGFBP buffering makes the hypoglycaemia risk plausibly greater, not smaller.

Research in humans

No published human studies of LR3 specifically. By contrast, mecasermin (Increlex), native rhIGF-1, is an FDA-approved medicine — since 2005, for severe primary IGF-1 deficiency. The approved product deliberately retains IGFBP binding. There is no approved LR3 product.

Animal and lab research

Work from the Ballard and Francis group (Adelaide) showed roughly threefold greater potency than native IGF-1 in rodents for weight gain and nitrogen balance after subcutaneous administration. A 1993 study measured plasma clearance of labelled IGF-1 and LR3-IGF-1 in rats and found clearance of the analogue to be roughly ten times faster; the authors concluded that the binding proteins in fact protect IGF-1 against rapid clearance 1. There is also extensive in vitro work using it as a cell proliferation reagent.

Caveats. There is no long-term toxicology or carcinogenicity programme of the kind that would be required for a medicine. The half-lives cited in the trade (20-30 hours, or 56-72 hours) contradict one another and cannot be traced to any study; they also rest on confusion between the half-life of free IGF-1 (10-20 minutes) and that of IGFBP-bound IGF-1 (12-15 hours). Material carrying a 'research use only' label is not manufactured or released to the standards for injectable medicines.

What it is used for

  • Used in practice for muscle building and recovery time, without any human evidence
  • Legitimate: as a growth factor in serum-free cell culture media in the manufacture of biological medicines

Dosing

Dose
20-50 mcg per day
Frequency
1x daily
Route
subcutaneous
Duration
cycles of approximately 4 weeks
  • These figures come solely from peptide vendors and bodybuilding forums. There is not a single dose-finding study — not in humans, and not as a medicine in animals.
  • With the approved rhIGF-1 product, dosing around a meal is mandatory because of hypoglycaemia: the label directs that INCRELEX "should be administered shortly before or after (± 20 minutes) a meal or snack", and that the dose be withheld if the patient cannot eat 2. No such protocol exists for LR3, while the risk is plausibly greater because of the absence of IGFBP buffering.
  • Diabetics using insulin or sulfonylureas face a direct and serious risk of losing control of blood glucose; hypoglycaemia is the first warning on the approved rhIGF-1 label 2.

These figures describe what the literature and published protocols report. They are not advice and not a dosing instruction.

Protocols

Four-week cycle

user protocol — not validated

Source: Peptide vendors and bodybuilding forums

This is not a validated schedule. It is a pattern that circulates among users and sellers, reproduced because it is what people actually follow — not because it has been tested. No trial established these doses, this interval or this duration, and nobody is checking what is in the vial. Treat every number below as an assertion, not a finding.

Weeks 1-420-50 mcg per day subcutaneously, usually as a single injection
After the cyclea break of comparable length before repeating

What this schedule omits matters more than what it states. The approved rhIGF-1 product requires dosing around a meal because of hypoglycaemia; nothing equivalent appears in these protocols, even though LR3 is bound by IGF binding proteins poorly and is therefore less buffered, not more. For anyone using insulin or a sulfonylurea that omission is the dangerous part.

Schedules are reproduced as their source states them. Units, IU and milligrams explains why the figures are not interchangeable between products.

Reconstitution

Vial sizes
0.1 mg, 1 mg, 5 mg
Solvent
bacteriostatic water (0.9% benzyl alcohol); some suppliers advise dilute acetic acid because of solubility
Storage
2-8 °C, do not freeze after reconstitution. The common shelf-life claims of 30-45 days are supplier statements, not stability research.

Worked example

1 mg vial + 2 ml bacteriostatic water = 500 mcg/ml. 50 mcg = 0.1 ml, that is 10 units on a U100 insulin syringe.

The fact that reconstitution instructions contradict one another between suppliers is in itself a quality signal. Do not shake.

Work it out for IGF-1 LR3

Safety

Side effects

  • Hypoglycaemia — the most concrete and immediate danger. IGF-1 activates the insulin receptor, and because LR3 does not bind IGFBPs the physiological buffer that normally dampens this action is absent. Hypoglycaemia heads the warnings and precautions on the label of the approved rhIGF-1 product 2
  • Growth of soft tissue and organs under sustained supraphysiological signalling, with acromegaly-like features
  • Lymphoid tissue hypertrophy - swelling of tonsils and adenoids with snoring, sleep apnoea and middle ear effusion; a labelled warning for the approved rhIGF-1 product 2
  • Intracranial hypertension with papilloedema, headache, nausea and visual complaints; also a labelled warning 2
  • Slipped capital femoral epiphysis during rapid growth, and progression of pre-existing scoliosis; both labelled warnings 2
  • Hypersensitivity and allergic reactions including anaphylaxis, a labelled warning for the approved product 2
  • Fluid and sodium retention
  • Injection site reactions

Do not use if

  • Active or suspected malignancy — "Malignant Neoplasia" is a listed contraindication for the approved rhIGF-1 product 2. IGF-1 is mitogenic and anti-apoptotic. A pooled meta-analysis of individual participant data from 19 studies found a positive association between circulating IGF-1 and prostate cancer risk 4; Mendelian randomisation supports a causal link with colorectal carcinoma. In acromegaly (chronically raised GH and IGF-1) the risk of colorectal adenomas and carcinomas is increased. This does not prove that exogenous LR3 causes cancer, but the direction of the evidence is consistent and that is why the approved analogue is contraindicated in neoplasia
  • Closed epiphyses - a listed contraindication for the approved product, alongside known hypersensitivity to mecasermin 2
  • Intravenous administration - the approved rhIGF-1 product is for subcutaneous use only
  • Diabetes mellitus, particularly when using insulin or sulfonylureas, without strict glucose monitoring
  • Pregnancy and breastfeeding: no data
  • Competitive athletes under the WADA code: prohibited at all times under S2.3, growth factors and growth factor modulators, which names "Insulin-like growth factor 1 (IGF-1, mecasermin) and its analogues" 53

Interactions

Additive hypoglycaemia with concurrent use of insulin, sulfonylureas and meglitinides; insulin users need a dose reduction 2. Concurrent use of growth hormone raises IGF-1 further and amplifies both the hypoglycaemia and the overgrowth risk. These interactions are inferred from the approved rhIGF-1 product; no interaction studies have been done on LR3 itself.

Sources