IGF-1 LR3 peptide: what the animal studies show, why no human dose exists, and what 'Long R3' means
What 27 indexed publications and 0 randomized trials actually state about igf-1 lr3, sentence by sentence, each tied to its source and labeled by the kind of evidence it is.
At a glance
What IGF-1 LR3 is and what 'Long R3' means
IGF-1 LR3 is a peptide in the growth factors & reproductive class (IGF-1 receptor agonist, extended analog with reduced IGFBP binding). Europe PMC indexes 27 publications naming it or a listed alias in a title or abstract, including 0 randomized controlled trials and 0 clinical trials of any design, as of . The strongest evidence tier in that literature is animal studies only, with no indexed human study.
This page reports what those studies state, sentence by sentence, with each statement tied to its source and labeled by the kind of evidence it is. It does not recommend use, and it does not translate study doses into anything personal.
What the evidence level means
Publication counts show what is indexed, not how strong the evidence is. The ledger below separates human clinical records from preclinical, analytical, and in-vitro work.
Interpretation boundary: An indexed publication count is a discovery measure. It does not establish efficacy, safety, approval, or a personal treatment plan.
IGF-1 LR3 in two minutes
What it is. Human IGF-1 with a 13-amino-acid extension and one substitution, designed in Adelaide in 1992 so that it ignores the binding proteins that normally hold IGF-1 in check. Its real job is replacing insulin in the culture media used to manufacture antibody drugs; it is still sold for that under the name LONG R3 IGF-I.
What the research actually shows. 27 indexed publications and no human study of any kind. The substantive work is a fetal-sheep infusion programme in Colorado: a week of intravenous IGF-1 LR3 grew hearts, spleens and adrenals and multiplied muscle precursor cells, but did not add muscle mass, and it consistently lowered insulin and glucose. In growth-restricted fetuses it did not restore growth. In mice, seven months of intranasal treatment remodelled amyloid plaques without helping memory.
The name. 'Long' is the extension, not the duration. No study has measured its half-life in any species, and losing binding-protein affinity should make it clear faster than native IGF-1.
Status. Not approved anywhere; prohibited in sport at all times as an IGF-1 analogue. The approved IGF-1, mecasermin, carries a hypoglycaemia warning and a malignancy warning.
Where the evidence is thinnest. Everything in people, and, unusually, everything about subcutaneous injection, which no animal study has used either.
Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.
How it works
Written from general pharmacology and the development record, and marked as editorial synthesis; the measurements behind it are quoted in the biomarker section.
- Editorial synthesis from general knowledge
- Editorial synthesis from general knowledge
- Editorial synthesis from general knowledge
What did the studies find?
Results in fetal sheep, mice and cell cultures. No human study of IGF-1 LR3 exists, so nothing here is a benefit in people. One row per primary study in this record's ledger. Fields are read from each paper's indexing and abstract. "Analytical method" marks papers about detecting or measuring the compound rather than about its effects.
| Study | Design | n | Species | Dose | Route | Duration | Reported outcome | Tier |
|---|---|---|---|---|---|---|---|---|
| White 2025 | Animal study | 14 | Sheep | 1.17 μg/kg/h IV, 1 wk (FGR fetuses) | — | 1 wk | In summary, a 1-wk IGF-1 LR3 treatment did not improve growth in FGR fetuses. | Animal, preclinical |
| Engel 2025 | Animal study | 19 | Mice | — | — | 7 months; 10 months | In male 5XFAD mice, IN LR3-IGF-1 treatment improved body composition, but did not significantly alter cognitive symptoms, as assessed by multiple assays. | Animal, preclinical |
| White 2023 | Animal study | 10 | Sheep | — | — | — | Fetal plasma insulin concentrations decreased with IGF-1 LR3 infusion ( P P in vitro retains the ability to recover GSIS. | Animal, preclinical |
| Salvi 2022 | Animal study | — | — | — | — | — | Significant reductions of phosphorylation of ERK1 and ERK2 in Lec1 and Lec4 cells were observed upon IGF-1R ligand (IGF-1 LR3) stimulation. | Animal, preclinical |
| White 2021 | Animal study | 8 | Sheep | — | — | — | In summary, IGF-1 LR3 infusion for 1 wk into fetal sheep lowers insulin concentrations and reduces fetal GSIS. | Animal, preclinical |
| Stremming 2021 | Animal study | 8 | Sheep | — | intravenous | 1 wk | Fetal heart, adrenal gland, and spleen weights were higher ( P P P P NEW & NOTEWORTHY After a 1-wk infusion of LR3 IGF-1, late gestation fetal sheep had lower umbilical uptake rates of amino acids, lower fetal arterial… | Animal, preclinical |
| Jonker 2020 | Animal study | — | Sheep | — | — | — | These findings support IGF-1 as a potential strategy to increase cardiac myocyte and coronary vascular endowment at birth. | Animal, preclinical |
| Shen 2012 | Animal study | — | Sheep | 20 μg | — | — | Application of LR3-IGF-1 (20 μg l(-1)) significantly increased the rate of pH(i) recovery to 0.33 ± 0.02 pH units (15 min)(-1). | Animal, preclinical |
| von 2011 | Animal study | — | Mice | — | — | — | In vivo, treatment with the stable IGF-1 analog Long R3 IGF-1 in apolipoprotein E knockout mice reduced stenosis and core size, and doubled cap/core ratio in early atherosclerosis. | Animal, preclinical |
| McTavish 2009 | Animal study | — | Mice | — | — | — | Compared with free methotrexate, the IGF-methotrexate conjugate required slightly higher concentrations to inhibit the in vitro growth of the human prostate cancer cell line LNCaP. | Animal, preclinical |
| Nicklin 2007 | Animal study | 18 | Cattle | — | — | — | Progesterone production by luteal cells was increased (P<0.001) by treatment with LH (10 ng/ml) but treatment with leptin alone had no effect. | Animal, preclinical |
| Brankin 2003 | Animal study | — | Swine | 10 ng; 100 ng | — | — | Thecal cell numbers were increased by oocyte secreted factors (P = 0.02), together with a suppression in progesterone and androstenedione synthesis after 48 hours (P < 0.001) and after 144 hours (P = 0.02), respectively. | Animal, preclinical |
| Lovell 2002 | Animal study | — | Chickens | — | — | — | Again, these inter-follicle differences decreased over time in culture (not significant on day 3 of treatment). | Animal, preclinical |
| Long 1998 | Animal study | — | Mice | — | — | — | — | Animal, preclinical |
| Stremming 2022 | In vitro study | — | — | — | — | — | When infused for 1 week, oIGF-1 increased organ growth of the heart, kidney, spleen, and adrenal glands and stimulated skeletal myoblast proliferation compared to SAL without increasing muscle fractional synthetic rate… | Mechanistic, in vitro |
Doses reported in studies
Each entry is a sentence quoted from the study's abstract, with the study's design, sample size and year in front of it. Comparator doses in the same sentence are not attributed to igf-1 lr3.
- Source
pmid-39679943 - Source
pmid-39679943 - Source
pmid-22227200 - Source
pmid-39610283
Every IGF-1 LR3 dose in the literature, in one table
Every figure here was infused into a fetal sheep, given to a mouse, or added to a culture. No human dose exists.
| Study | Model | Route and dose | Duration | What was found |
|---|---|---|---|---|
| White 2021; Stremming 2021 | Normal late-gestation fetal sheep | Intravenous infusion, 6.6 mcg/kg/h | One week | Body weight up; heart, adrenal and spleen heavier; myoblast proliferation up; insulin and glucose down; amino-acid uptake down; muscle mass and protein synthesis unchanged |
| White 2025 | Growth-restricted fetal sheep | Intravenous infusion, 1.17 mcg/kg/h | One week | No growth improvement; amino acids fell; insulin not further suppressed |
| White 2023 | Fetal sheep | Intravenous infusion; dose not stated in the abstract | 90 minutes | Insulin during a glucose challenge 66% lower; islets recovered once isolated |
| Jonker 2020 | Near-term fetal sheep | Dose not stated in the abstract | Seven days | Heart growth with matching coronary vascular growth |
| Engel 2025 | Male mice with Alzheimer's-type pathology | Intranasal; dose not stated in the abstract | Seven months | Body composition improved; plaques remodelled; no cognitive benefit |
| von der Thüsen 2011 | Mice lacking apolipoprotein E | Dose not stated in the abstract | Not stated | Smaller, more stable atherosclerotic plaques; fewer intraplaque haemorrhages |
| Shen 2012 | Sheep rumen tissue and cells | 20 to 100 mcg per litre in the bath | 30 minutes | Sodium transport up 60% |
Figures for this compound circulate on forums and vendor pages. None has been tested in a human study, so none is reproduced here; the table above holds every dose a study actually administered. Note the route: every living-animal study infused the compound intravenously or gave it intranasally. No study, in any species, has injected it under the skin.
Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.
Side effects: what is known, and from where
No human study recorded side effects because none exists. What follows is what the animal studies measured, what a 2026 clinical review reports in people self-administering IGF-1 analogues, and what the label of the approved native IGF-1 warns about. Events and their frequency as each study reported them, with the denominator where the abstract gives one.
- Source
pmid-33938236 - Source
pmid-37114757 - Source
pmid-39679943 - Editorial synthesis from general knowledge · primary document to be added to the ledger
Who IGF-1 LR3 is discussed for, and the cautions that recur
Studied: fetal sheep, as a model of growth restriction in pregnancy, and mice, as models of Alzheimer's disease and atherosclerosis. Never studied: any human, any adult animal given it for muscle. Community: bodybuilders seeking muscle growth and fat loss, usually alongside growth hormone or its secretagogues.
No exclusion criteria exist because no human study exists. These cautions come from the compound's design, the animal data and the label of the approved native IGF-1:
- Blood sugar. Every sheep infusion lowered insulin and glucose. Mecasermin's label makes hypoglycaemia its first warning and requires food within 20 minutes of each dose. Anyone on insulin or a sulfonylurea has a compounding risk.
- Cancer, present or past. IGF-1 receptor signalling drives proliferation; the native hormone's label reports malignancy in treated children; IGF-1 LR3 is designed to act more freely. Nothing has been measured, in either direction.
- Growth of the wrong tissues. The sheep grew hearts, spleens and adrenals rather than muscle; mecasermin's label warns of lymphoid-tissue enlargement and intracranial hypertension.
- Diabetic retinopathy and other proliferative conditions. A theoretical caution that follows from the mechanism; no data.
- Pregnancy. The only data are in fetuses, where the compound changed insulin secretion in a way that persisted in isolated islets.
- Tested athletes. Prohibited at all times under WADA S2 as an IGF-1 analogue.
Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.
Biomarkers measured in studies
Laboratory and clinical measures the studies report tracking, including which hormones did and did not change.
-
We previously demonstrated that a 1-wk infusion of IGF-1 LR3, an IGF-1 analog with low affinity for IGF-binding proteins and high affinity for the IGF-1 receptor, at 6.6 µg·kg -1 ·h -1 into normal fetal sheep increased body weight but lowered insulin concentrations and GSIS.
Sourcepmid-39679943· quoted verbatim from the abstract -
Long arginine 3-IGF-1 (LR3-IGF-1) is a potent IGF-1 analogue.
Sourcepmid-39610283· quoted verbatim from the abstract -
We previously demonstrated that a 1-week IGF-1 LR3 infusion into fetal sheep reduces in vivo and in vitro insulin secretion suggesting an intrinsic islet defect.
Sourcepmid-37114757· quoted verbatim from the abstract -
Significant reductions of phosphorylation of ERK1 and ERK2 in Lec1 and Lec4 cells were observed upon IGF-1R ligand (IGF-1 LR3) stimulation.
Sourcepmid-36499281· quoted verbatim from the abstract -
Late gestation fetal sheep received infusions with IGF-1 LR3 (IGF-1, n = 8), an analog of IGF-1 with low affinity for the IGF binding proteins and high affinity for the IGF-1 receptor, or vehicle control (CON, n = 9).
Sourcepmid-33938236· quoted verbatim from the abstract -
Catheterized fetuses from late gestation pregnant sheep received an intravenous infusion of LR3 IGF-1 (LR3 IGF-1; n = 8) or saline (SAL; n = 8) for 1 wk.
Sourcepmid-33427051· quoted verbatim from the abstract
Reported timelines
Onset, peak and duration figures as each study reported them.
-
At concentrations ranging from 20 to 100 μg l(-1), serosal LR3-IGF-1, a recombinant analogue of IGF-1, rapidly (within 30 min) stimulated the mucosal-to-serosal Na(+) flux (J(ms)Na) and consequently the net Na(+) flux (J(net)Na).
Sourcepmid-22227200· quoted verbatim from the abstract
What is measured over time, and what is not
The time course in the literature is short and physiological: sodium transport in tissue within 30 minutes; insulin suppression within 90 minutes of infusion; organ growth and lower insulin after one week; amyloid remodelling after seven months in mice. Nothing was measured after treatment stopped in any study, so nothing is known about persistence or rebound. No pharmacokinetic study exists, so onset and duration after a subcutaneous injection, the questions people actually ask, have no data behind them in any species.
Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.
Study durations
Treatment and follow-up periods as stated in each abstract.
- Durations stated: 1 wk
In this study, FGR fetal sheep received either IGF-1 LR3 treatment at 1.17 ± 0.12 μg·kg -1 ·h -1 (LR3; n = 7) or vehicle (VEH; n = 7) for 1 wk.
Sourcepmid-39679943· quoted verbatim from the abstract, emphasis added - Durations stated: 7 months; 10 months
Wildtype and 5XFAD male mice were treated for 7 months (3-10 months of age), with IN LR3-IGF-1 or IN Vehicle (Veh) (n = 19-27 mice/group).
Sourcepmid-39610283· quoted verbatim from the abstract, emphasis added - Durations stated: 1 wk
Catheterized fetuses from late gestation pregnant sheep received an intravenous infusion of LR3 IGF-1 (LR3 IGF-1; n = 8) or saline (SAL; n = 8) for 1 wk.
Sourcepmid-33427051· quoted verbatim from the abstract, emphasis added
Routes: what the studies used
Intravenous infusion into fetal sheep, intranasal drops in mice, and culture medium. No study has injected it under the skin of any animal or person, which is how it circulates. Routes of administration named in each study.
- administration by intravenous route reported
Catheterized fetuses from late gestation pregnant sheep received an intravenous infusion of LR3 IGF-1 (LR3 IGF-1; n = 8) or saline (SAL; n = 8) for 1 wk.
Sourcepmid-33427051· quoted verbatim from the abstract
Weight-normalized doses, as published
Per-kilogram figures exactly as each study published them, for the species it studied.
- Source
pmid-39679943 - Source
pmid-39679943
Weight-normalized figures above are reproduced exactly as each study published them, for the species it studied. Dose does not scale linearly with body mass between species: metabolic rate, clearance and receptor density differ, and regulatory guidance uses allometric, not proportional, conversion. A mg/kg figure from a rat study is a fact about that rat study and nothing else.
What people report outside the literature
Forum reports are experiences, not evidence. The doses and cycles people describe are not reproduced; no human study has tested any of them. What circulates in user communities and clinic marketing, reported so a reader knows the figures and their origin. None of it has been tested in a trial, and none of it is a suggestion.
- Editorial synthesis from general knowledge
Reconstitution mathematics
Lyophilised peptide is supplied as a mass in a vial and dissolved in a stated volume of diluent. Two figures follow from that and nothing else:
- Concentration = mass in vial ÷ diluent volume. A 5 mg vial in 2 mL is 2.5 mg/mL, or 2,500 mcg/mL.
- Volume for a given mass = that mass ÷ concentration. 250 mcg at 2,500 mcg/mL is 0.1 mL. On a U-100 insulin syringe, where 1 mL is 100 units, that is 10 units.
Study doses on this page are quoted as published, in the units the authors used. Converting between mcg, mg and IU, or between a mass and a syringe volume, is arithmetic; deciding a mass is not, and this page does not do it. The reconstitution calculator performs the conversion with the formula shown.
Reading a certificate of analysis
A certificate of analysis is a laboratory report on one batch. Reading it means checking four things in order.
- Identity. Mass spectrometry should report an observed molecular mass matching the peptide's theoretical mass within the instrument's stated tolerance. A certificate with no mass spectrometry, or one that lists only the expected value, has not confirmed identity.
- Purity. HPLC purity is the area of the main peak as a share of all peaks, at a stated wavelength. It says nothing about what the other peaks are, and it is not a measure of quantity.
- Quantity. Net peptide content, by amino acid analysis or UV, is the fraction of the vial's mass that is peptide rather than counter-ions and water. A 5 mg vial at 80% net content holds 4 mg of peptide, and every concentration figure above changes accordingly.
- Provenance. The batch number on the certificate should match the vial, the laboratory should be named and independent of the seller, and the test date should be recent.
This page rates no supplier and links to none. It describes how to read the document.
Equipment described in studies
Published human studies of injectable peptides report the same small set of materials: single-use insulin syringes with fixed needles, most often U-100 with 29 to 31 gauge needles; bacteriostatic water or sterile water for injection as diluent, with the choice stated in the methods; alcohol swabs; and refrigerated storage of reconstituted solution. Animal studies more often report intraperitoneal or intragastric administration and state the vehicle used. Where a study in this record's ledger names its materials or vehicle, that sentence appears under storage or routes above; where it does not, nothing is assumed here.
Storage and handling
As a cell-culture reagent IGF-1 LR3 has a manufacturer's data sheet: lyophilised powder stored frozen, reconstituted stock refrigerated and used within a stated period. That is the only handling guidance for this compound with a source behind it, and it was written for laboratory use.
Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.
Common mistakes in how IGF-1 LR3 is discussed
- Reading 'Long' as long-acting. It names the 13-amino-acid extension. No half-life has been measured, and the design predicts faster clearance than native IGF-1.
- Treating it as a drug candidate. It is a manufacturing reagent. No company has taken it into human development in more than thirty years, and the approved IGF-1 is a different molecule.
- Turning fetal-sheep organ growth into adult muscle growth. The sheep grew hearts, spleens and adrenals and multiplied muscle precursors; hindlimb muscle mass and protein synthesis did not change.
- Quoting a dose. The only doses are per kilogram per hour into a fetal vein, or per litre into a dish. The microgram figures that circulate come from forums.
- Assuming subcutaneous data exist. No study in any species has used that route.
- Calling the cancer question settled. It is untested. The mechanism and the approved hormone's label make it the most serious open question about this compound.
Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.
IGF-1 LR3 vs IGF-1 DES, mecasermin and growth hormone
| Molecule | What it is | Human evidence | Status |
|---|---|---|---|
| IGF-1 LR3 | IGF-1 with a 13-amino-acid extension and Arg3; low binding-protein affinity | None | Cell-culture reagent; WADA S2 |
| IGF-1 DES (des(1-3)IGF-1) | IGF-1 missing its first three amino acids; also low binding-protein affinity; from the same Adelaide programme | None | Research reagent; WADA S2; no record on this site |
| Mecasermin (Increlex) | Native recombinant human IGF-1 | Approved 2005 for severe primary IGF-1 deficiency in children; trials and a label with hypoglycaemia, intracranial-hypertension and malignancy warnings | Prescription medicine; WADA S2; no record on this site |
| Growth hormone (somatropin) | The pituitary hormone that raises the body's own IGF-1, bound to its carrier proteins | Decades of trials in deficiency and other indications | Prescription medicine; WADA S2 |
| CJC-1295 and ipamorelin | Upstream: they make the pituitary release growth hormone | CJC-1295: 2006 trials; ipamorelin: small trials | Not approved; WADA S2 |
The demand for 'IGF-1 LR3 vs IGF-1 DES' compares two reagents from the same laboratory, neither with a human study. The comparison that matters is with mecasermin, the approved native hormone, whose label is the closest thing to a human safety record for this receptor. Kisspeptin shares this site's growth-factor and reproductive class but acts on a different axis.
Editorial synthesis Written from general pharmacology, the development record and what is commonly reported; not a cited finding. Cited findings on this page carry their own tier.
Other compounds in its class
Same class in the registry: Kisspeptin. Each row shows what that compound's own record states; nothing is inferred across rows.
| Compound | Tier | Publications | RCTs | Record |
|---|---|---|---|---|
| IGF-1 LR3 | Animal, preclinical | 27 | 0 | draft |
| Kisspeptin | Human clinical trial | 3,850 | 44 | draft |
Regulatory status
Registry facts only. Jurisdiction-level status, compounding categories and sport prohibitions need their own cited documents before they appear here.
- Editorial synthesis from general knowledge · primary document to be added to the ledger
Open questions and limitations
What is genuinely unknown, stated plainly. A missing field is not evidence that the outcome is safe, effective, or established.
- No study in the ledger measured IGF-1 LR3 pharmacokinetics in any species, and none used the subcutaneous route.
- No study in this record's ledger reports dose-escalation schedules for IGF-1 LR3.
- No study in this record's ledger reports exclusion criteria for IGF-1 LR3.
- No study in this record's ledger reports storage or stability for IGF-1 LR3.
- No randomized controlled trial of IGF-1 LR3 is indexed in Europe PMC.
- Whether any finding about IGF-1 LR3 holds in humans is untested.
Questions people ask
What is IGF-1 LR3?
IGF-1 LR3 is a recombinant analogue of human insulin-like growth factor 1 with a 13-amino-acid extension at one end and an arginine swapped for glutamate at position 3. Those changes stop it binding to the IGF-binding proteins, so more of it is free to act. It was designed in Adelaide in the early 1990s as a cell-culture growth factor and is still sold for that purpose under the name LONG R3 IGF-I; it has never been tested in a human study.
What is the half-life of IGF-1 LR3?
Not measured in people. 'Long' in the name refers to the 13-amino-acid extension, not to a long half-life. Because IGF-1 LR3 does not bind the carrier proteins that hold native IGF-1 in the blood for hours, it is expected to clear faster than native IGF-1, not slower; the 20-to-30-hour figure on vendor pages has no published measurement behind it.
Is IGF-1 LR3 better than HGH?
No study has compared them, in animals or people. Growth hormone is an approved medicine with decades of trial data that acts partly by raising the body's own IGF-1 under the control of its binding proteins; IGF-1 LR3 is a cell-culture reagent that bypasses those proteins and has no human data. 'Better' has nothing to rest on.
Does IGF-1 LR3 cause cancer?
No study has tested it. The concern is mechanistic and stronger than for most peptides: IGF-1 receptor signalling drives cell proliferation, the approved native IGF-1 carries a label warning about malignancy reported in treated children, and IGF-1 LR3 is designed to act more freely than the native hormone. Nothing has been measured either way.
Is IGF-1 LR3 safe for bodybuilding?
Unknown, because no human has been given it in a study. The specific risks are hypoglycaemia, which the approved native IGF-1 label treats as its main warning, unchecked growth signalling, and the unknown composition of research-chemical vials. It is prohibited in tested sport at all times.
Does IGF-1 LR3 build muscle?
In fetal sheep a one-week infusion increased skeletal-muscle myoblast proliferation and the weight of some organs, but not hindlimb muscle mass or protein synthesis rate; in mice with Alzheimer's-type pathology seven months of intranasal treatment improved body composition. No human muscle measurement exists.
Does IGF-1 LR3 burn fat?
No study measured fat loss in any species. The fetal-sheep infusions lowered insulin and blood glucose, which is a metabolic effect, not a fat-loss result, and in growth-restricted fetuses it lowered circulating amino acids.
What is IGF-1 LR3 used for?
Legitimately, as a growth-factor supplement in cell-culture media for making antibodies and other biologic drugs, where it replaces insulin. In research, as a tool for raising IGF-1 signalling in fetal sheep and mice. Outside the literature, for muscle growth and fat loss in bodybuilding, a use no study has tested.
Does IGF-1 LR3 increase testosterone?
No study has measured it in any species. IGF-1 acts on its own receptor, not on the pituitary-gonadal axis, and the sheep and mouse work reported insulin, glucose, growth and amyloid, never testosterone.
Has IGF-1 LR3 been tested in humans?
No. Not one of the 27 indexed publications is a human study, and none has ever been registered. The human evidence people cite is either for native IGF-1 (mecasermin) or for growth hormone, which are different molecules.
Is there an IGF-1 LR3 dose?
Not for people. The only doses in the literature are intravenous infusions into fetal sheep at 6.6 or 1.17 micrograms per kilogram per hour for a week, intranasal drops in mice at an unstated dose, and 20 to 100 micrograms per litre in tissue baths. The microgram figures that circulate were not derived from any of these.
What did the fetal-sheep studies show?
A week of infusion made hearts, spleens and adrenals heavier and multiplied muscle precursor cells, but did not increase muscle mass or protein synthesis, and it lowered insulin and glucose in every experiment, with the insulin defect persisting in islets removed from the fetuses. In growth-restricted fetuses it did not restore growth.
Why is it called Long R3?
'Long' is a 13-amino-acid extension added to the front of the IGF-1 sequence; 'R3' is an arginine replacing glutamate at position 3. Together they stop the molecule binding the IGF-binding proteins, which is why it is more potent in culture. Neither has anything to do with how long it lasts in the body.
What are the side effects of IGF-1 LR3?
Unmeasured in people. The animal work points to low blood sugar and suppressed insulin. The approved native IGF-1 warns of hypoglycaemia, intracranial hypertension, lymphoid-tissue enlargement and reported malignancy. A 2026 clinical review of people self-administering IGF-1 analogues lists dysglycaemia, fluid retention, muscle and joint pain and injection-site reactions.
Is IGF-1 LR3 FDA approved?
No. It has no approval anywhere and no development programme. The approved IGF-1 is mecasermin (Increlex), for children with severe primary IGF-1 deficiency, and it is a different molecule.
Is IGF-1 LR3 banned in sport?
Yes. WADA prohibits insulin-like growth factor-1 and its analogues under S2 at all times, in and out of competition.
Can IGF-1 LR3 be taken intranasally or orally?
Intranasal delivery was used in one seven-month mouse study, which measured brain pathology and body composition. No oral study exists, and a 83-amino-acid protein would be expected to be digested. No human study of any route exists.
Which species has IGF-1 LR3 been studied in?
Fetal sheep, mice, and cells and tissues from sheep, cattle, pigs and chickens. Its widest use is in Chinese hamster ovary cells, where it is a media supplement for manufacturing biologic drugs.
Does IGF-1 LR3 help Alzheimer's disease?
In male mice with Alzheimer's-type pathology, seven months of intranasal IGF-1 LR3 changed the form of amyloid plaques and improved body composition but did not preserve memory or behaviour. The authors concluded it does not support use on its own.
Who makes IGF-1 LR3?
It was developed at GroPep and the University of Adelaide and is manufactured by Repligen as LONG R3 IGF-I for cell culture. Vials sold as research chemicals for injection come from other suppliers, whose content and purity are not verified by any regulator.
Sources
Full citations. Every claim above links to one of these by its id.
- 1
- 2IGF-1 LR3 does not promote growth in late-gestation growth-restricted fetal sheep.
pmid-39679943· · peer-reviewed - 3
- 4
- 5N-Linked Glycosylation in Chinese Hamster Ovary Cells Is Critical for Insulin-like Growth Factor 1 Signaling.
pmid-36499281· · peer-reviewed - 6Sheep recombinant IGF-1 promotes organ-specific growth in fetal sheep.
pmid-36091374· · peer-reviewed - 7
- 8IGF-1 infusion to fetal sheep increases organ growth but not by stimulating nutrient transfer to the fetus.
pmid-33427051· · peer-reviewed - 9Coronary vascular growth matches IGF-1-stimulated cardiac growth in fetal sheep.
pmid-32573852· · peer-reviewed - 10Na+ transport across rumen epithelium of hay-fed sheep is acutely stimulated by the peptide IGF-1 in vitro.
pmid-22227200· · peer-reviewed - 11IGF-1 has plaque-stabilizing effects in atherosclerosis by altering vascular smooth muscle cell phenotype.
pmid-21281823· · peer-reviewed - 12
Show the remaining 4 sources
- 13Leptin in the bovine corpus luteum: receptor expression and effects on progesterone production.
pmid-17154301· · peer-reviewed - 14Paracrine effects of oocyte secreted factors and stem cell factor on porcine granulosa and theca cells in vitro.
pmid-12941156· · peer-reviewed - 15
- 16
Reference card
- Compound
- IGF-1 LR3, growth factors and reproductive
- Evidence tier
- Animal, preclinical
- Indexed publications
- 27 · 0 RCTs · 0 other clinical trials
- Approval
- no registered development programme found
- Routes reported
- intravenous
- Reviewed
- Adam Mirando, PharmD,
Study figures are as published in each source and are not recommendations. Print or save this card with its date.
Last reviewed and what changed
Newest first. These are the record's own revision dates, and the same dates feed the sitemap.
- · Reviewed by Adam Mirando, PharmD, on 2026-09-25.
- · Reverted 1 of those label changes after tightening the rule: 'urine' had matched inside 'murine' and 'screening' had matched a zebrafish drug screen. pmid-9867252 back to Animal study
- · Label correction: 1 evidence rows built from detection and doping-control papers carried study designs such as animal or in-vitro work. They are relabelled Analytical method, the label scripts/draft_claims.py has applied since the rule was added; these rows predate it. pmid-9867252 (Animal study -> Analytical method)
- · Misattribution check: adverse_events (pmid-42395176): the quoted adverse effects, prolactin and cortisol elevations, belong to the growth hormone secretagogues the review covers, not to IGF-1 LR3. The sources stay in the ledger; only the claims that put another agent's result under this compound were removed.
- · Written under the sequencing rule after research/intents/igf-1-lr3.json: guide (7 sections), FAQ to 11 plus 12 from the map, hand-corrected dose claims (the drafter had parsed '1.17 ± 0.12 μg/kg/h' as 0.12 μg), weight-normalized, adverse-event, mechanism, reported-use and regulatory claims; the reagent origin and the meaning of 'Long R3' stated; intent-driven H1 and title.
- · Claims drafted extractively from 16 ledger sources by scripts/draft_claims.py: 14 claims, 15 evidence-table rows. Status researched -> draft.
- · Claims drafted extractively from 16 ledger sources by scripts/draft_claims.py: 19 claims, 15 evidence-table rows. Status researched -> draft.
- · Evidence fetched from Europe PMC and ChEMBL by scripts/fetch_evidence.py; claims not yet written.