compound
IGF-1 LR3
An engineered analog of a hormone that exists as an approved medicine, covered claim by claim: the sheep and cattle literature that is its whole published record, and the 2025 paper whose title reports no growth.
- Primary sources Registry records and papers are read at the source, not through summaries. Read the methodology
- Every claim graded Each claim about what a compound does carries an evidence tier and a numbered citation. How grades derive
- Sells nothing No cart, no price, and no product page anywhere on this site. Conflict disclosure
- Corrections logged Errors are fixed and recorded in a permanent public log, never edited away. Corrections log
IGF-1 LR3 is a modification of a hormone that already exists as a licensed medicine. That makes it unusual in this catalogue and it makes the comparison unusually clean: the unmodified version has a manufacturer, a label, an approved population and a post-marketing registry, and the modified version has none of those.
The modification itself is straightforward to describe. Native IGF-1 circulates mostly bound to carrier proteins that keep it in reserve. LR3 is engineered to evade those carriers and to bind the receptor strongly, so more of it is free and it acts for longer.
What is unusual here is that the compound's own literature exists and points somewhere other than the marketing. It has been studied in fetal sheep and in beef cattle, and the most recent paper naming it reports that it did not promote growth in the animals it was given to.
| Property | Value | Source |
|---|---|---|
| Category | Engineered analog of insulin-like growth factor 1, sold as a research chemical for muscle growth | PMID 39679943 |
| Also known as | Long R3 IGF-1, LR3 IGF-1, Long(R3)-IGF-1 | PMID 10370861 |
| What the modification does | Low affinity for the IGF binding proteins and high affinity for the IGF-1 receptor, so it evades the carriers that normally hold circulating IGF-1 in reserve | PMID 39679943 |
| Registered human trials | None. Of 29 registry records naming mecasermin or recombinant human IGF-1 as an intervention, not one names LR3 or Long R3 | ClinicalTrials.gov, read 23 August 2026 |
| Species studied | Fetal sheep and beef cattle. No study in a person has been published | PMID 33938236 |
| Anti-doping status | Covered by the WADA 2026 Prohibited List at S2.3, which names insulin-like growth factor 1 and mecasermin and extends to their analogues. Prohibited at all times, and a non-Specified Substance | WADA 2026 Prohibited List |
Not medical advice
This page reports what has been documented about a compound. It is not medical advice, not a diagnosis, not a dosing protocol, and not a recommendation to obtain or use anything described here. Talk to a licensed clinician about anything concerning your health. Read the full disclaimer.
Reviewed against editorial standards Updated
Key takeaways
- A registry sweep on 23 August 2026 returned 29 records naming mecasermin or recombinant human IGF-1 as an intervention. Not one of them names LR3 or Long R3, so there is no registered trial of this analog at any phase in any country.
- The most recent study naming the compound is titled for its result: IGF-1 LR3 did not promote growth in late-gestation growth-restricted fetal sheep. Growth promotion is the reason the compound is sold. [Animal] [1]
- Three studies from the same programme converge on an effect on the pancreas rather than on muscle. A one-week infusion into fetal sheep reduced glucose-stimulated insulin secretion, and the 2021 paper attributes it to a defect intrinsic to the islets. [Animal] [2] [3]
- The closest thing in the literature to the muscle claim is a 1999 infusion study in beef heifers losing weight on restricted feed. It reports a tendency for whole-body and skeletal muscle protein to be conserved, alongside a marked fall in the plasma concentrations of every amino acid measured and of glucose. [Animal] [4]
- The unmodified version of this protein is an approved medicine. Mecasermin is licensed for growth failure in children two years and older with a severe deficiency of it, which is a different population and a different purpose from an adult with normal levels.
- REGISTERED HUMAN TRIALS
- 0
- SPECIES STUDIED
- 2
- NUMBERED SOURCES
- 12
- EVIDENCE GRADE
- D
Who researches IGF-1 LR3?
Most readers arrive here from the muscle claim, and the useful content for them is what the compound's own studies measured rather than what IGF-1 does in general.
A second group arrives comparing it against the approved version. That comparison is the clearest one on this site: same protein family, one with a label and a registry and one with neither.
A tested athlete has the shortest answer on this page. The prohibited list names the parent and extends to analogues, so the modification changes nothing about that status.
What is IGF-1 LR3?
Plain-English version: a laboratory-modified copy of a growth hormone the body makes, changed so the proteins that normally hold it in reserve cannot grab it.
Insulin-like growth factor 1 is a protein the body makes, mostly in the liver and mostly in response to growth hormone. In circulation almost none of it travels free: binding proteins hold it, which controls how much reaches tissue and for how long.
IGF-1 LR3 changes that arrangement deliberately. The molecule carries a substitution at the third position and a thirteen amino acid extension on the front end, and the 2025 study describing it summarises the consequence as low affinity for the binding proteins and high affinity for the receptor [1]. More of it stays free and it persists longer.
That is the whole design and it is worth being precise about what it implies. A molecule engineered to evade the body's own reserve system is not simply a stronger version of the hormone; it is one that removes a control the body uses. Nothing in the published record establishes what removing that control does in an adult person, because no such study exists.
Native human IGF-1 with a substitution at position 3 and a thirteen amino acid extension at the front · Approximately 9,100 Da, against roughly 7,600 Da for native IGF-1
How strong is the evidence, claim by claim?
Every claim area this compound is discussed for gets a row, including the ones with the weakest support. The tier records what the row rests on, and the last column states what that work can and cannot show. Each tier links to its definition on the methodology page.
| Evidence Area | What Has Been Studied | Evidence Level | What It Can and Cannot Show |
|---|---|---|---|
| Muscle growth and body composition | The claim the compound exists for. Two studies name the analog and measure something related to growth. A 1999 intravenous infusion in beef heifers losing weight on restricted feed measured whole-body and skeletal muscle protein metabolism. A 2025 study infused it into late-gestation growth-restricted fetal sheep and measured growth [1] [4] [12] | [Animal] | The 2025 study reports in its title that the analog did not promote growth in those animals. The 1999 cattle study reports a tendency rather than a result, in animals under caloric restriction, and in the same experiment the infusion markedly reduced the plasma concentrations of all amino acids measured and of glucose. Neither study involves a person, neither involves an adult seeking muscle gain, and no registered trial of the analog exists in any species for this use |
| Effects on insulin and glucose | The effect the compound's own literature returns to most often, and it is not the one it is sold for. A one-week infusion into late-gestation fetal sheep reduced glucose-stimulated insulin secretion, which a 2021 paper traces to a defect intrinsic to the pancreatic islets. A 2023 follow-up found the attenuation during an acute infusion did not persist once islets were isolated. Separately, the 1999 cattle infusion markedly reduced plasma glucose [2] [3] [4] | [Animal] | Fetal sheep and cattle, at infusion rates chosen for those experiments. Nothing here establishes what happens in an adult person. What it does establish is that the compound's own published record contains a repeated pancreatic effect, which is worth a reader's attention precisely because it is not the effect the compound is marketed on |
| Its place in the performance-enhancing market | A 2026 review in Frontiers in Endocrinology covers performance-enhancing drugs marketed as research compounds and names IGF-1 Long R3 among them, alongside the GHRH analogues, the growth hormone releasing peptides, ipamorelin, hexarelin and AOD-9604. It describes reported adverse effects spanning endocrine and metabolic disturbance [5] [7] | [Anecdote] | A review of self-administration practice and clinical encounters is not a trial and does not measure whether the compound does what it is sold to do. It is cited here because it is the only current published work that addresses this compound as it is actually used, rather than as an infusion in a research animal |
Rolled up, that puts IGF-1 LR3 at evidence grade D Animals and anecdote . No completed human study of this compound for any use. The claim set is animal, in-vitro, and anecdote. A grade describes the quality of the research, not whether something works and not whether anyone should use it. The derivation is published.
How IGF-1 LR3 is thought to work
The mechanism here is not in dispute and it is also not the interesting question. What IGF-1 does is well characterised. What a version engineered to evade the body's reserve system does in an adult person is not characterised at all.
1. Evading the binding proteins, escaping the carrier proteins that normally keep the hormone in reserve (established as the design)
Circulating IGF-1 is almost entirely bound to carrier proteins. Those carriers set how much is available to tissue at any moment, which makes them a control system rather than an obstacle.
The analog is built with low affinity for those carriers and high affinity for the receptor. The design intent is more free hormone acting for longer, and the 2025 sheep study states the property in exactly those terms. [Animal] [1] [9] [10] [11]
2. The overlap with insulin signalling, the receptor it acts on is closely related to the one insulin uses (observed repeatedly in sheep and cattle)
The IGF-1 receptor and the insulin receptor are closely related, and the literature on this analog keeps landing on glucose and insulin rather than on muscle. Fetal sheep infused for a week showed reduced glucose-stimulated insulin secretion traced to the islets themselves, and cattle infused intravenously showed a marked fall in plasma glucose.
This is the part of the record a reader is least likely to have seen and most likely to need, because it describes an effect on a system the compound is not sold to affect. [Animal] [2] [3] [4]
What we do not know
What the analog does in an adult person, by any route, at any amount. No study exists.
Whether the pancreatic effects seen in fetal sheep have any counterpart in an adult. Nothing published addresses it.
Whether the 6.6 micrograms per kilogram infusion rate reported in the sheep programme abstract is stated the same way in the full text. This site read the abstracts only.
Whether the analog has any regulatory position of its own. It has not been assumed to inherit the approved drug's.
What this evidence can and cannot show
These results come from Fetal sheep and beef cattle for the compound itself. in Continuous infusion into fetal sheep; intravenous infusion in cattle under caloric restriction., not from people. An animal model is a deliberate simplification: the injury is created on purpose, the animal is young and healthy, the dose is scaled to body weight in a way that does not translate directly, and the outcome is measured at a fixed point rather than lived with. Cell and tissue work is a further step removed, because the concentrations that produce an effect in a dish are often far above anything a body reaches. Mechanism is a reason to run a trial. It is not a substitute for one, and compounds that looked mechanistically convincing have failed in people many times.
Has IGF-1 LR3 been tested in humans?
There is no human record for this analog, and the table sets out what a reader is most likely to be shown instead.
The registry sweep on 23 August 2026 queried the analog's names alongside mecasermin, Increlex, iPlex and recombinant human IGF-1, then filtered to records whose interventions actually name one of those drugs. That filter matters here: an unfiltered query returns 135 records, because IGF-1 is a widely measured biomarker and most of those studies are measuring it rather than giving it.
| Study | People | What was done | Result | Evidence level |
|---|---|---|---|---|
| IGF-1 LR3 itself | None | No registered trial at any phase, in any country, for any indication | There is no human record | [Anecdote] |
| Mecasermin trials | 29 records, up to 1378 in a registry | The unmodified protein, developed and approved as a medicine for a rare pediatric deficiency | Covered on its own page. A different molecule and a different population | [Human RCT] |
| The fetal sheep programme | None | Continuous infusion, measuring growth and insulin secretion | Reported in the claims table above, including the 2025 result on growth | [Animal] |
| The 1999 cattle study | None | Intravenous infusion in beef heifers under restricted feeding | A tendency to conserve protein, alongside a marked fall in amino acids and glucose | [Animal] |
Why we are not calling this proof
The mecasermin trials belong to a different molecule. The analog was engineered specifically to behave differently from it, which is the point of the modification, so results from one do not carry to the other in either direction.
The absence of any registration is not a failed test. It means nobody has taken the analog into a registered study, so nothing is established about what it does in a person.
Benefits: what the research shows
The claims table holds what is claimed and what sits behind it. This section is the shape of the record as a whole.
The honest bottom line on benefits
The compound's own literature exists, which is more than several entries in this catalogue can say, and it points away from the marketing rather than toward it. The most recent study naming the analog reports no growth promotion, and the effect that recurs across the programme is on insulin secretion.
None of that establishes what happens in an adult person, because that study has not been done. It does mean a reader deciding on the basis of published evidence is deciding on fetal sheep and beef cattle.
How long IGF-1 LR3 stays in the body
The property that defines this molecule is a pharmacokinetic one: it evades the binding proteins, so it stays free longer than the native hormone. That is the design and it is described in the sheep literature.
What has never been measured is what that produces in a person. There is no human half-life, no exposure figure and no route comparison for the analog, because no human study has been run.
The infusion rates used in the animal work were chosen for those experiments and were delivered as continuous infusions into research animals, one of them a fetus. They do not describe a route or a schedule anyone else uses.
No human pharmacokinetic data exists for the analog. [Animal] [1] [4]
What is documented about dosing
Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.
Commonly cited protocols (extrapolated, not validated)
Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.
| Study | What was given | Frequency | Duration | Notes |
|---|---|---|---|---|
| Fetal sheep programme | An infusion rate stated per kilogram in the source papers | Continuous infusion | One week in the studies reporting insulin effects | Read from abstracts. The full texts were not read, and the figure should be confirmed before it is relied on |
| Beef heifers, 1999 | An intravenous infusion described in the source paper | Continuous infusion | Eight hours | Animals under restricted feeding. Amino acids and glucose both fell markedly |
| Any human use | Nothing documented | Nothing documented | Nothing documented | No registered or published human study of this analog exists |
Commonly cited protocols (extrapolated, not validated) circulate for this compound in microgram amounts by injection. They did not come from a study of people, because no study of people exists.
The animal figures cannot be scaled across. They were continuous infusions into a research preparation, one of them a fetus in utero, at rates chosen to answer a question about that preparation. There is no human route, no human exposure measurement and no pharmacokinetic bridge, so there is nothing to scale and nothing to scale it with.
Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.
Main routes people compare, and what each source class actually reported, are set out on the documented protocols page.
Reported effects and what has been measured
What has been measured, and in what
The measurements that exist come from fetal sheep and from beef cattle and were designed to answer physiological questions rather than to characterise safety in a person.
The finding that recurs is on the pancreas. A one-week infusion into fetal sheep reduced glucose-stimulated insulin secretion, traced in the 2021 paper to a defect intrinsic to the islets. The 1999 cattle infusion markedly reduced plasma glucose and every amino acid measured. [Animal] [2] [3] [4]
What has not been characterised
Long-term exposure in a person has not been characterised in any published study, by any route, because no study in a person exists.
The molecule is engineered to evade the binding proteins that regulate how much free hormone reaches tissue. What removing that control does over time in an adult is not addressed anywhere in the published record. [Animal] [1]
What has been measured about IGF-1 LR3, and what has never been studied
Talk to a licensed clinician about anything concerning your health.
Sourcing and quality
What a credible product should show
The approved version of this protein is manufactured under a regulatory file with a defined identity. The analog is not, and there is no approved reference standard for it, so a certificate has nothing external to be checked against.
The modification is thirteen extra amino acids and a substitution. A product labelled as the analog might be native IGF-1, the analog, a partially processed intermediate, or something else, and only analysis distinguishes them.
Red flags
IGF-1's general biology cited as evidence for the analog. The analog was engineered specifically to behave differently from native IGF-1.
Mecasermin's approval or trials cited on a page selling the analog. They belong to the unmodified protein and to a rare pediatric deficiency.
The growth claim offered without the 2025 study, whose title reports that the analog did not promote growth in the animals it was given to.
Any dosing figure at all. There is no human study of the analog from which one could come.
Will it show on a drug test?
Covered by the WADA 2026 Prohibited List at section S2.3, growth factors and growth factor modulators, whose entry reads insulin-like growth factor 1 (IGF-1, mecasermin) and its analogues. An engineered analog is what that phrase describes.
Prohibited at all times, in and out of competition. The class carries no permitted window.
Non-Specified, which is the category without the reduced-sanction route that a Specified Substance can qualify for.
Storage
No storage guidance is given here. Storage belongs to a characterised formulation, and no characterised formulation of this analog exists outside a research supplier's own specification.
Regulatory status, as of 23 August 2026
| Body | Position | Date | Document |
|---|---|---|---|
| No agency | Not an approved drug in any indication, anywhere | Read 23 August 2026 | ClinicalTrials.gov and the absence of any regulatory file |
| ClinicalTrials.gov | No registration naming LR3 or Long R3, across 29 records naming mecasermin or recombinant human IGF-1 as an intervention | Swept 23 August 2026 | ClinicalTrials.gov v2 API |
| WADA | Covered at S2.3 by the entry naming insulin-like growth factor 1 and mecasermin and extending to their analogues. Prohibited at all times. Non-Specified Substance | 2026 list, read 23 August 2026 | WADA 2026 Prohibited List |
| FDA, 503A Bulks List | This site has not established a position for the analog and does not state one. It has not been assumed to inherit the approved drug's status | Open item as of 23 August 2026 | Recorded as unverified rather than asserted |
The analog has no agency position of its own because no agency has been asked for one. It has not been submitted for approval and it is not the subject of an investigational application on the public record.
The anti-doping entry is the one unambiguous regulatory fact here, and it is unusual in covering the analog explicitly rather than by inference. The list names the parent protein and the approved drug and then extends to their analogues, which is what this molecule is by construction.
This section is dated and re-checked on review. It records agency actions and their documents, not evidence about an effect, and carries no evidence tier.
IGF-1 LR3 compared with other performance peptides
| Compound | Evidence grade | What the human record covers | Read more |
|---|---|---|---|
| Mecasermin | Graded on its own page | The unmodified protein, approved as a medicine for growth failure in children two years and older with a severe deficiency, with 29 registry records behind it | /peptides/mecasermin/ |
| Native IGF-1 | Not covered separately | The hormone the body makes, held in reserve by binding proteins. This analog is built to evade that reserve system | Described in the mechanism section above |
| Follistatin-344 and ACE-031 | Graded on the performance group page | The other compounds sold for muscle growth covered by this site, with separate and unrelated evidence bases | /peptides/groups/performance/ |
The comparison that matters is with mecasermin, and it is the cleanest one on this site. Same protein family, one modified and one not, one sold and one prescribed.
The second row is the caution behind the first. The analog exists because someone wanted the hormone to behave differently, so evidence about the hormone is not evidence about the analog.
What IGF-1 LR3 typically costs
Frequently asked questions
Has IGF-1 LR3 been tested in humans?
No. A registry sweep on 23 August 2026 returned 29 records naming mecasermin or recombinant human IGF-1 as an intervention, and not one of them names LR3 or Long R3.
What is the difference between IGF-1 LR3 and IGF-1?
The analog carries a substitution at the third position and a thirteen amino acid extension at the front. The 2025 sheep study summarises the consequence as low affinity for the binding proteins and high affinity for the receptor, so more of it stays free and it acts for longer.
Does the research show it builds muscle?
The two studies that name the analog and measure something related to growth are a 1999 infusion in beef heifers and a 2025 infusion in fetal sheep. The 2025 paper reports in its title that it did not promote growth in those animals. The cattle study reports a tendency in animals under restricted feeding.
What species has it actually been studied in?
Fetal sheep and beef cattle. There is no published study in a person.
What does it do to blood sugar?
In the published animal work it lowers it. A one-week infusion into fetal sheep reduced glucose-stimulated insulin secretion, traced to a defect intrinsic to the islets, and the 1999 cattle infusion markedly reduced plasma glucose. What that means in an adult person is not established.
Is mecasermin the same thing?
No. Mecasermin is the unmodified recombinant protein and it is an approved medicine. The analog was engineered specifically to behave differently from it.
Do mecasermin's approval and trials apply to this?
No. They belong to a different molecule and to a rare pediatric deficiency. The modification is the reason the analog exists and the reason evidence does not carry across.
Is it banned in sport?
Yes. The WADA 2026 Prohibited List at S2.3 names insulin-like growth factor 1 and mecasermin and extends to their analogues. It is prohibited at all times, in and out of competition, and it is a non-Specified Substance.
Is there a dose?
No amount has been established for a person, and there is no human study from which one could be derived.
What is the most recent research?
A 2025 paper in the American Journal of Physiology: Endocrinology and Metabolism, reporting that the analog did not promote growth in late-gestation growth-restricted fetal sheep, and a 2026 review in Frontiers in Endocrinology covering performance-enhancing peptides marketed as research compounds, which names it among them.
References
- White A, Stremming J, Wesolowski SR, Al-Juboori SI, Dobrinskikh E, Limesand SW, Brown LD, Rozance PJ. IGF-1 LR3 does not promote growth in late-gestation growth-restricted fetal sheep. Am J Physiol Endocrinol Metab. 2025. PMID 39679943 DOI 10.1152/ajpendo.00259.2024 Describes the analog as having low affinity for IGF-binding proteins and high affinity for the IGF-1 receptor. Read as an abstract; the full text was not read.
- White A, Stremming J, Boehmer BH, Chang EI, Jonker SS, Wesolowski SR, Brown LD, Rozance PJ. Reduced glucose-stimulated insulin secretion following a 1-wk IGF-1 infusion in late gestation fetal sheep is due to an intrinsic islet defect. Am J Physiol Endocrinol Metab. 2021. PMID 33938236 DOI 10.1152/ajpendo.00623.2020
- White A, Stremming J, Brown LD, Rozance PJ. Attenuated glucose-stimulated insulin secretion during an acute IGF-1 LR3 infusion into fetal sheep does not persist in isolated islets. J Dev Orig Health Dis. 2023. PMID 37114757 DOI 10.1017/S2040174423000090
- Hill RA, Hunter RA, Lindsay DB, Owens PC. Action of long(R3)-insulin-like growth factor-1 on protein metabolism in beef heifers. Domest Anim Endocrinol. 1999. PMID 10370861 DOI 10.1016/s0739-7240(99)00015-6 Reports a tendency for whole-body and skeletal muscle protein to be conserved, alongside markedly reduced plasma concentrations of all amino acids measured and of glucose.
- Dominikowski A, Rękoś Z, Olejarz M, Szczepanek-Parulska E, Domin R, RuchaŁa M. The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration. Front Endocrinol (Lausanne). 2026. PMID 42395176 DOI 10.3389/fendo.2026.1822475 Names IGF-1 Long R3 among agents marketed as research compounds. Read in full on 23 August 2026.
- ClinicalTrials.gov. Registry sweep for mecasermin, Increlex, mecasermin rinfabate, iPlex, rhIGF-1, IGF-1 LR3 and Long R3 IGF-1, run through the v2 API on 23 August 2026 and filtered to records whose interventions name one of those drugs. Twenty-nine records survive the filter and none names LR3 or Long R3. An unfiltered query returns 135, because IGF-1 is a widely measured biomarker. ClinicalTrials.gov. 2026. ClinicalTrials.gov
- World Anti-Doping Agency. The 2026 Prohibited List. Section S2.3, Growth Factors and Growth Factor Modulators, carries the entry: Insulin-like growth factor 1 (IGF-1, mecasermin) and its analogues. The S2 class heading states that the class is prohibited at all times, in and out of competition, and that all substances in it are non-Specified. Read in full on 23 August 2026. World Anti-Doping Agency. 2026. WADA 2026 Prohibited List
- US Food and Drug Administration. INCRELEX (mecasermin) injection prescribing information, BLA021839, Ipsen Biopharmaceuticals, Inc. Read via the openFDA drug label API on 23 August 2026. Cited here for the approved population of the unmodified protein, which is a different molecule from the analog this page covers. openFDA drug label. 2026. Increlex label
- Stremming J, Heard S, White A, Chang EI, Shaw SC, Wesolowski SR, Jonker SS, Rozance PJ, Brown LD. IGF-1 infusion to fetal sheep increases organ growth but not by stimulating nutrient transfer to the fetus. Am J Physiol Endocrinol Metab. 2021. PMID 33427051 Part of the same fetal sheep programme, cited for the programme's design rather than for a finding about the analog specifically.
- Jonker SS, Giraud GD, Chang EI, Elman MR, Louey S. Coronary vascular growth matches IGF-1-stimulated cardiac growth in fetal sheep. FASEB J. 2020. PMID 32573852 Part of the same fetal sheep programme.
- Stremming J, White A, Donthi A, Batt DG, Hetrick B, Chang EI, Wesolowski SR, Seefeldt MB, McCurdy CE, Rozance PJ, Brown LD. Sheep recombinant IGF-1 promotes organ-specific growth in fetal sheep. Front Physiol. 2022. PMID 36091374 Cited to show what the unmodified protein does in the same preparation the analog was tested in.
- Lu Z, Liu N, Huang H, Wang Y, Tu T, Qin X, Wang X, Zhang J, Su X, Tian J, Bai Y, Luo H, Yao B, Zhang H. Recombinant expression of IGF-1 and LR3 IGF-1 fused with xylanase in Pichia pastoris. Appl Microbiol Biotechnol. 2023. PMID 37261455 Cited for how the analog is produced, not for any biological finding.