IGF-1 LR3 Dosage Guide 2026: What Was Actually Given

What does an IGF-1 LR3 dosage calculator actually calculate?

Volume, and nothing else: a vial size, a water amount, a syringe type and a microgram figure go in. Out comes a concentration, a draw volume and a unit count. No calculator anywhere can supply the one number this compound is missing, which is how many micrograms a person takes.

Both boxes want milligrams, and this compound is usually written in micrograms: a thousand micrograms is one milligram, so 50mcg is typed as 0.05. That single decimal place is where the arithmetic most often goes wrong, and we took the conversion apart in micrograms versus milligrams.

IGF-1 LR3 dosage chart: what was given, and the species it went into

Species gets its own column, and one row goes to each source: the chart holds the exogenous IGF-1 LR3 amounts a named study or product document puts on the record, printed beside the animal or the dish that received them, the route and the schedule. Amounts people report giving themselves are deliberately not in it. No tier column appears anywhere in it, because the published record has nothing to fill one with.

This is a sample of the animal literature, not a census of it: searched on 2 August 2026 for the query "LR3IGF-I" OR "LongR3-IGF-I" OR "Long R3 IGF-I" OR "Long-R3-IGF-I" OR "Long [Arg3]-IGF-I" OR "IGF-1 LR3" OR "IGF1-LR3" OR "LR3 IGF-1" OR "long R3IGF-I", each across all fields, PubMed returned 109 records, most of them cell-culture work. The rows below are the ones we read for ourselves and could pin to a named species, amount, route and duration. Other published administrations exist, and any page claiming to hold all of them, this one included, would be claiming more than it had read.

The species column decides what the number means: it decides what the number means. Eight of the nine rows below are animal rows, and five of those eight arrived by implanted pump, by continuous infusion or inside an implanted gel rather than through a syringe. The last row is not an animal amount at all, it is a concentration in a culture dish. Not one row is a human row, because there is no human row to print.

One molecule, several spellings: IGF-1 LR3, IGF1 LR3, igf lr3, Long R3 IGF-1 and Long [Arg3]-IGF-I all name the same 9 kDa protein. The papers cited at the bottom of this page write it LR3IGF-I, LongR3-IGF-I, Long-R3-IGF-I, IGF1-LR3 and Long [Arg3]-IGF-I; the reagent sheet writes IGF-I LR3. Everything here applies to all of them.

The conversion we are not doing: a microgram-per-day figure delivered continuously into a 150g rat, a 2kg piglet or a fetal lamb is not a human daily amount, and nothing in the sources at the bottom of this page converts one into the other. Any page that hands over a human microgram figure derived from those rows added a step the research did not.

The conversion we are doing: micrograms into syringe units, further down. That one is arithmetic, and it holds whatever the microgram figure is and wherever it came from.

Is there a human dose of IGF-1 LR3?

Not one that any study has established: searches of the ClinicalTrials.gov v2 application programming interface run on 2 August 2026 for the search terms "LR3 IGF", "Long R3 IGF-1" and "IGF-1 LR3" each returned a total count of 0 studies. The same interface, searched for mecasermin on the same day, returned 40.

The literature says the same thing in its own words: the 2021 anti-doping method paper that developed the detection assay for this exact family opens by noting that LongR3-IGF-I and its siblings "were never approved for use in humans" while being "readily available as black market products for bodybuilding" (Mongongu, Drug Test Anal).

And PubMed carries no trial either: searched on 2 August 2026 for the query ("LR3 IGF" OR "Long R3 IGF") with the clinical trial publication type filter applied across all fields, PubMed returned 0 records. The query is printed here in full so that anyone can run it again.

What that absence is and is not: the same database holds 109 records under the nine spellings of the name, so the zero is not a broken query. It is the specific absence of a human trial, sitting inside a real and mostly preclinical literature.

What the manufacturer's own paperwork says it is for: the product information sheet for a commercially sold IGF-1 LR3 describes the protein as a cell-culture reagent and closes with the line "PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED."

Which is why this page publishes no human microgram figure. The absence is not an editorial position we adopted for caution. It is what a trial registry search and a literature database search both return, and what the manufacturer's own paperwork says the material is for.

Why is IGF-1 LR3 described as more potent than IGF-1?

Because of what it does not bind, not what it does: the whole design is a molecule that largely escapes the IGF binding proteins. Ballard's 1993 comparison measured IGF-I as having "approximately 1000 fold higher affinity" than LR3IGF-I toward IGFBP-3, IGFBP-4, total rat plasma binding proteins and the binding protein secreted by L6 myoblasts.

The manufacturer's sheet puts the same property more conservatively: it states that IGF-1 LR3 "has >100-fold reduced affinity for IGF-binding proteins (IGFBPs), which reduces availability of IGFs in cell culture". Two named sources, two different multiples, both pointing the same way.

At the receptor it is weaker, not stronger: Tomas records that LR3IGF-I "binds 3-fold less well than IGF-I to the type 1 IGF receptor". The potency does not come from a better fit at the target. It comes from more of the molecule reaching the target.

The cleanest proof of that is the experiment where it loses.

Francis ran exactly that control: in cell lines that secrete binding proteins into the medium the potency order was Long [Arg3]-IGF-I and des(1-3)IGF-I first, then Long [Gly3]-IGF-I, then Long IGF-I, then IGF-I last. In chicken embryo fibroblasts, "a cell line that does not secrete detectable IGFBPs into the medium", Long [Arg3]-IGF-I "was less potent than IGF-I".

What that means for any potency multiple you read: it is a property of the system the measurement was taken in, not a fixed number carried by the molecule. Ballard reports 5 to 10 fold greater potency in cultured L6 myoblasts and 6 fold in the rat growth measurements. Tomas 1992 reports about 2.5 fold in dexamethasone-treated rats. Francis reports less than 1 fold, meaning weaker, in a cell line with no binding proteins around.

How long does IGF-1 LR3 last in the blood?

The published answer is the opposite of the popular one: Ballard's clearance experiments found that "LR3IGF-I was shown to be removed from the plasma much more rapidly than was IGF-I, a difference reflecting the poor association of LR3IGF-I with plasma IGFBPs".

The control that settles the mechanism: the same paper repeated the comparison in pregnant rats, where binding protein levels are markedly reduced. There, "only the clearance of IGF-I was affected to produce a clearance rate almost as rapid as that found with LR3IGF-I". Take the carrier proteins away and IGF-I starts behaving like LR3, which is the direction the mechanism predicts.

A second, much more recent measurement agrees: after one intramuscular administration of 100mcg per kg in rats, Mongongu's assay detected unchanged Des(1-3)-IGF-I and R3-IGF-I "until 24 h after administration", while "LongR3-IGF-I disappeared rapidly after 4 h". One of its N-terminal degradation products, Des(1-11)-LongR3-IGF-I, outlasted the intact molecule and was detected up to 16 hours.

Why the popular figure survives anyway: a long half-life is the obvious story to tell about a molecule engineered to dodge its carrier proteins. It is also backwards. Those carrier proteins are what keeps circulating IGF-I from being cleared, and a molecule that skips them loses that protection along with the restriction.

What is genuinely missing here: a human pharmacokinetic measurement. Both figures above are rat figures. Mongongu notes that the same degradation products appeared after incubating the analogs in human whole blood in vitro, "suggesting that observations in rats may be extrapolated to humans", which is the authors' own hedge and not a human result.

Is IGF-1 LR3 the same as the prescription IGF-1?

No, and the difference is the entire point of the molecule: the approved molecule is mecasermin, recombinant human IGF-1 with the native sequence, marketed as Increlex. IGF-1 LR3 is that sequence deliberately altered so that it binds the carrier proteins far more weakly. One is the hormone; the other is a reagent engineered to behave unlike it.

Two approvals, not one, and the second is gone: the regulator's own application database returns two approved mecasermin products. Increlex, BLA 021839, is prescription and still marketed. Iplex, mecasermin rinfabate, BLA 021884, was approved on 12 December 2005 and its record now reads discontinued. Neither one is an analogue of the kind this page is about, and searching the same database for the LR3 spellings returns no matching product at all.

What the approved label covers, in its own words: Increlex "is indicated for the treatment of growth failure in pediatric patients 2 years of age and older with severe primary IGF-1 deficiency or with growth hormone (GH) gene deletion who have developed neutralizing antibodies to GH". That is the whole indication.

The numbers that label carries: a starting range of 0.04mg to 0.08mg per kg twice daily and a maximum of 0.12mg per kg twice daily, from a 40mg per 4mL multiple-dose vial at 10mg per mL. Those are mecasermin figures, tied to that indication and that population, and they belong to a different molecule from the one this page is about.

The warning on that label that travels furthest: "Severe hypoglycemia leading to hypoglycemic seizures has been observed with INCRELEX treatment. Because INCRELEX has insulin-like hypoglycemic effects it should be administered shortly before or after (± 20 minutes) a meal or snack." That hazard belongs to IGF-1 signaling itself, which is the one thing the two molecules genuinely share.

Why the distinction matters when reading a protocol page: a page that reassures about IGF-1 LR3 by pointing at an approved IGF-1 product has pointed at a different molecule, on a different indication, in children. The upstream drugs that raise IGF-1 rather than replacing it are a third category again, worked through on our page comparing growth hormone against the peptides that release it.

Where do the internet doses come from?

There are two ways to dodge this question: skip it, or answer it with a tiered chart built out of animal data. We do neither, and the reason is that we could not find the step between the two columns below in either of the two literature databases we searched. The queries behind that absence are printed at the bottom of this page, with the controls that prove each half of them can return a hit.

Not one figure on this page is offered as yours, and no human study has established one for anybody to offer.

The half-life question is the one a reader can settle in a minute, and it is worth doing because it is checkable in a way a dose claim is not. Ballard's rats cleared LR3 faster than IGF-I, and Mongongu's rats had no intact LongR3-IGF-I left after four hours. Both abstracts are linked at the bottom of this page.

IGF-1 LR3 reconstitution: what a 1mg vial does at four water volumes

The question people actually type: how much bacteriostatic water goes into a 1mg IGF-1 LR3 vial. The water volume is a decision taken at the bench, not a specification printed on the glass, and it is that decision which fixes the concentration. Nothing in the sources at the bottom of this page reconstituted a 1mg vial of it for injection, so there is no tested volume to report.

What the one real preparation document specifies, and what it is for: the reagent product sheet describes reconstitution in sterile water to at least 0.1mg per mL, with optional dilution afterward into bovine serum albumin at a final concentration of 0.1 to 1%. That is a bench protocol for a culture dish, and the albumin step alone marks it as belonging to a different world from a syringe.

So the table below sticks to the one thing that can be settled: it runs the arithmetic for a 1mg vial at four water volumes, adds two 5mg rows for comparison, and shows what one syringe unit is worth in each case. The general version, with any vial and any water volume, is in concentration versus dose and in the reconstitution calculator.

Why the 1mg vial makes the water choice bite: a milligram is a small amount of powder spread across a barrel marked in hundredths of a milliliter. At 1mg in 0.5mL one unit carries 20mcg, so a one-unit misread moves the amount by 20mcg. At 1mg in 3mL one unit carries 3.33mcg, and the same misread moves it by a sixth as much. Same vial, same protein, six times the resolution.

The cost of that resolution: total volume. The same microgram figure sits in a six times larger draw at 3mL than at 0.5mL, so a barrel of any given size runs out six times sooner. A 0.3mL barrel is 30 units either way, but at 3mL those 30 units are worth 100mcg and at 0.5mL they are worth 600mcg. The 50mcg figure this page keeps returning to is 0.15mL on the 3mL mix, half of that barrel, and 0.025mL on the 0.5mL mix.

Two of the rows land on the same place from different directions: 1mg in 1mL and 5mg in 5mL both give 1,000mcg per mL, because concentration is a ratio and neither the vial nor the water decides it alone. That is worth knowing before comparing two charts that quote different vials.

How many units is 50mcg of IGF-1 LR3?

A sixfold spread across four ordinary mixes: on a 1mg vial with 1mL of water, 50mcg reads as 5 units on a U-100 syringe. The same vial with 2mL reads 10 units. With 0.5mL it reads 2.5 units, which is not a whole mark. With 3mL it reads 15 units.

Where those numbers come from: 1mg in 1mL is 1,000mcg per mL, and one unit on a U-100 barrel is a hundredth of a milliliter, so one unit carries 10mcg and 50mcg lands on five of them. Every other row is the same division with a different denominator.

Which is why a bare "5 units" means nothing: that reading is 50mcg on one reconstitution, 100mcg on another and 25mcg on a third, and the three are indistinguishable on the barrel until the concentration is named. The syringe measures volume. It has never measured mass.

One assumption sits under every count above: they are all U-100 counts. On the other scale still in circulation the same mark carries two and a half times the volume the count was worked out for, and that factor compounds with whichever concentration row produced the count rather than replacing it. The two scales have their own page.

What's not known yet?

Still not an approved medicine: no approved product contains IGF-1 LR3, in the regulator records we checked, and the two approved IGF-1 products that database does return are both a different molecule, one of them discontinued and the marketed one carrying a pediatric indication.

Banned in sport, at all times: the 2026 World Anti-Doping Agency Prohibited List places "Insulin-like growth factor 1 (IGF-1, mecasermin) and its analogues" under section S2.3, growth factors and growth factor modulators, in a class marked "PROHIBITED AT ALL TIMES (IN- AND OUT-OF-COMPETITION)".

Detectable, on a published method: Mongongu's 2021 work validated immunopurification followed by high resolution mass spectrometry for LongR3-IGF-I spiked into human serum, and tested detectability after a single intramuscular administration in rats. The window there was short for the intact molecule and longer for one of its degradation products.

Four holes, and none of them is small:

• No human dose-ranging study, and no registered trial to produce one. Every study-administered amount in the chart above went into an animal.
• No human pharmacokinetic measurement. The clearance result and the detection result on this page are both rat results, and the human part is an in vitro blood incubation the authors label as suggestive.
• No long-term human safety study in the peer-reviewed record we searched. A 2026 review in Frontiers in Endocrinology sorts the compounds it reviewed into four evidence tiers and puts IGF-1 LR3 in the bottom one, for compounds that "have no peer-reviewed human studies", and the FDA adverse event system returns no match under the four spellings of the name we searched. Both are null results rather than safety findings, and neither of them rules out an unpublished or differently named study, or harm that nobody has written down.
• No verified data on the community schedules that circulate for it. The same review collected those online protocols and printed them as behavioural data, stating that they are "not evidence-based treatment strategies" and "MUST NOT be interpreted as clinically validated or safe".

A page that fills those four holes with a number filled them in itself.

Bigger than all four, because it applies before any of them: the identity of what is in the vial. Kohler's 2010 case report analyzed one black market injection vial and characterized its contents as Long-R3-IGF-I carrying a hexahistidine tag on the C-terminus, joined by the linker amino acids Leu-Glu. That tag is a purification handle from protein chemistry, normally removed when it sits on the N-terminus, and the authors write that the effects of the His-tagged form in humans "have not been elucidated or described".

Their own read on where it came from: the vial's contents "may rather be a by-product from biochemical studies than synthesized for injection purposes". One vial is one vial, and one characterization is not a survey. What it does establish is that a vial sold to be injected can turn out to hold a purification construct off a protein chemistry bench.

How this page is sourced

Read off the papers and the documents themselves: each research figure here came out of the document it is credited to, and never out of another site's account of it. Eleven of the twelve journal papers were read from the PubMed record on 2 August 2026, Tomas 1992 from the full text hosted at Europe PMC, and the 2026 review from its PubMed Central full text on 3 August 2026. Each printed identifier was checked against the source that issues it.

Twenty-one sources, none of them a study of what a person takes: twelve peer-reviewed papers, one manufacturer product sheet, two regulator records, one international anti-doping standard, and five database searches run for this page.

Why five of the entries are searches rather than documents: several claims on this page are absences, and an absence has no document to point at. The query, the date, the count and a control that proves the query can return a hit are the whole evidence, so they are cited like anything else. An absence claim with no printed query is a claim with no source.

What is deliberately absent from the list: commercial dosing pages. We do not name or link peptide sellers, and a source we cannot name is a source a reader cannot check, so rather than cite one anonymously we cut the claims that rested on it. Where the community protocols themselves are the point, we cite the peer-reviewed review that collected them instead of the pages that publish them. That is why this page reports no community dosing tiers.

Where the rules behind that live: the standard we hold every citation to is written up in full on the methodology page, and any figure here that turns out to need a correction is corrected against it.

Last reviewed: 2 August 2026.

1. 1

   Francis GL, Ross M, Ballard FJ, et al. Novel recombinant fusion protein analogues of insulin-like growth factor (IGF)-I indicate the relative importance of IGF-binding protein and receptor binding for enhanced biological potency. J Mol Endocrinol. 1992;8(3):213-23. Source for the construct, the Glu-3 to Arg substitution, the porcine growth hormone extension, the potency order in binding-protein-secreting lines, and the chicken embryo fibroblast reversal. doi:10.1677/jme.0.0080213. PMID 1378742.

2. 2

   Tomas FM, Knowles SE, Owens PC, et al. Insulin-like growth factor-I (IGF-I) and especially IGF-I variants are anabolic in dexamethasone-treated rats. Biochem J. 1992;282(Pt 1):91-7. Full text read at Europe PMC, PMC1130894, on 2 August 2026. Source for the three LR3IGF-I arms of 44, 111 and 278 micrograms per day, the matching IGF-I arms of 695, 278 and 111 micrograms per day, the methods sentence setting the variant amounts 2.5-fold lower, the 6g against 19g against 18g body weight comparison, the 3-methylhistidine figures, the 45% gut weight rise, and the 3-fold weaker type 1 receptor binding. doi:10.1042/bj2820091. PMID 1371669.

3. 3

   Tomas FM, Knowles SE, Chandler CS, et al. Anabolic effects of insulin-like growth factor-I (IGF-I) and an IGF-I variant in normal female rats. J Endocrinol. 1993;137(3):413-21. Source for the 14-day osmotic pump delivery, the 278 micrograms per day IGF-I arm and its 18 to 26% effects, the 44 micrograms per day LR3IGF-I equivalence, and the 213 micrograms per day human growth hormone control. doi:10.1677/joe.0.1370413. PMID 8371075.

4. 4

   Ballard FJ, Walton PE, Bastian S, et al. Effects of interactions between IGFBPs and IGFs on the plasma clearance and in vivo biological activities of IGFs and IGF analogs. Growth Regul. 1993;3(1):40-4. Source for the approximately 1000-fold binding protein affinity difference, the 5 to 10 fold L6 myoblast potency, the 6-fold growth potency, the faster plasma clearance of LR3IGF-I, and the pregnant rat control. No DOI was ever registered for this article; the PubMed record is the locator. PMID 7683526.

5. 5

   Mongongu C, Coudore F, Domergue V, et al. Detection of LongR3-IGF-I, Des(1-3)-IGF-I, and R3-IGF-I using immunopurification and high resolution mass spectrometry for antidoping purposes. Drug Test Anal. 2021;13(7):1256-1269. Source for the never-approved-for-human-use statement, the single 100 micrograms per kilogram intramuscular rat administration, the four-hour disappearance of intact LongR3-IGF-I, the degradation products out to 16 hours, and the oxidized forms found in black market products. doi:10.1002/dta.3016. PMID 33587816.

6. 6

   Kohler M, Thomas A, Walpurgis K, et al. Detection of His-tagged Long-R3-IGF-I in a black market product. Growth Horm IGF Res. 2010;20(5):386-90. Source for the hexahistidine tag on the C-terminus, the Leu-Glu linker, and the authors' statements that the effects of the tagged form in humans have not been elucidated and that the material may be a by-product of biochemical studies. doi:10.1016/j.ghir.2010.07.001. PMID 20675162.

7. 7

   Tomas FM, Walton PE, Dunshea FR, Ballard FJ. IGF-I variants which bind poorly to IGF-binding proteins show more potent and prolonged hypoglycaemic action than native IGF-I in pigs and marmoset monkeys. J Endocrinol. 1997;155(2):377-86. Source for the pig bolus amounts of 20 and 50 micrograms per kg for the IGFs including LR3IGF-I, the 2 to 3 fold greater glucose-lowering potency of the variants, and the longer cumulative suppression. The marmoset arm of that study compared IGF-I and des(1-3)IGF-I and is not an LR3 figure. doi:10.1677/joe.0.1550377. PMID 9415072.

8. 8

   Hammon H, Blum JW. Endocrine and metabolic changes in neonatal calves in response to growth hormone and long-R3-insulin-like growth factor-I administration. Biol Neonate. 1998;73(2):121-8. Source for the calf amount of 50 micrograms per kg per day, twice daily for 7 days, fed with colostrum or milk replacer in one group and injected subcutaneously in another, and for the finding that the fed route had no effect while the injected route lowered plasma glucose and insulin. doi:10.1159/000013968. PMID 9483305.

9. 9

   Dunshea FR, Chung CS, Owens PC, Ballard JF, Walton PE. Insulin-like growth factor-I and analogues increase growth in artificially-reared neonatal pigs. Br J Nutr. 2002;87(6):587-93. Source for the neonatal pig infusion amounts of 2, 4 or 8 micrograms per hour over 8 days, the second experiment at 8 micrograms per hour for 9 days followed by 16 micrograms per hour for 9 more, the 2kg starting weight, and the increased daily gain in the LR3IGF-I animals over the second half of that second experiment. doi:10.1079/BJNBJN2002574. PMID 12067429.

10. 10

    White A, Stremming J, Wesolowski SR, et al. IGF-1 LR3 does not promote growth in late-gestation growth-restricted fetal sheep. Am J Physiol Endocrinol Metab. 2025;328(1):E116-E125. Source for the growth-restricted fetal sheep amount of 1.17 plus or minus 0.12 micrograms per kg per hour over one week, the 6.6 micrograms per kg per hour used in the same group's earlier normally grown fetuses, and the finding that fetal body weights were not different between treated and vehicle groups. doi:10.1152/ajpendo.00259.2024. PMID 39679943.

11. 11

    Clark AR, Adams AT, McKinley TO, et al. Provisional treatment of volumetric muscle loss with insulin-like growth factor 1 releasing muscle void fillers. J Surg Res. 2026;317:461-466. Source for the 28 microgram and 280 microgram amounts delivered from an implanted hydrogel muscle void filler in adult male Lewis rats, soluble or encapsulated, the increased muscle weight at the high encapsulated amount at 28 days, and the absence of any change in torque, fiber size or fiber count. doi:10.1016/j.jss.2025.11.043. PMID 41418663.

12. 12

    STEMCELL Technologies Inc. Product Information Sheet: Human Recombinant IGF-I LR3, ACF, catalog #100-2060, document #10000029772, version 00. Source for the 9 kDa predicted mass, E. coli expression, the 98% SDS-PAGE purity, the 11.7ng per mL EC50 in transfected MCF-7 cells, the 0.1 EU per microgram endotoxin limit, the greater-than-100-fold reduced binding protein affinity, the acetonitrile and trifluoroacetic acid formulation, the sterile water and bovine serum albumin preparation section, and the research-use-only statement. Retrieved 2 August 2026, HTTP 200. Product information sheet PDF.

13. 13

    INCRELEX (mecasermin) injection, solution, for subcutaneous use. Ipsen Biopharmaceuticals, Inc. DailyMed structured product label, version 21, published 7 August 2025. Indications and Usage for the pediatric severe primary IGF-1 deficiency indication; Dosage and Administration for the 0.04 to 0.08 mg/kg twice daily starting range and the 0.12 mg/kg twice daily maximum; Warnings and Precautions for the hypoglycemia text; Description for the 40 mg per 4 mL multiple-dose vial. Read 2 August 2026. DailyMed label.

14. 14

    U.S. Food and Drug Administration. Drugs@FDA record for INCRELEX, BLA 021839, applicant Ipsen. The regulator record checked for whether any approved product contains an IGF-1 analogue rather than native mecasermin. Retrieved 2 August 2026, HTTP 200. accessdata.fda.gov.

15. 15

    U.S. Food and Drug Administration, openFDA Drugs@FDA application programming interface, queried 2 August 2026 on the products.active_ingredients.name field. "IGF-1 LR3", "LONG R3 IGF-1" and "LONGR3-IGF-I" each returned HTTP 404 and "No matches found!". The control query "MECASERMIN" returned HTTP 200 and a total of 2, so the zero is a real zero and not a dead endpoint: BLA 021839, INCRELEX, marketing status prescription, and BLA 021884, IPLEX, mecasermin rinfabate recombinant, marketing status discontinued, original approval dated 12 December 2005. Source for the absence of any approved LR3 product and for the two-product mecasermin count. openFDA Drugs@FDA query.

16. 16

    World Anti-Doping Agency. The 2026 Prohibited List, International Standard, effective 1 January 2026. Section S2, page 8: growth factors and growth factor modulators, listing "Insulin-like growth factor 1 (IGF-1, mecasermin) and its analogues", in a class headed "PROHIBITED AT ALL TIMES (IN- AND OUT-OF-COMPETITION)". Retrieval note, rechecked 3 August 2026: the canonical link below answers a plain request with HTTP 202, an empty body and an Amazon Web Services firewall challenge header, and answers a request carrying an ordinary desktop browser user-agent with a 2,419-byte JavaScript challenge page. Neither response is the document, so the text above was read instead from the copy the International Testing Agency serves under the same filename: HTTP 200, a valid 382,029-byte, 26-page PDF whose first page reads "This List shall come into effect on 1 January 2026" and whose page 8 carries section S2.3 and the IGF-1 analogues entry quoted above. The canonical link is printed unchanged because it is the document's home. 2026 Prohibited List PDF, canonical. Copy that resolves.

17. 17

    ClinicalTrials.gov v2 application programming interface. Studies endpoint queried with countTotal enabled for the search terms "LR3 IGF", "Long R3 IGF-1" and "IGF-1 LR3", each returning a total count of 0, and for "mecasermin", returning 40. Run 2 August 2026. Registry search.

18. 18

    National Library of Medicine, PubMed E-utilities esearch endpoint. Two searches run 2 August 2026. First, ("LR3 IGF"[All Fields] OR "Long R3 IGF"[All Fields]) AND "clinical trial"[Publication Type], returning a count of 0; the control mecasermin AND "clinical trial"[Publication Type] returned 5 on the same endpoint that day, so the filter is live. Second, a synonym sweep across LR3IGF-I, LongR3-IGF-I, Long R3 IGF-I, Long-R3-IGF-I, Long [Arg3]-IGF-I, IGF-1 LR3, IGF1-LR3, LR3 IGF-1 and long R3IGF-I, returning 109 records. Source for the absence of a human trial in the peer-reviewed literature and for the size of the published record the dosage chart samples from. PubMed search.

19. 19

    U.S. Food and Drug Administration, openFDA drug adverse event application programming interface, covering the FDA Adverse Event Reporting System. Queried 2 August 2026 on the patient.drug.medicinalproduct field for "IGF-1 LR3", "IGF1 LR3", "LONG R3 IGF-1" and "LONGR3-IGF-I", each returning HTTP 404 and "No matches found!". The control query on patient.drug.openfda.substance_name for "MECASERMIN" returned HTTP 200 and a total of 805 reports, so the zero is a real zero. Source for the statement that no adverse event record appears under this compound's own name, which is an absence of records and not a safety finding. openFDA adverse event query.

20. 20

    Dominikowski A, Rekos Z, Olejarz M, et al. 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;17:1822475. Published 18 June 2026. A narrative review that searched PubMed, Google Scholar and the Cochrane Library from January 1989 to January 2026 and assigned every compound it reviewed to one of four evidence tiers. Its own limitations section says compound selection was driven by the agents most often met in clinical practice and most prominent on unregulated platforms, "rather than by an exhaustive bibliographic enumeration", so it is not a census of the class. Source for the bottom tier, which the review defines as "no peer-reviewed human studies, with claims resting on preclinical extrapolation and grey-literature user narratives", and for its placement of IGF-1 LR3 in that tier. Also the source for its handling of the online protocols it collected, which it prints as behavioural data that are "not evidence-based treatment strategies" and "MUST NOT be interpreted as clinically validated or safe". That table carries reported microgram figures, and this page prints none of them. Read from the PubMed Central full text, PMC13322892, on 3 August 2026. doi:10.3389/fendo.2026.1822475. PMID 42395176.

21. 21

    National Library of Medicine PubMed E-utilities esearch endpoint, and the Europe PMC REST search endpoint, both looking for a published animal-to-human dose conversion. On PubMed, 3 August 2026, the nine-spelling name query AND ("human equivalent dose" OR allometric* OR "body surface area" OR "interspecies scaling"), each across all fields, returned a count of 0. On that endpoint the same day, all four of those conversion terms alone returned 31,281 records and the nine-spelling name query alone returned 109 records, so each half of the query retrieves on its own. On Europe PMC, 3 August 2026, the same nine names and the same four conversion terms written against the TITLE_ABS field returned a hit count of 0; on that endpoint the same day, the four conversion terms alone returned 30,567 records and the nine names alone returned 107 records. Source for the statement that no peer-reviewed animal-to-human conversion for this compound was found on either of these two databases. Every count here is the control it is printed beside, run with the terms named beside it and no others. PubMed control query.