Peptide Decoding

IGF-1 LR3 vs IGF-1 DES

LR3 lasts longer and DES binds its receptor harder, and neither has ever been tested in a published human trial. Both are engineered versions of a hormone your body makes, modified to escape the proteins that normally hold IGF-1 inactive. Mecasermin, sold as Increlex, is real IGF-1, FDA approved, with a measured half-life and a label.

  • Muscle
  • No human trials of either
  • An approved version exists
Published September 8, 2026
Research vials labeled IGF-1 DES and IGF-1 LR3, one milligram each, under low blue light
The short answer

There is an approved IGF-1 drug. Neither of these is it.

One was built to last. One was built to hit harder and clear fast. Neither has been given to a person in a study.

IGF-1 LR3 and IGF-1 DES at a glance
AttributeIGF-1 LR3IGF-1 DES
Length83 amino acids67 amino acids
How it differs from IGF-113 residues added, plus one swappedThree residues removed from the front
Half-lifeSources give 6 to 30 hours [5]Sources give 20 minutes to 8 hours [5]
Human trialsNoneNone
FDA statusNot approvedNot approved
An approved IGF-1 existsMecasermin, Increlex [1]Mecasermin, Increlex [1]

The half-life figures conflict because no human study has measured either compound.

Research vial labeled IGF-1 LR3, one milligram, containing white lyophilized powder
Long acting · Systemic · Cell-culture origin

IGF-1 LR3

Native IGF-1 with thirteen extra amino acids stuck on the front and one residue swapped. Both changes stop it being captured by the binding proteins that normally hold IGF-1 in reserve. In plain terms: a version engineered to stay free and stay around, originally made as a laboratory reagent for growing cells.

Length83 amino acids
Modification13-residue extension plus Arg3
Human trialsNone
Originally made asA cell culture reagent
Research vial labeled IGF-1 DES, one milligram, containing white lyophilized powder
Short acting · Local · Naturally occurring

IGF-1 DES

Native IGF-1 with the first three amino acids cut off. Binding proteins grip that short front section, so removing it produces a molecule that stays free and binds its receptor more tightly. In plain terms: a shorter, sharper version, and one that occurs naturally in colostrum and fetal brain tissue.

Length67 amino acids
ModificationGly-Pro-Glu removed
Human trialsNone
Occurs naturallyYes, in colostrum
The numbers

Nobody can agree on the numbers, because nobody has measured them

Read four sources on these compounds and you get four different half-lives.

Native IGF-1 has a problem. Almost all of it is immediately captured by binding proteins, held inactive and released slowly. Free IGF-1 lasts about ten minutes. Both compounds on this page are attempts to get around that, using opposite strategies.

LR3 adds. Thirteen amino acids on the front end, plus a swap at position three from glutamate to arginine. The swap disrupts the binding protein contact directly, and the extension slows clearance.

DES subtracts. It removes the first three residues, Gly-Pro-Glu, the exact section binding proteins grip. Less of it gets captured, and what remains binds the receptor more tightly than native IGF-1 does.

The conflicting numbersFour sources · one set of compounds · no human measurement
LR3 half-life
6 hours · 20 to 30 hours
DES half-life
20 minutes · 20 to 30 minutes · 4 to 8 hours in rodents
DES receptor affinity
Slightly higher · 2 to 10 times higher · 5 to 10 times higher
LR3 receptor affinity
Roughly equivalent · slightly reduced
LR3 binding protein reduction
1000-fold · or to 2 to 4 percent of native
DES binding protein reduction
50-fold · 100-fold · or to 10 to 15 percent of native

A five-fold spread on LR3's half-life is not a rounding difference. It is the difference between dosing once a day and dosing twice. These figures conflict because there is no human measurement to settle them. [5] The numbers come from cell culture, from rodents, and from each other.

Mecasermin, the approved version, has a half-life of about 5.8 hours in growth hormone deficient patients. That figure was measured and printed on an FDA label, which is why there is only one of it. [1]

Native IGF-170 residues
First three: Gly-Pro-Glu
IGF-1 LR383 residues
13 added at the front · position 3 substituted, Glu to Arg
IGF-1 DES67 residues
First three removed
Native chain Added by LR3 Gly-Pro-Glu, or the substituted position Removed by DES
One adds thirteen to the front, one removes three. Both are aiming at the same binding site.

Same target, opposite methods. Add a shield, or remove the handle.

Different consequences. Adding slows clearance. Removing sharpens receptor binding.

Neither is the approved one. That is 70 amino acids, unmodified, and it is called mecasermin. [1]

Side by side

Everything that differs

IGF-1 LR3 compared with IGF-1 DES
AttributeIGF-1 LR3IGF-1 DES
Full nameLong R3 IGF-1Des(1-3)IGF-1
Length83 amino acids67 amino acids
Change from native13-residue N-terminal extension plus Glu3 to Arg3N-terminal Gly-Pro-Glu removed
Occurs naturallyNo, synthetic onlyYes, in bovine colostrum and human fetal brain
Binding protein escapeYes, by disrupting the contact siteYes, by removing the contact site
Receptor affinitySources say equivalent or slightly reduced [5]Sources say slightly to ten times higher [5]
Half-lifeSources say 6 to 30 hours [5]Sources say 20 minutes to 8 hours [5]
Practical framingSustained systemic signalShort local pulse
Human trialsNoneNone
Originally developed asA cell culture reagentA naturally occurring fragment, later synthesized
FDA statusNot approvedNot approved
Approved alternativeMecasermin, Increlex, NDA 021839 [1]Mecasermin, Increlex, NDA 021839 [1]
The evidence, in the order it arrived

One approval, one accidental drug, and no trials of either compound here.

0
Published human trials of either compound [5]
6 to 30 h
The range of half-lives circulating for LR3 [5]
5.8 h
The measured half-life of the approved IGF-1, from its label [1]
1970s and 1980s
IGF-1
Endocrinology literature

The hormone, and its keepers

IGF-1 is characterized as the hormone through which growth hormone produces most of its effects on tissue. Its binding proteins are identified soon after, along with the reason free IGF-1 is so scarce.

1980s
IGF-1 DES
Protein isolation studies

Found, not invented

Des(1-3)IGF-1 is isolated from bovine colostrum and from human fetal brain tissue. It is a naturally occurring truncation, and it turns out to bind the IGF-1 receptor more tightly than the full molecule. [2]

1990s
IGF-1 LR3
Cell culture reagent catalogs

Engineered for a dish, not a person

LR3 is engineered, and its intended use is laboratory work. It was designed as a cell culture reagent, a way to drive cell growth without binding proteins soaking up the signal. [3]

It was never developed as a medicine, so there is no development program behind it, no toxicology package built for human use, and no reason anyone would have built one.

2005
Native IGF-1
FDA approval · NDA 021839

Mecasermin is approved as Increlex

Recombinant native human IGF-1, for severe primary IGF-1 deficiency in children aged two and over. It has a label, a measured half-life of about 5.8 hours, a documented hypoglycemia risk and a dosing protocol tied to food. [1]

March 2023
Trofinetide
FDA approval · NDA 217026

The offcut becomes a drug

Trofinetide is approved as Daybue for Rett syndrome. It is a synthetic analog of glypromate, Gly-Pro-Glu, the exact tripeptide removed from IGF-1 to produce DES. [4]

So the three amino acids cut off to make one research compound became the basis of a different approved drug for an unrelated condition.

Today
Both
Secondary sources only

Still no human trial of either

Neither LR3 nor DES has appeared in a published human clinical trial. Both are sold as research chemicals, and the figures quoted for both come from cells, rodents and each other. [5]

Today
IGF-1 DES
Animal studies, reviewed in J Cell Sci

The site injection premise, tested in animals

Localized IGF-1 elevation in skeletal muscle did not augment exercise-induced hypertrophy, after wheel running or after resistance training. Growth appeared in muscle that was already growing, not in adult trained muscle. [6]

There is an FDA approved IGF-1, and almost nobody buying these compounds seems to know it exists. Mecasermin is recombinant human IGF-1, approved in 2005, with a real label, a measured half-life of 5.8 hours, a known hypoglycemia risk and a dosing schedule tied to meals. [1] LR3 and DES are engineered analogs with no human trial of any kind, and one of them was made to grow cells in a dish. [3] The numbers reflect that gap. That is not a small disagreement between careful sources. It is what happens when a number is repeated for two decades without anyone measuring it.

IGF-1 DES and IGF-1 LR3 vials side by side on a white surface
Two engineered analogs with no human data, and an approved version neither of them is.
How does each one work?

The same obstacle, approached from opposite directions.

The obstacle. More than 95 percent of IGF-1 in your blood is bound to carrier proteins, chiefly IGFBP-3, which hold it in reserve and release it gradually. Bound IGF-1 does nothing while it waits. The arrangement is not accidental. IGF-1 drives cells to grow and divide, and a body that let it circulate freely would have very poor control over cell growth.

IGF-1 LR3 adds a shield

The thirteen-residue extension and the arginine substitution both interfere with binding protein contact. More stays free, and the extension also slows clearance. The result is described as a sustained systemic signal.

That framing follows from the half-life rather than from any measurement in a person. If LR3's half-life is really six hours rather than thirty, the distinction narrows considerably. Nobody has measured it. [5]

IGF-1 DES removes the handle

Binding proteins grip the first three residues. Take them away and there is nothing to grip. DES also binds the IGF-1 receptor more tightly than native IGF-1, though how much more tightly is one of the numbers nobody agrees on. [5]

A compound lasting twenty minutes is mostly gone before it travels far, which is where the local framing comes from, and where the site injection idea comes from with it.

And the local injection idea has been tested, in animals, and it did not work. DES is sold for site injection, the premise being that putting a short-acting IGF-1 analog near a muscle grows that muscle. Researchers have looked at the underlying question by overexpressing IGF-1 directly in the skeletal muscle of mice and rats, which is a stronger version of the same intervention.

Localized IGF-1 elevation did not augment exercise-induced hypertrophy, either after wheel running or after resistance training. [6] Growth appeared in muscle that was already growing, during postnatal development or during regeneration after damage, and not in adult muscle already responding to training. That is animal work, and it is the nearest anyone has come to testing the site injection premise. It points against it.

Both carry the same underlying concern. Escaping the binding proteins means removing the control system your body uses to keep IGF-1 signaling in check. IGF-1 also cross-reacts with the insulin receptor. That is the mechanism behind the hypoglycemia risk documented on the approved product's label. [1]

Also in this family

These are not the only IGF-1 variants sold

Two more sit in the same category, with the same problem.

MGF, or mechano growth factor, is a 24 amino acid fragment produced when the IGF-1 gene is spliced differently under mechanical load. The idea behind it is appealing: your muscle makes a local repair signal when you work it, so supplying that signal directly should help. It was identified by Goldspink's group and the underlying biology is real. [9]

No completed randomized trial of exogenous MGF exists, and one independent laboratory found no proliferative effect on primary human myoblasts, which is a direct replication failure of the central claim. [9] PEG-MGF attaches polyethylene glycol to extend how long it lasts. Same evidence position, plus a modification that has never been tested in a person either.

Why this belongs here. Four IGF-1 derived compounds are sold for muscle, and the number with a published human trial is zero. The variation between them is in engineering, not in evidence. Full files: MGF and PEG-MGF.

Key differences

What separates them

Shared: both escape IGF binding proteins · both act on the IGF-1 receptor · both are injected · neither has a human trial · neither is FDA approved · both carry hypoglycemia and IGF-1 axis concerns

IGF-1 LR3

StrategyAdds 13 residues plus a substitution
Length83 amino acids
Occurs naturallyNo
DurationLonger, and the figure is disputed
FramingSustained systemic signal
OriginBuilt as a cell culture reagent
Receptor affinityEquivalent or slightly reduced
Specific concernSustained exposure and axis suppression

IGF-1 DES

StrategyRemoves 3 residues
Length67 amino acids
Occurs naturallyYes, in colostrum
DurationShorter, and the figure is disputed
FramingShort local pulse
OriginIsolated from tissue, later synthesized
Receptor affinityHigher, by a disputed amount
Specific concernHigher receptor affinity, unmeasured in people

Summary compiled from published research and regulatory records.

What nobody has answered

Four gaps, and the first covers everything else

Nobody has run a human trial of either compound.Not for muscle, not for anything. Every figure in circulation traces to cell culture, rodents, or another website. [5]

Nobody has measured either half-life in a person.The six to thirty hour range for LR3 is not a disagreement between careful studies. It is an absence of studies. [5]

Nobody knows what long-term binding protein escape does, and the background makes it worth asking.The binding protein system is how the body regulates IGF-1 signaling, and both compounds are designed to defeat it. Large observational studies link higher natural IGF-1 levels to higher rates of several cancers. A UK Biobank analysis of 394,388 people found associations with breast, prostate, colorectal, melanoma, kidney and thyroid cancers, and with lower rates of several others. [7] A review pooling 96 studies and over 110,000 people found higher IGF-1 raised overall cancer risk by roughly 15 percent. [8] Two things to hold onto: those studies measured the IGF-1 people naturally have, not IGF-1 raised by an analog engineered to escape regulation, and association is not causation. The approved IGF-1 product is contraindicated in active or suspected malignancy for the same reason. [1]

Nobody has compared them either.No study has put LR3 against DES, so the systemic-versus-local framing rests on half-life figures that are themselves disputed. [5]

Safety and buying

The approved version has a label. These have inherited concerns and no data.

Evidence register3 fields · 12 entriesCompiled from the mecasermin label, published research and US market conditions
01Documented

From the approved IGF-1's label

These are measured risks for real IGF-1, and both compounds act on the same receptor.

  • Hypoglycemia, documented and managed on the label with dosing tied to food intake [1]documented
  • The label requires a meal or snack shortly before or after each dose [1]documented
  • Tonsillar hypertrophy and intracranial hypertension are listed warnings [1]documented
  • Contraindicated in active or suspected malignancy [1]documented
02Unstudied

Both compounds here

Nobody has run these studies. That is different from a clean result.

  • Either compound in a human being, in any published trial [5]not studied
  • The actual half-life of either, in a person [5]not studied
  • What sustained binding protein escape does over months, against a background linking IGF-1 to cancer risk [7][8]not studied
  • Whether the systemic and local framing holds at allnot studied
03Supply

What you are buying

An approved product exists and neither of these is it.

  • LR3 is widely sold as a cell culture reagent, and that grade is not made for injection [3]identity
  • Mecasermin is a prescription drug with GMP manufacturing and known contents [1]comparison
  • Testing of seized peptides found purity between 5 and 75 percent, plus arsenic and lead [10]analysis
  • One US lab reported problems in almost 30 percent of samples, including bacteria [11]testing

*Where this page says nothing is established, it means nobody has studied it. It does not mean a compound is safe.

Card 1 needs a note. Those risks are documented for mecasermin, native IGF-1 given to children with a deficiency, under supervision, with blood sugar monitoring. They are listed here because both compounds on this page act on the same receptor, and because they are the only measured human safety data that exists anywhere near this subject. They are not measurements of LR3 or DES. Both compounds escape the binding proteins that moderate native IGF-1, so the concerns plausibly apply at least as strongly. Nobody has checked. Our guide on reading a certificate of analysis covers what to look for in a research vial.

Sport and regulatory status

Both prohibited, and neither is the approved IGF-1

Sport

Prohibited at all times

Section S2.1 of the 2026 WADA Prohibited List covers growth factors, and IGF-1 and its analogues are named. [12] Both compounds here are IGF-1 analogues, prohibited at all times, in and out of competition. Everything in S2 is a non-specified substance, carrying a default four year ban for a first violation. Detection methods for IGF-1 analogues exist and have been in use for years, and the analytical literature specifically covers modified forms. Assuming an engineered analog is invisible because it is not the native molecule is the wrong assumption.

Regulatory status

Neither compound is approved

Mecasermin is approved. Sold as Increlex, it is recombinant native human IGF-1, seventy amino acids, unmodified. The FDA approved it in 2005 under NDA 021839 for severe primary IGF-1 deficiency in children aged two and over. It carries a label, a dosing protocol tied to meals because of hypoglycemia risk, and post-approval monitoring. [1] Neither LR3 nor DES is approved anywhere. Neither has been submitted. Neither has a human trial behind it to submit. Check the current regulatory status page for how these categories are moving.

LR3's usual sales category matters here. It is widely sold as a cell culture reagent, and that is what it was designed to be. Reagent-grade material is made to a standard suited to a dish of cells, not to a person. Those are different specifications. [3] One more thing shows how differently these molecules have been treated: the three amino acids removed from IGF-1 to produce DES, Gly-Pro-Glu, are the basis of trofinetide, approved as Daybue for Rett syndrome in March 2023. [4] The offcut got a development program, a trial and an approval. The compound it was cut from did not.

Common questions

Questions people ask

What is the difference between IGF-1 LR3 and IGF-1 DES?

LR3 has thirteen extra amino acids on the front plus one residue swapped, making it 83 amino acids long. DES has three amino acids removed from the front, making it 67. Both changes stop binding proteins from capturing the molecule, and they do it in opposite ways.

Which one lasts longer?

LR3, though by how much is genuinely unclear. Sources give its half-life as anywhere from 6 to 30 hours and give DES anywhere from 20 minutes to 8 hours. Neither has been measured in a person.

Is IGF-1 LR3 FDA approved?

No. LR3 has never been approved. There is an FDA approved IGF-1 product called Increlex, and it contains mecasermin, native unmodified IGF-1, not LR3.

Are there any human studies on IGF-1 LR3 or DES?

No published human clinical trials exist for either compound. Everything written about them traces to cell culture work, rodent studies, or other websites.

Why do different sites give different half-lives?

Because nobody has measured them in a human. The figures come from animals and cell work, get quoted without the species attached, and then get copied. A five-fold spread on LR3 is the result.

What are the risks of IGF-1 analogs?

The measured risks come from mecasermin's label: hypoglycemia serious enough to require dosing with food, tonsillar hypertrophy, intracranial hypertension, and a contraindication in active or suspected cancer. Those are for native IGF-1 under medical supervision. Both compounds here escape the binding proteins that moderate native IGF-1.

Does injecting IGF-1 DES at a site grow that muscle?

No study supports it. The closest evidence comes from animals, where overexpressing IGF-1 directly in skeletal muscle did not augment exercise-induced hypertrophy after either wheel running or resistance training. It did produce growth in muscle that was already growing, during development or after damage. That points against the site injection premise rather than for it.

Do these raise cancer risk?

No study has looked at these compounds specifically. What exists is a body of observational work linking higher natural IGF-1 levels to higher rates of several cancers, including a UK Biobank analysis of 394,388 people. Those measured natural levels, not analogs designed to escape regulation, and the approved IGF-1 product is contraindicated in active or suspected malignancy.

What is the correct IGF-1 LR3 dosage?

No published human study establishes one. The figures in circulation, commonly 40 to 100 micrograms daily for LR3 and 50 to 150 micrograms for DES, come from community practice rather than from any trial. The only IGF-1 product with a published dosing protocol is mecasermin, dosed at 0.04 to 0.12 mg/kg twice daily with food, in children with a diagnosed deficiency.

What is IGF-1 LR3 used for?

It has no approved use anywhere. It was developed and is still widely sold as a cell culture reagent, a way to drive cell growth in a laboratory dish. It is bought for muscle growth, and no human trial has tested it for that or anything else.

What are the side effects of IGF-1 LR3?

No human trial has recorded any, because none exists. The measured side effects for native IGF-1 come from mecasermin's label and include hypoglycemia serious enough to require dosing with food, tonsillar hypertrophy and intracranial hypertension. Both compounds here escape the binding proteins that moderate native IGF-1, so those concerns plausibly apply at least as strongly.

Is IGF-1 DES natural?

It occurs naturally in bovine colostrum and human fetal brain tissue, so it was discovered, not designed. That says nothing about whether injecting it is safe or effective, and neither question has been studied.

Are they banned in sport?

Yes, both. IGF-1 and its analogues are named under section S2.1 of the 2026 Prohibited List, prohibited at all times.

The published record

What Europe PMC and ClinicalTrials.gov hold for each, on the same rule.

IGF-1 LR3 has 91 records to IGF-1 DES's 209. 18 original human studies against 59.

The published record

Research index

91

Records indexed for IGF-1 LR3

28 in humans, 18 of them original studies.

Browse the records

In animalsPro
In the labPro
ReviewsPro
Senior author sharePro

Counted from Europe PMC indexing, not read by a person. Human means indexed under humans, which includes reviews and work on human cells. Original studies exclude reviews and lab work on human cells.Last updated 11 September 2026.

The published record

Research index

209

Records indexed for IGF-1 DES

91 in humans, 59 of them original studies.

Browse the records

In animalsPro
In the labPro
ReviewsPro
Senior author sharePro

Counted from Europe PMC indexing, not read by a person. Human means indexed under humans, which includes reviews and work on human cells. Original studies exclude reviews and lab work on human cells.Last updated 11 September 2026.

References

What this page is built on

  1. 01INCRELEX (mecasermin) injection prescribing information. FDA approval 2005, NDA 021839. FDA label. Recombinant human insulin-like growth factor-1, 70 amino acids, identical to endogenous IGF-1. Approved for severe primary IGF-1 deficiency in pediatric patients aged 2 and over. Half-life approximately 5.8 hours in growth hormone deficient patients. Dosing 0.04 to 0.12 mg/kg twice daily. Hypoglycemia is a documented risk requiring administration shortly before or after a meal or snack. Warnings include tonsillar hypertrophy and intracranial hypertension. Contraindicated in active or suspected malignancy.
  2. 02Des(1-3)IGF-1 identification and characterization. Originally isolated from bovine colostrum and human fetal brain tissue. A naturally occurring truncation of IGF-1 lacking the N-terminal Gly-Pro-Glu tripeptide, with markedly reduced IGFBP binding and higher IGF-1 receptor affinity than native IGF-1.
  3. 03IGF-1 LR3 origin and use. An 83 amino acid analog comprising a 13-residue N-terminal extension and a Glu3 to Arg3 substitution. Developed and sold primarily as a cell culture reagent for serum-free and reduced-serum culture systems. Reagent-grade material is not manufactured to injectable specification.
  4. 04DAYBUE (trofinetide) prescribing information. FDA approval March 2023, NDA 217026. Trofinetide is a synthetic analog of glypromate, the tripeptide Gly-Pro-Glu, which is the N-terminal fragment removed from IGF-1 to produce Des(1-3)IGF-1. Approved for Rett syndrome.
  5. 05Conflicting figures for IGF-1 LR3 and IGF-1 DES. No published human pharmacokinetic study exists for either compound. Values in circulation across secondary sources: LR3 half-life given as 6 hours and as 20 to 30 hours; DES half-life given as 20 minutes, 20 to 30 minutes, and 4 to 8 hours in rodents; DES receptor affinity given as slightly higher, 2 to 10 times higher and 5 to 10 times higher than native; LR3 receptor affinity given as roughly equivalent and as slightly reduced; IGFBP binding reduction given as 1000-fold and as 2 to 4 percent of native for LR3, and as 50-fold, 100-fold and 10 to 15 percent of native for DES. These figures cannot be reconciled and none traces to a human measurement.
  6. 06Localized IGF-1 overexpression and exercise-induced hypertrophy. Paul AC, Rosenthal N. 2002, and Lee S, et al. 2004, as reviewed in "A growth stimulus is needed for IGF-1 to induce skeletal muscle hypertrophy", J Cell Sci. 2010;123(6):960. Animal studies. Localized elevation of IGF-1 in skeletal muscle did not augment exercise-induced muscle hypertrophy after wheel running or after resistance training. Hypertrophic effects appeared during active growth, in postnatal development or in regeneration, and not in adult trained muscle.
  7. 07Watts EL, et al. Circulating insulin-like growth factor-1 and risk of total and 19 site-specific cancers: cohort study analyses from the UK Biobank. Cancer Res. 2020;80(18):4014. PMID 32856611. Human cohort study, 394,388 participants. Higher IGF-1 associated with breast, prostate, colorectal, melanoma, kidney and thyroid cancers, and with lower rates of lung, ovarian, head and neck, and liver cancers. Measured natural IGF-1 levels, not analog administration.
  8. 08Chen W, et al. Phenotypes and genotypes of insulin-like growth factor 1, IGF-binding protein-3 and cancer risk: evidence from 96 studies. Eur J Hum Genet. 2009. PMID 19491931. Meta-analysis, more than 110,000 people. Higher IGF-1 associated with roughly 15 percent higher overall cancer risk.
  9. 09MGF and PEG-MGF evidence position. MGF is a 24 amino acid E-peptide produced by alternative splicing of the IGF-1 gene under mechanical load, identified by Goldspink's group. No completed randomized controlled trial of exogenous MGF exists, and one independent laboratory reported no proliferative effect on primary human myoblasts, a direct replication failure of the central claim. PEG-MGF is a pegylated version with no human trial either.
  10. 10Janvier S, Cheyns K, Canfyn M, Goscinny S, De Spiegeleer B, Vanhee C, Deconinck E. Impurity profiling of the most frequently encountered falsified polypeptide drugs on the Belgian market. Talanta. 2018;188:795-807. DOI 10.1016/j.talanta.2018.06.023. Peer-reviewed analytical study. Purity 5 to 75 percent, plus arsenic and lead.
  11. 11NBC Washington. Lab finds problems in 30% of peptide vials tested. December 2024. News report of commercial laboratory testing, not peer reviewed.
  12. 12World Anti-Doping Agency. The 2026 Prohibited List, section S2.1, covering growth factors including IGF-1 and its analogues. Effective 1 January 2026. Regulatory document. Everything in S2 is a non-specified substance, prohibited at all times.
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