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Research peptide — not a dietary supplement
IGF-1 LR3 is a research compound, not a regulated dietary supplement. It is typically administered by injection and sold “for research use only.” The evidence below is largely preclinical (animal and in-vitro) or early-stage, so no evidence score is assigned. This page is provided for transparency and education — it is not a recommendation to use. Consult a qualified healthcare provider, and be aware that purity, dosing, and legal status vary by jurisdiction.
What the evidence says
Most IGF-1 LR3 studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality studies published 2003–2025.
Based on 8 studies
Confidence
LowBy outcome
The current evidence for IGF-1 LR3 is insufficient to assign an evidence score, based on 8 indexed studies. A grey-market injectable 'research peptide' with NO human efficacy trials of the analog itself — the muscle-growth marketing is extrapolated from cell-culture and animal work. IGF-1 LR3 (Long R3 IGF-1) is a synthetic, engineered analog of human IGF-1: three residues are changed and a 13-amino-acid extension is added so it binds the IGF-1 receptor normally but barely binds the IGF-binding proteins that normally regulate native IGF-1. The result is a far longer-acting, less-regulated IGF-1 signal — which is exactly why bodybuilders inject it and exactly why it is concerning. It was created as a laboratory reagent (it drives cell proliferation in culture and organ/myoblast growth in fetal-sheep infusions), not as a medicine. There has never been a published human trial of IGF-1 LR3 for muscle, strength, or anything else. It is not an approved drug or a regulated supplement; it is an unregulated grey-market injectable. Activating the IGF-1 axis carries theoretical cancer-promotion risk (IGF-1 receptors are overexpressed on many tumors), and in animal infusions it suppressed insulin secretion and lowered blood glucose — a real hypoglycemia signal. This entry exists to inform, not to recommend. Representative study: PMID 36091374.
Mecasermin (IGF-1)
Mostly mechanism / observationalThe pharmaceutical-grade version of IGF-1 — an FDA/EMA-approved prescription injectable, but approved ONLY for a rare childhood growth disorder (severe primary IGF-1 deficiency / Laron syndrome), where it genuinely raises height velocity in clinical trials. It is the regulated counterpart to the grey-market igf-1-lr3 peptide bodybuilders inject, and shares the same core risks. Crucially, there is NO trial supporting its off-label use for muscle, performance, or anti-aging in healthy adults — and IGF-1's documented harms (hypoglycemia, intracranial hypertension, lymphoid/tonsillar hypertrophy, and a theoretical cancer concern because IGF-1 is mitogenic) are real. Not a dietary supplement, not a longevity drug.
Last reviewed June 2026 · evidence from 8 studies · how we score
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
Long R3 Insulin-like Growth Factor-1 (LR3 IGF-1)
A grey-market injectable 'research peptide' with NO human efficacy trials of the analog itself — the muscle-growth marketing is extrapolated from cell-culture and animal work. IGF-1 LR3 (Long R3 IGF-1) is a synthetic, engineered analog of human IGF-1: three residues are changed and a 13-amino-acid extension is added so it binds the IGF-1 receptor normally but barely binds the IGF-binding proteins that normally regulate native IGF-1. The result is a far longer-acting, less-regulated IGF-1 signal — which is exactly why bodybuilders inject it and exactly why it is concerning. It was created as a laboratory reagent (it drives cell proliferation in culture and organ/myoblast growth in fetal-sheep infusions), not as a medicine. There has never been a published human trial of IGF-1 LR3 for muscle, strength, or anything else. It is not an approved drug or a regulated supplement; it is an unregulated grey-market injectable. Activating the IGF-1 axis carries theoretical cancer-promotion risk (IGF-1 receptors are overexpressed on many tumors), and in animal infusions it suppressed insulin secretion and lowered blood glucose — a real hypoglycemia signal. This entry exists to inform, not to recommend.
Scored at the bottom of Emerging because there has never been a published human trial of the LR3 analog; all evidence is cell-culture and fetal-animal work, with real theoretical cancer and hypoglycemia risks and no quality-controlled product.
IGF-1 LR3 ('Long R3 IGF-1') is a synthetic analog of human insulin-like growth factor-1, engineered for the laboratory rather than the clinic. Two modifications define it: the glutamate at position 3 is replaced by arginine (the 'R3'), and a 13-amino-acid N-terminal extension is added (the 'Long').
Together these changes drastically reduce its affinity for the IGF-binding proteins (IGFBP-1 through -6) that normally sequester ~99% of circulating native IGF-1, while preserving high affinity for the IGF-1 receptor.
The practical consequence is a molecule that delivers a much more potent and far longer-lasting IGF-1-receptor signal than native IGF-1 at the same dose — which is precisely why it became a popular cell-culture reagent and, separately, a grey-market bodybuilding injectable.
IGF-1-receptor activation drives the PI3K/Akt/mTOR and ERK/MAPK pathways that promote cellular proliferation, protein synthesis, and survival.
In real experiments on the LR3 analog specifically, that signaling translates into: bioactive cell proliferation in recombinant-protein assays (Lu et al., 2023); proliferation of cultured bovine satellite cells (the muscle stem cells; Reiter et al., 2014) and fetal-sheep cardiomyocytes via ERK and PI3K (Sundgren et al., 2003); and, when infused into late-gestation fetal sheep, increased organ growth (heart, kidney, spleen, adrenals) and stimulated skeletal-myoblast proliferation (Stremming et al., 2022).
Here is the load-bearing caveat that must lead any honest reading: there has never been a published human trial of IGF-1 LR3 — not for muscle growth, strength, fat loss, recovery, or safety.
Every muscle/anabolic claim made for it is preclinical (cells and animals) or extrapolated from the biology of native IGF-1, and native IGF-1 is NOT the same molecule: it is regulated by binding proteins that the LR3 analog deliberately evades, so even the native-IGF-1 evidence base cannot be cleanly transferred.
The same fetal-sheep work that shows growth also shows the downside: a one-week IGF-1 LR3 infusion suppressed glucose-stimulated insulin secretion and lowered both insulin and glucose (White et al., 2021; 2023) — a concrete hypoglycemia mechanism.
And the IGF-1 axis itself is a recognized cancer-relevant pathway: IGF-1 receptors are overexpressed on many tumor types, which is why LR3-IGF-1 has been used as a tumor-targeting vehicle in oncology research (McTavish et al., 2009).
Chronically amplifying an unregulated IGF-1 signal therefore carries a theoretical risk of promoting growth of existing or nascent tumors, plus acromegalic/organ-overgrowth concerns inherent to any strong growth-factor agonist.
On top of the pharmacology, IGF-1 LR3 is an unapproved, unregulated grey-market injectable: identity, purity, dose, and sterility are not guaranteed, and injecting non-sterile peptide material carries infection and contamination risk independent of the molecule.
The evidence here is scored well below 3 and flagged Emerging: a genuine, interesting preclinical signal for cell and organ growth, with zero human data, real metabolic and oncologic theoretical risks, and no legitimate or quality-controlled product — sandboxed out of all goal- and stack-based recommendations.
IGF-1 LR3 carries an Arg-for-Glu substitution at position 3 plus a 13-residue N-terminal extension. These changes sharply reduce binding to the IGF-binding proteins (IGFBPs) that normally regulate native IGF-1, while keeping high affinity for the IGF-1 receptor — producing a more potent, longer-lasting IGF-1 signal. Demonstrated as 'low affinity for IGF binding proteins and high affinity for the IGF-1 receptor' in animal/cell work (White et al., 2021); never characterized in a human trial.
Binding the IGF-1 receptor activates the PI3K/Akt/mTOR and ERK/MAPK cascades that drive protein synthesis, cell proliferation, and survival. In cultured fetal-sheep cardiomyocytes, LR3 IGF-1-stimulated proliferation required both ERK and PI3K signaling (Sundgren et al., 2003). Established in cells/animals only.
How IGF-1 LR3 works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Tap node to isolate • Pinch to zoom • Tap edge for research
No legitimate or recommended dose — IGF-1 LR3 is an unapproved grey-market research chemical with no human dosing data and no quality control. We do NOT provide a dosing protocol. There has never been a human trial to establish a safe or effective dose; the only published dosing is in animals (e.g., fetal-sheep infusions) and does not translate to a human regimen.
Can be taken without food
| Form | Type |
|---|---|
| 💊None — unapproved grey-market research chemical | Recommended |
There is no legitimate pharmaceutical form. IGF-1 LR3 is an engineered IGF-1 analog used as a cell-culture reagent and in animal research; it is not a medicine or a dietary supplement.
Minimum: 1 weeks
Optimal: 1 weeks
Cycling: Not required
Note: No approved or validated timing — the analog has never been tested in humans. This library does not endorse or schedule its use.
Dose-response data unavailable. The current published research for IGF-1 LR3 does not provide sufficient dose-specific outcome data to generate reliable dose-response curves.
Refer to the Dosage & Timing section above for recommended dose ranges based on available evidence.
There has never been a published human efficacy or safety trial of IGF-1 LR3 itself. Every muscle/anabolic effect below is from cells or animals (mostly fetal sheep and cell cultures). Native-IGF-1 human data does NOT transfer cleanly — the LR3 analog is deliberately engineered to evade the binding proteins that regulate native IGF-1.
Purified LR3 IGF-1 shows bioactivity comparable to standard IGF-1 in cell-proliferation assays (Lu et al., 2023), and stimulates proliferation of cultured muscle satellite cells (Reiter et al., 2014). Cell-culture findings — not a demonstrated human muscle effect.
Prior work infusing the LR3 IGF-1 analog into late-gestation fetal sheep increased fetal organ growth and stimulated skeletal-myoblast proliferation; the same group's sheep-specific IGF-1 construct (developed to overcome LR3's limitations) then increased growth of the heart, kidney, spleen, and adrenal glands and stimulated myoblast proliferation over a 1-week infusion (Stremming et al., 2022). A growth signal — but in fetal animals, and including visceral-organ overgrowth, not just muscle.
A one-week fetal-sheep IGF-1 LR3 infusion suppressed glucose-stimulated insulin secretion and lowered plasma insulin and glucose (White et al., 2021). This is the documented basis for the hypoglycemia risk users report. Animal data.
IGF-1 receptors are overexpressed on many tumor types, which is why LR3-IGF-1 has been used as a tumor-targeting vehicle in oncology research (McTavish et al., 2009). Chronically amplifying an unregulated IGF-1 signal carries a theoretical risk of promoting existing or nascent tumors — never quantified in human LR3 users.
No human has been studied taking IGF-1 LR3, so its side-effect and long-term safety profile in people is genuinely unknown. On top of that it is an unregulated grey-market injectable with no identity/purity/sterility guarantee, adding infection and contamination risk independent of the molecule.
Avoid — there are no human trials of the analog, no approved use, and no quality-controlled product. Preclinical cell/animal growth signals do not justify human self-injection.
Avoid — IGF-1-axis activation is a recognized theoretical tumor-promotion risk.
Avoid — IGF-1 LR3 suppressed insulin and lowered glucose in animals; hypoglycemia risk is real and could compound glucose-lowering medications.
Avoid entirely — a potent growth-factor agonist, completely unstudied in human pregnancy.
IGF-1 LR3 cross-talks with the insulin axis and lowered insulin/glucose in animal infusions. Combining it with insulin, sulfonylureas, or other hypoglycemic agents could compound blood-sugar lowering and precipitate hypoglycemia. No human interaction data exist.
Stacking with growth hormone or other growth-promoting agents would further amplify IGF-1-axis signaling and the associated organ-overgrowth and cancer-promotion concerns. Never studied in humans.
Tip: IGF-1 LR3 lowered insulin and glucose in animal infusions, and IGF-1-receptor activation has insulin-like effects. Hypoglycemia is a plausible and potentially dangerous effect; human frequency is unknown because no human has been studied.
Tip: IGF-1 receptors are overexpressed on many cancers; chronically amplifying an unregulated IGF-1 signal is a recognized theoretical cancer-promotion concern. Never quantified in human LR3 users.
Tip: Animal LR3 infusion increased visceral-organ growth; strong sustained IGF-1 agonism raises acromegalic/organ-overgrowth concerns. Unstudied in humans.
Tip: Grey-market injectable material has no identity/purity/sterility guarantees; reconstituting and injecting it carries contamination and infection risk independent of the molecule.
The commonly studied dose of IGF-1 LR3 is No legitimate or recommended dose — IGF-1 LR3 is an unapproved grey-market research chemical with no human dosing data and no quality control. We do NOT provide a dosing protocol. There has never been a human trial to establish a safe or effective dose; the only published dosing is in animals (e.g., fetal-sheep infusions) and does not translate to a human regimen.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
Timing is flexible for IGF-1 LR3 — consistent daily use matters more than the time of day. There is no validated human dosing schedule because the analog has never been tested in humans.
IGF-1 LR3 should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are hypoglycemia (low blood sugar), theoretical promotion of tumor growth (IGF-1 axis), organ / acromegalic overgrowth. Use caution if any of these apply to you: Not an approved medicine and not a regulated dietary supplement — unapproved grey-market injectable research chemical; do not self-source; No human safety data of the LR3 analog exists — every safety conclusion would be an extrapolation from cells, animals, or native IGF-1; Any personal or family history of cancer — IGF-1-axis activation is a theoretical tumor-promotion risk.
Insulin (bodybuilding use)
Mostly mechanism / observationalInsulin is a life-saving prescription hormone for diabetes — and, used illicitly by bodybuilders as an off-label 'anabolic,' one of the most dangerous performance drugs in existence. The theory is nutrient partitioning: insulin drives glucose and amino acids into muscle and suppresses muscle-protein breakdown. But there is NO controlled evidence that insulin builds muscle or improves performance in healthy, non-diabetic athletes — and a non-diabetic who injects it risks profound, sometimes FATAL hypoglycemia (coma, seizures, brain injury, death), plus fat gain. This is a harm-reduction reference documenting a popular, deadly misuse, NOT a recommendation and NOT a dietary supplement.
LR3-IGF-1 stimulates proliferation of cultured muscle satellite cells (Reiter et al., 2014), and fetal-sheep LR3 IGF-1 infusion stimulated skeletal-myoblast proliferation in vivo (Stremming et al., 2022). This is the proposed route to muscle growth — demonstrated in cells and fetal animals, never in adult humans.
A one-week IGF-1 LR3 infusion into fetal sheep lowered plasma insulin and glucose and suppressed glucose-stimulated insulin secretion (White et al., 2021) — a concrete mechanism for the hypoglycemia risk reported anecdotally with grey-market use. Animal data only.
There are no human drug-interaction data for IGF-1 LR3 of any kind; interactions cannot be reliably predicted.
Tip: No human has ever been studied on IGF-1 LR3 — the side-effect profile in people is genuinely unknown. This is itself the warning.