The two IGF-1 analogs popular in bodybuilding — LR3 for sustained systemic IGF-1 elevation, DES for localized pre-workout hypertrophy.
Both are IGF-1 analogs that resist binding-protein sequestration. LR3 is engineered; DES is a naturally occurring truncation of native IGF-I (originally isolated from bovine colostrum and human fetal brain, now produced recombinantly for research). They address native IGF-1's two main pharmacological problems (short half-life and high binding-protein sequestration):
Both raise tissue IGF-1 action more than native IGF-1 would at equivalent doses (~2-3× per microgram in vivo for LR3, up to ~10× in vitro for DES in IGFBP-rich media). Both carry the same IGF-1-pathway concerns: cancer-axis risk via IGF-1R-mediated mitogenic signaling, hypoglycemia (insulin receptor cross-binding is continuous, not threshold), and suppression of endogenous GH/IGF-1 via somatotropic-axis feedback (mostly LR3-specific — DES is too short-acting at typical doses to drive sustained suppression).
Neither LR3 nor DES is FDA-approved for any human indication. The only FDA-approved IGF-1 product is mecasermin (Increlex) — recombinant native rhIGF-I, approved for severe primary IGF-1 deficiency in pediatric patients ≥ 2 years (NDA 021839); it is not LR3 and not DES. WADA prohibits IGF-1 and its analogues at all times under S2.3 (Growth Factors and Growth Factor Modulators, 2026 Prohibited List). Both compounds are sold as research chemicals only.
Both bind and activate the IGF-1 receptor — driving protein synthesis, satellite cell activation, and the protein-synthesis machinery that drives hypertrophy. New-fiber formation (hyperplasia) is mechanistically plausible and shown preclinically; human hyperplasia data with LR3 or DES specifically is absent. Both also engage the insulin receptor at low affinity (~1/100th of insulin's), which produces dose-dependent hypoglycemia at every dose level — IR cross-binding is continuous, not threshold. Per microgram, DES drives a more potent and more prolonged hypoglycemic action than native IGF-I (Tomas 1997 in pigs and marmosets, PMID 9415072).
Commonly cited as 20–30 hour half-life, though biochemistry argues for shorter plasma residence with longer downstream signaling. Functionally a once-daily compound. Comparable in effect to direct HGH in terms of IGF-1 pathway, without needing the pituitary. Note: chronic LR3 also suppresses your own GH and IGF-1 production via long-loop hypothalamic feedback (Conlon 1995 guinea pig PMID 7561636; Dunaiski 1997 pig PMID 9488001) — the basis for not stacking LR3 with GH secretagogues (CJC-1295, ipamorelin, sermorelin). The human numbers come from Arvat 1997 (PMID 9005975): after 2 U of rhGH intravenously, the GH response to GHRH was 86.1% inhibited while the response to hexarelin was 32.1% inhibited — so a GHRH analogue is all but switched off, and a ghrelin-receptor agonist is blunted rather than abolished. Worth reading precisely: that experiment raised GH, not IGF-1, and the ghrelin-side compound was hexarelin, not ipamorelin. "Ineffective" is too strong for the ghrelin side; "substantially blunted" is what the data supports.
Short plasma half-life (minutes-scale per animal data; the commonly-cited "~20 minutes" lacks a peer-reviewed human PK study). Up to ~10× the potency of native IGF-I in cell-based protein-synthesis assays (where IGFBPs sequester intact IGF-I and DES escapes that sequestration; Ballard 1987, PMID 2962574; Carlsson-Skwirut 1989, PMID 2469478) — receptor affinity itself is similar to native IGF-I. The "localized" injection-into-trained-muscle framing reflects pharmacokinetics (clearance is fast enough that most of the dose stays peri-injection before systemic dilution), not molecular tissue targeting; no human imaging or biopsy study of DES site-localized hypertrophy is published.
IGF-1 is one of the few anabolic agents theorized to induce actual new muscle-fiber formation (hyperplasia). Evidence in humans is weak; preclinical animal data is stronger.
| Benefit | Evidence |
|---|---|
| Muscle hypertrophy | Strong animal data (rat anabolism in catabolic states: dexamethasone, gut resection, renal restriction). No peer-reviewed human RCT for hypertrophy with either LR3 or DES exists. Anabolic synergy with training is community-reported, not trial-validated. |
| Fat loss | IGF-1 pathway activation contributes to lipolysis; modest compared with HGH and tesamorelin, which act on adipose more directly via GHR-mediated lipolysis. |
| Tissue repair | IGF-1R signaling drives satellite-cell activation and protein-synthesis upregulation in injured tissue; animal models of gut resection (Lemmey 1991, PMID 1996625) and renal mass restriction (Martin 1991, PMID 1928375) show accelerated recovery with DES specifically. Human data with LR3 or DES is absent. |
| Metabolic effects | Acute low-dose administration can transiently improve insulin sensitivity; chronic supraphysiological exposure drives the opposite effect (insulin resistance) — same class effect documented for rhGH and tesamorelin. Hypoglycemia is dose-dependent at every dose level. |
IGF-1’s role in bodybuilding is overhyped in forums. For most users the benefit-to-side-effect ratio is worse than CJC-1295 + Ipamorelin or tesamorelin.
Build your protocol, log every dose, monitor your body's response, and get reminders so you never miss a dose.
Start Tracking FreeAlmost every claim made for LR3 and DES is extrapolated from native IGF-1. It is worth knowing the handful of studies that carry the weight, and what each one does and does not establish.
The closest thing to human evidence for IGF-1 on muscle. Nineteen postabsorptive subjects received a 6-hour intra-arterial infusion of rhIGF-I into one forearm at 1.8, 6.0 or 10.0 mcg/kg/h.
| Protein synthesis | Rose 49–74% at all three doses (p < 0.05) |
| Protein degradation | Fell about 45%, but only at the two higher doses |
| Forearm blood flow | Up 75%, 213% and 159% by dose |
| Glucose uptake | Unchanged at the low dose; 4–6× at the higher two |
The detail that matters most is the control arm. The contralateral, non-infused forearm showed no change at all in glucose, lactate or phenylalanine handling — even though recirculation pushed systemic IGF-I as high as 517 ng/mL. Fryburg concluded the effects "appear dependent on the route of administration."
Read that against how LR3 is actually used. This was continuous intra-arterial infusion into a single limb, not a daily subcutaneous bolus, and simply having high IGF-1 in the blood did not reproduce the effect in the other arm.
Mice received viral-mediated IGF-I gene transfer into the hindlimb, with or without 2,500 rad of gamma radiation to destroy satellite-cell proliferative capacity. Radiation removed roughly half the IGF-I hypertrophic effect, implying the other half comes from direct paracrine/autocrine action on existing myofibres.
This is the source of the widely repeated "half of IGF-1's growth is satellite cells" line. It is a real result, in mice, using sustained local gene overexpression — not an injected analogue.
Most of the evidence above is native IGF-1. This one used IGF-1 LR3 specifically, delivered to rats with volumetric muscle loss in a hydrogel void filler at 28 mcg or 280 mcg.
The high dose increased muscle weight at 28 days. It produced no difference in specific or maximum torque, and no change in fibre size or fibre count. The authors concluded LR3 did not enhance neuromuscular function or fibre hypertrophy.
Mass went up; function and fibres did not. That is a useful corrective to the assumption that anything raising IGF-1 signalling necessarily builds working muscle, and it happens to be one of the few published results on the exact molecule people are injecting.
IGF-1 pathway biology is thoroughly established (Yoshida 2020, PMID 32858949, for the mechanistic review). Evidence that injecting an IGF-1 analogue subcutaneously produces muscle growth in healthy humans does not exist — not weakly, not at all. The human work is acute infusion; the growth work is animal, mostly native IGF-1, and mostly delivered in ways nobody replicates with a syringe.
Not medical advice. These figures describe what is reported in the literature and what practitioners and communities do — not a recommendation, and for most compounds here no human dose-finding study exists. Talk to a qualified healthcare provider.
A higher convention of 40–80 mcg/day also circulates widely. This guide stays at the lower band deliberately. The failure mode at the top of the range is not a wasted dose — it is hypoglycemia, which the licensed product's label records as having caused seizures, and LR3 is specifically engineered to evade the binding proteins that normally buffer IGF-1 activity. There is no human dose-finding study for LR3 at any dose, so neither number is validated; the asymmetry in what going too high costs is the reason for preferring the lower one.
Both can cause hypoglycemia, and the licensed IGF-1 product's label does not describe this as a nuisance effect: severe hypoglycemia leading to hypoglycemic seizures has been observed with mecasermin. Eat a carb-containing meal shortly before or after injection, monitor for shakiness, dizziness and sweating, and keep fast carbohydrate available. The Increlex label recommends preprandial glucose monitoring at initiation and until a tolerated dose is established — a reasonable practice to copy even though the indication and dose do not transfer. Start at the low end.
Pre-filled with a typical IGF-1 LR3 and DES setup. Edit any field — the draw updates live.
Insulin syringe — 100 units = 1 mL
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Not medical advice. These figures describe what is reported in the literature and what practitioners and communities do — not a recommendation, and for most compounds here no human dose-finding study exists. Talk to a qualified healthcare provider.
IGF-1 LR3 is fragile and requires acidic diluent — bacteriostatic water at neutral pH causes the peptide to aggregate within days. Use 0.6% acetic acid (also sold as “peptide reconstitution solution”) instead.
1 mg vial + 1 mL 0.6% acetic acid = 1000 mcg/mL
| Dose | Volume | Syringe Units |
|---|---|---|
| 20 mcg | 0.02 mL | 2 units |
| 50 mcg | 0.05 mL | 5 units |
| 100 mcg | 0.10 mL | 10 units |
Very small draw volumes — use a 0.3 mL insulin syringe for precision.
Mecasermin (Increlex) is recombinant human IGF-1, licensed for growth failure in children with severe primary IGF-1 deficiency. It is not LR3 or DES, and its dosing does not transfer — it is native IGF-1 with normal binding-protein regulation, given at 0.04–0.12 mg/kg twice daily, a milligram scale that is not comparable to microgram LR3 precisely because LR3 is built to escape those binding proteins. But its label is the closest thing to a real human adverse-effect record for sustained IGF-1 receptor agonism, and it lists more than this guide previously did:
Several of these were studied in growing children over years, so they do not map cleanly onto an adult running a six-week cycle. They are included because the alternative — describing IGF-1 safety purely from community report — leaves out the only systematic human record that exists.
IGF-1R signaling is mitogenic and anti-apoptotic, and human observational and Mendelian-randomization evidence supports a probable causal association between higher circulating IGF-1 and risk of incident colorectal cancer, with positive observational signals for prostate and postmenopausal breast cancer. The supraphysiological IGF-1R activation produced by LR3 or DES is outside the range of any prospective human safety dataset, so extrapolation is uncertain. Active or prior malignancy is a contraindication for LR3 and DES specifically because there is no human safety data at supraphysiological doses to argue otherwise. The cancer-axis exposure is more direct than with GHRP/GHRH peptides, which raise IGF-1 only via endogenous pituitary GH and are subject to feedback ceiling.
IGF-1 LR3 and DES is a research peptide not approved by the FDA for human use. It is sold only as a research chemical, and StackTrax does not endorse or facilitate personal use.
Quality varies enormously among research-chemical suppliers. At minimum, look for:
Lyvn does not carry IGF-1 LR3 and DES. They are the vendor we recommend elsewhere on this site, and they publish the full independent panel per batch — which makes their catalogue a useful yardstick for the criteria above even on a compound they do not stock. We are not recommending a specific supplier for IGF-1 LR3 and DES itself, because we have no basis to.
For research use only. Not for human consumption. 21+.
Build your protocol, log every dose, monitor your body's response, and get reminders so you never miss a dose.
Start Tracking FreeNo. IGF-1 LR3 has never been FDA approved. There IS an FDA-approved recombinant IGF-1 product — Increlex (mecasermin) — but that is NATIVE IGF-1 (70 amino acids), not the LR3 analog. Increlex is approved for severe primary IGF-1 deficiency in children. IGF-1 LR3 (83 amino acids with an R3 substitution and N-terminal extension) has no human regulatory approval anywhere and is sold only as a research-grade cell-culture reagent or research chemical.
Community-practice dosing is 20–50 mcg subcutaneously once daily, typically post-workout or before bed. These figures come from bodybuilding forums and clinic convention — there is no peer-reviewed human dose-finding study for LR3 IGF-1 in hypertrophy use. The "20–30 hour half-life" widely cited in community sources is extrapolation; no peer-reviewed human PK study of LR3 specifically exists.
IGF-1 LR3 requires 0.6% acetic acid (NOT bacteriostatic water). BAC water degrades the peptide. A typical reconstitution is 1 mg of LR3 + 1 mL of 0.6% acetic acid, yielding 1 mg/mL. A 20 mcg dose draws to 0.02 mL (2 units on a 100-unit insulin syringe), 50 mcg = 0.05 mL (5 units). Refrigerate immediately after reconstitution.
No. Increlex (mecasermin) is recombinant native human IGF-1 produced as a pharmaceutical product for FDA-approved use in severe primary IGF-1 deficiency. IGF-1 LR3 is an engineered analog developed primarily as a cell-culture reagent. They share the same receptor (IGF-1R) but are chemically distinct.
Both are IGFBP-resistant IGF-1 analogs. LR3 has an N-terminal extension and an R3 substitution that give it a long plasma residence — community framing is "systemic IGF-1 elevation." DES is a naturally occurring truncation (missing the N-terminal tripeptide Gly-Pro-Glu) with a very short circulating half-life (minutes) — community framing is "site-localized post-workout injection into the trained muscle." LR3 is the daily systemic version; DES is the post-workout local version.
Yes. IGF-1 LR3 is prohibited at all times under WADA S2.3 (Growth Factors and Growth Factor Modulators) as an analog of IGF-1. No therapeutic-use exemption is available.
Disclaimer: This guide is for educational and informational purposes only and is not intended as medical advice, diagnosis, or treatment. The compounds discussed are not FDA approved for human use. Always consult a qualified healthcare provider before starting any new supplement or peptide protocol. StackTrax does not sell peptides or supplements directly — purchase links go to third-party vendors. StackTrax is not responsible for the products, quality, or business practices of any third-party vendor.
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StackTrax guides cover peptides and compounds that are not FDA-approved for the uses discussed. The dosing, reconstitution, and safety information is compiled from published research and community protocols for educational purposes only.
Before using any compound mentioned here, consult a qualified healthcare provider. StackTrax does not sell, prescribe, or recommend these substances for personal use.