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), which become ineffective once exogenous IGF-1 has shut down the somatotroph response.
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 FreeBoth can cause hypoglycemia. Eat a carb-containing meal within 30 minutes of injection, monitor for shakiness / dizziness / sweating, and have fast carbs available. Start at the low end of the dose range to assess response.
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.
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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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:
StackTrax’s preferred partner NextGen Peptides does not currently carry IGF-1 LR3 and DESin their catalog, which is why you don’t see a direct purchase link here. Other major research-chemical suppliers carry it; we don’t specifically recommend one for this compound.
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. This page contains affiliate links — StackTrax may earn a commission on purchases at no extra cost to you.
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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.
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