IGF-1 LR3
Long-[Arg³] Insulin-like Growth Factor 1 · 83-AA IGF-1 analog
IGF-1 LR3 is a long-acting synthetic analog of human insulin-like growth factor 1, engineered with an arginine substitution at position 3 plus a 13–amino-acid N-terminal extension so it largely escapes the IGF-binding proteins that normally buffer IGF-1. That escape lets more free peptide reach the IGF-1 receptor, which is the real basis for its reputation as "stronger and longer-lasting" than native IGF-1 — not, as is often claimed, a slow clearance (rat data actually show faster clearance). It is sold as a cell-culture growth reagent, has no approved human use and no human trials, and is prohibited in sport (WADA).
The short version
IGF-1 LR3 is a lab-modified version of IGF-1, a natural growth signal your body makes (mostly in the liver, in response to growth hormone).
The change is deliberate: normally IGF-1 is grabbed and held by carrier proteins in the blood, which limits how much is active at any moment. LR3 is built to slip past those carriers, so more of it stays free and switches on the growth-signal receptor. That is why it is described as stronger and longer-acting than plain IGF-1.
Almost everything known about it comes from cell-dish and animal studies — it is sold as a research reagent for growing cells, not as a medicine. It is not an approved drug, has never been tested in humans as a therapy, and is banned in competitive sport.
Molecular identity
Specs
- Molecular weight
- 9,111.45 g/mol
- Molecular formula
- C400H619N111O115S9
- CAS / UNII
- 143045-27-6 · M9L22Y19H9
- Sequence (83 AA)
- MFPAMPLSSLFVNGPRTLCGAELVDALQFVCGDRGFYFNKPTGYGSSSRRAPQTGIVDECCFRSCDLRRLEMYCAPLKPAKSASigma-Aldrich I1271
- Structure / class
- 83-AA IGF-1 analog: native IGF-1 70-AA core (Glu3→Arg) + 13-AA N-terminal extension from methionyl porcine GHSigma-Aldrich I1271
- Physical form
- Lyophilized powder (E. coli–expressed recombinant); reconstitute for cell-culture useSigma-Aldrich I1271
- Molecular target
- IGF-1 receptor (IGF-1R) agonist; very low IGF-binding-protein (IGFBP) affinitySigma-Aldrich I1271
- Half-life
- No human PK data; in rats cleared as fast as / faster than native IGF-1PMID 7693845
- Regulatory status
- Research reagent; not FDA-approved; prohibited in sport (WADA S2.3, IGF-1 analogues)WADA Prohibited List
Plain English
Mechanism
IGF-1 LR3 turns on the IGF-1 receptor (IGF-1R), a switch on the cell surface that drives growth. When it binds, the receptor fires two main internal signal chains: the PI3K–Akt–mTOR pathway, which tells the cell to build protein and stay alive (the anabolic, muscle-building side), and the Ras–MAPK pathway, which tells the cell to divide and multiply (proliferation, also called hyperplasia — making more cells, not just bigger ones).
The clever part is what the modifications do. Native IGF-1 is mostly bound up by six carrier proteins called IGF-binding proteins (IGFBPs), which act like a sponge that soaks up free hormone. The arginine swap at position 3 plus the 13–amino-acid extension make LR3 bind those sponges very poorly, so a much larger free fraction reaches the receptor. Importantly, this is why it is "more potent" — but only where IGFBPs are present: in lab dishes with no binding proteins, LR3 is actually weaker than native IGF-1 (Francis 1992). So the often-quoted "about 3× stronger" is a setting-dependent figure, not a fixed property.
Because the IGF-1 receptor and the insulin receptor are close cousins, IGF-1 and its analogs can also nudge the insulin side and lower blood sugar — in animals, LR3 infusion dropped circulating glucose and insulin. This receptor cross-talk is the mechanism behind the hypoglycemia (low-blood-sugar) risk people are warned about.
Why people reach for it
Potential benefits
IGF-1 LR3 is the long-acting, systemic base of the muscle-growth peptides — the one people build a bulk cycle around. Here's what draws them to it.
- Build muscle past your usual ceiling — Its headline appeal. LR3 switches on the IGF-1 receptor and the PI3K–Akt–mTOR pathway — the body's main protein-building signal — and the modifications let far more of it stay free and active than native IGF-1, which is why it's reached for to push hypertrophy.
- Grow new muscle cells, not just bigger ones — Through the Ras–MAPK arm it drives proliferation (hyperplasia) — more muscle cells, not only enlarged existing ones — the property that makes it stand out from a simple anabolic.
- An all-day anabolic base — Its long functional action comes from escaping the IGF-binding proteins so more free peptide keeps reaching the receptor, giving a once-daily, whole-body signal that holds through a training block — the systemic foundation other peptides layer onto.
- Channels nutrients into worked muscle — Dosed post-workout it lands when the receptor is most stimulus-primed and blood flow to the trained muscle is up, which is why people time it to feed recovery and growth into the tissue they just trained.
- Pairs cleanly with a local pulse — Because it's the long systemic lever, it slots naturally next to a short, targeted one — most commonly IGF-1 DES for a post-workout local hit while LR3 holds the background.
Sources:PMID 1378742PMID 39638246PMID 8053901PMID 9572822
What people reach for IGF-1 LR3 for, drawn from what the research reports (cell and animal studies — no human trials) and how it's used — not proven human outcomes or medical claims.
Implied timing
Best time to dose
Implied best time
Post-workout (or morning)
Most people take IGF-1 LR3 once daily after training — and on rest days at a consistent morning time — to drive the growth signal into recently worked muscle.
- Dosing post-workout puts the anabolic signal where it's wanted: the IGF-1 receptor is most stimulus-primed right after training and blood flow to the worked muscle is elevated, so the peptide is channeled toward the tissue you just trained. A carbohydrate-and-protein meal afterward complements it (and helps blunt the blood-sugar dip).
- LR3 is long-acting in function — it escapes the IGF-binding proteins so more free peptide keeps reaching the receptor — which means once-daily dosing is enough; you don't need to chase the clock with multiple hits.
- On rest days there's no workout to anchor to, so a consistent morning time is the practical default — it keeps the IGF-1-axis elevation steady across the cycle.
- One timing caution drives from the mechanism, not the hour: LR3 lowers blood glucose via insulin-receptor cross-talk, so the dose is tied to a carbohydrate-containing meal and never taken fasted before sleep.
No study establishes an ideal time of day for IGF-1 LR3 — this is reasoned from its mechanism and how it's actually used. As a rule of thumb most peptide dosing lands in the midday-to-evening window; for LR3 the lean is post-workout, with a consistent morning slot on rest days.
Sources:PMID 39638246PMID 8053901
How to run it
Dosing & protocol
IGF-1 LR3 is used here as a subcutaneous injection — the form sold as a research peptide and the route the on-page calculator is built for. No human trial has set a dose; the ranges and schedule below are bodybuilding-community and practitioner convention extrapolated from animal work. Read this as a map of how people actually run LR3 — not a validated prescription.
Community convention, not trial-proven: no human clinical trial has ever tested IGF-1 LR3 in humans, and it is not an FDA-approved drug. It is prohibited in sport (WADA S2.3). Every number here is a usage pattern extrapolated from animal research, not evidence.
Tiered dose ranges
Most protocols land between 20–50 mcg per day subcutaneously; experienced users occasionally go higher.
- Entry / first cycle:
- 20–30 mcg once daily — standard starting range to assess tolerance and gauge the blood-sugar response before scaling.
- Standard:
- 40–50 mcg once daily — the core community range for an anabolic / body-composition cycle.
- Higher range:
- Up to ~100 mcg/day reported by experienced users — substantially increases hypoglycemia risk and is the upper end seen in community logs, not a recommendation.
Subcutaneous administration
LR3 is injected into subcutaneous fat; site, timing, and carbohydrate proximity are the critical choices.
- Injection site:
- The abdomen (keeping an inch or two clear of the navel), the love-handle area, or the outer thigh. Rotate sites each dose to prevent local irritation and lipohypertrophy (fatty nodules from repeated injection into the same spot).
- Measuring the dose:
- Drawn on a U-100 insulin syringe from the reconstituted vial. At the standard mix (1 mg vial + 1 mL BAC water = 1,000 mcg/mL): 20 mcg = 2 IU · 30 mcg = 3 IU · 50 mcg = 5 IU. The calculator handles any vial size.
- Time of day:
- Most commonly injected post-workout, when the muscles have a direct need for the growth signal — see Best time to dose above. Some users dose on rest days at a consistent morning time. Avoid dosing before sleep without food on board — the blood-sugar drop during sleep can be significant.
- Food window — critical:
- Do NOT inject fasted or without carbohydrates nearby. IGF-1 LR3 lowers blood glucose via insulin-receptor cross-talk. Inject within 15–30 minutes of a carbohydrate-containing meal, or keep fast-acting carbs (glucose tabs, juice) on hand to counter any hypoglycemic episode.
Cycle & washout
LR3 is run in defined blocks rather than indefinitely — both to limit sustained pro-proliferative signaling and to prevent IGF-1 receptor down-regulation.
- Standard cycle:
- 4–6 weeks of daily dosing is the most commonly cited block length. Some practitioners cap at 4 weeks and others push to 8; the shorter end is more conservative given the sustained growth-signaling concern.
- Washout:
- Equal or longer off period — typically 4–8 weeks. The theoretical rationale is receptor sensitivity restoration, though this has not been studied for LR3 in people.
- No indefinite use:
- Sustained IGF-1-receptor activation is mechanistically pro-proliferative (drives cell division, resists apoptosis), and a higher IGF-1 axis is epidemiologically linked to several cancers. The time-limited pattern reflects that theoretical concern, not a studied LR3-specific finding.
Reconstitution at a glance
The on-page calculator does this live; the quick reference for the standard 1 mg vial:
- Mixing:
- 1 mg vial + 1 mL bacteriostatic water = 1,000 mcg per mL. On a 100-unit (1 mL) U-100 insulin syringe: 20 mcg = 2 IU · 30 mcg = 3 IU · 40 mcg = 4 IU · 50 mcg = 5 IU.
- Why 1 mL:
- Gives a 1:1 ratio that keeps the math simple — each 1 IU on the syringe equals exactly 10 mcg of peptide at this dilution.
Substrate the signal needs
Nutritional cofactor precision
IGF-1 LR3 is the muscle-growth signal itself — the same messenger growth hormone normally works through — so its cofactor logic is the most direct of the GH family: SUPPLY the building substrate, MITIGATE the hypoglycemia it creates, and AMPLIFY via the stimulus it is designed to amplify. This is IGF-1 physiology applied to LR3, not an LR3 nutrition study.
Reasoned from IGF-1's PI3K–Akt–mTOR and insulin-receptor cross-talk mechanisms — not a clinical LR3 cofactor trial. Supplement and nutrition doses are community and sports-nutrition convention.
SUPPLY the substrate: protein + leucine
IGF-1's anabolic job is to drive protein synthesis via Akt/mTOR — without the raw material, the signal fires with nothing to build.
- Protein target:
- 1.8–2.2 g per kilogram of body weight per day (about 0.8–1.0 g per pound). Note: food-restricted animals given LR3 failed to preserve muscle and actually increased protein breakdown — the growth signal requires an energy surplus, not a deficit.
- Leucine timing:
- 3–5 g of leucine around the training session (or alongside the dose on rest days). Leucine is the specific amino acid that co-activates mTOR — it is the key that turns the lock IGF-1 unlocks. A leucine-rich source (whey, chicken, eggs) at the post-workout meal directly serves the signal.
- Calorie surplus:
- A modest caloric surplus (roughly 200–400 kcal above maintenance) ensures the anabolic signal has energy to work with, not just maintenance calories to sustain baseline turnover.
MITIGATE the cost: carbohydrate timing for hypoglycemia
IGF-1 LR3 lowers blood glucose by cross-reacting with the insulin receptor — this is the real, documented risk, not a theoretical footnote.
- Carb-containing meal window:
- Inject within 15–30 minutes of a meal that includes carbohydrates (30–60 g is a reasonable target). Having glucose in circulation when LR3 peaks blunts the drop. Injecting fasted or before bed without food is when hypoglycemic episodes are most likely.
- Fast-acting carbs on hand:
- Some users keep glucose tablets (15–20 g), juice, or a small sports drink accessible when dosing — especially during the first cycle when the individual glucose response is unknown.
- Chromium picolinate (glucose handling support):
- 200–400 mcg chromium picolinate daily — supports insulin sensitivity and glucose disposal. Not a substitute for carb timing but a background support for anyone running LR3 alongside a training block.
- Magnesium glycinate:
- 300–400 mg before bed — magnesium is required for insulin-receptor function and glucose metabolism; suboptimal magnesium worsens glucose swings and is common in athletes under training load.
- Do NOT stack with insulin:
- Combining LR3 with exogenous insulin adds two blood-sugar-lowering agents — the community calls this the "most dangerous" IGF stack. In animals the LR3 + insulin combination drove large weight gain but would compound hypoglycemia risk severely in humans. Described here as a known community practice, not an endorsed one.
AMPLIFY: resistance training as the stimulus
IGF-1 is the signal that grows what you train — without the training stimulus, the signal has no specific target to amplify.
- Resistance training is the co-driver:
- The IGF-1 axis amplifies the mechanical growth stimulus from progressive overload. Animal hypertrophy data (even native IGF-1 studies) consistently show the growth signal produces the largest effect in loaded, worked tissue. Training hard during a cycle is not optional — it is the context the peptide is mechanistically designed to act in.
- Training timing alignment:
- Post-workout dosing is the most common approach, placing LR3 when the IGF-1 receptor is most stimulus-primed and blood flow to worked muscle is elevated. Rest-day dosing (at a consistent morning time) is also used to maintain baseline IGF-1-axis elevation through the cycle.
Combinations + timing
Stacking notes + timing windows
LR3 is the systemic, long-acting base of the IGF-1 axis. Its best partners either divide labor with it (short local vs. long systemic), push the upstream axis that generates natural IGF-1, or extend recovery. Doubling another pro-growth signal would push the same lever twice — the entries below are complementary levers only.
Combination rationale reasoned from complementary mechanisms — none of these stacks has human safety or outcome data, and LR3 itself has no human trial, so any pairing is doubly unproven. Doses are community convention; 'reached for' describes where users go, not a proven indication.
LR3 + IGF-1 DES
Division of labor — DES is the short, local, post-workout pulse; LR3 is the systemic long-acting base.
- Why it works:
- IGF-1 DES is a 67-AA truncated form missing the first three amino acids, which makes it substantially more potent at the receptor but also very short-acting (minutes, not hours) and thought to act more locally at the injection site. LR3 provides the sustained systemic IGF-1-axis elevation; DES provides the acute, localized post-workout pulse. Different half-lives, different distribution — complementary, not the same lever.
- The protocol:
- LR3 20–50 mcg subcutaneously once daily (base dose, often morning or post-workout) + IGF-1 DES 50–100 mcg injected near trained muscle immediately post-workout, on training days only. Run both on the same 4–6 week cycle timeline.
- Outcome:
- The combination users reach for to pair a systemic anabolic base with a targeted post-workout pulse. Both compounds lower blood glucose — carbohydrate timing on both doses is non-negotiable.
LR3 + Ipamorelin / CJC-1295
GH-axis pairing — Ipamorelin and CJC-1295 raise natural GH, which raises endogenous IGF-1, complementing the exogenous LR3.
- Why it works:
- Ipamorelin (a GHRP — ghrelin-receptor agonist) triggers a GH pulse without the cortisol/prolactin spike of older GHRPs. CJC-1295 (a GHRH analog) extends that pulse. Together they push the top of the GH→IGF-1 axis; LR3 adds exogenous IGF-1 at the bottom. Honest caveat: there is partial overlap — the body's own IGF-1 production rises from the GH secretagogues, so this is axis elevation plus exogenous analog, not two fully independent levers. Monitoring IGF-1 blood levels during this stack is the responsible approach.
- The protocol:
- Ipamorelin 200–300 mcg + CJC-1295 (with DAC) 2 mg twice weekly, injected subcutaneously — on an empty stomach or post-workout for GH pulse optimization. LR3 20–50 mcg/day as above. Keep the stack's total duration to the LR3 cycle length (4–6 weeks).
- Outcome:
- Reached for on body-composition cycles where users want the full GH–IGF-1 axis engaged. The GH secretagogue side also contributes improved sleep quality and recovery, which is a different outcome from LR3's direct anabolic signaling.
LR3 + BPC-157 / TB-500 (recovery layer)
Adding a soft-tissue recovery layer to the growth signal — BPC-157 repairs, TB-500 migrates repair cells.
- Why it works:
- BPC-157 supports connective-tissue and gut healing and drives angiogenesis (new blood vessels to the repair zone). TB-500 promotes migration of repair cells into injured tissue. LR3's anabolic signal and these recovery peptides work on different biology — growth signaling vs. tissue healing — so the combination addresses both the build and repair sides of a hard training block. Three different levers.
- The protocol:
- LR3 20–50 mcg/day as above + BPC-157 250–500 mcg/day subcutaneously + TB-500 on its own loading-and-maintenance schedule (typically a 2–4 mg weekly loading dose for the first 4–6 weeks, then a 1–2 mg/week maintenance). Co-inject or use nearby sites, rotating across the week.
- Outcome:
- Reached for on mass-and-recovery cycles — particularly where connective tissue (tendons, ligaments) is under stress from the added training load a growth cycle demands.
Insulin + LR3 — known-dangerous, flagged honestly
In animals, LR3 + insulin produced far more weight gain than either alone. In people, it stacks two blood-sugar-lowering agents — the most dangerous community practice on this page.
- The mechanism risk:
- LR3 lowers blood glucose via insulin-receptor cross-talk. Exogenous insulin lowers blood glucose directly. Combining both creates additive hypoglycemic pressure — severe hypoglycemia (blood sugar below 70 mg/dL, potentially much lower) can cause confusion, seizure, or cardiac event. This is not a theoretical risk; it is a documented mechanism.
- Why the community does it anyway:
- The rat tumour-bearing model (PMID 8053901) showed LR3 + insulin synergized dramatically for weight gain — that data circulates in bodybuilding communities as justification. The rat model is not a human safety study.
- Our position:
- Described here so readers understand what is being combined and why the risk is real — not as an endorsed protocol. If you encounter this stack, understand that fast-acting carbohydrates on hand, knowing the signs of hypoglycemia, and avoiding fasted dosing are the minimum harm-reduction steps. Ideally, avoid the combination.
Reconstitution math
Reconstitution calculator
Reconstitution calculator
Calculated for a 1 mL U-100 insulin syringe (100 units/mL).
Units per dose
5
Draw to this mark on a U-100 syringe
- Volume per dose
- 0.05 mL
- Doses per vial
- 20
- Concentration
- 1 mg/mL
One vial lasts
- Daily
- 20 days
- Every other day
- 40 days
- 5×/week
- 28 days
Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.
From the studies
Side effects from research
There is no human safety data for IGF-1 LR3 — the points below come from animal studies and from what is known about the IGF-1 axis generally.
Hypoglycemia (low blood sugar) is the best-documented and most immediate risk: IGF-1 analogs lower glucose through insulin-receptor cross-talk, shown directly in animals, and the risk is much worse when stacked with insulin. A theoretical but serious concern is cancer promotion — sustained IGF-1-receptor signaling is pro-proliferative and anti-apoptotic (it tells cells to divide and resists their programmed death), and a higher IGF-1 axis is epidemiologically linked to several cancers; this has not been studied for LR3 specifically. Animal work also adds a counterintuitive caution: under metabolic stress, LR3 was not uniformly anabolic and actually increased muscle protein breakdown in some rats, so it is not a guaranteed muscle-builder. Other extrapolated concerns include organ overgrowth and acromegaly-type effects from chronic excess.
As reported in literature
Research dosing ranges
These are doses from the published studies — all animal or cell-culture, since no human data exist. They are shown separately so research figures are never mistaken for a human dose. A key clearance fact lives here too: in rats, LR3 was cleared from plasma roughly ten times faster than native IGF-1 (because the IGFBP sponge that normally prolongs IGF-1 is bypassed), which directly contradicts the popular "20–30 hour half-life" claim that has no primary source.
| Dose | Route | Model | Outcome | Sources: |
|---|---|---|---|---|
| 98 nmol/kg/day | SC infusion (7 days) | Rat (food-restricted) | Modest weight gain; did NOT spare muscle — raised protein breakdown in adults | PMID 11472075 |
| 200–500 mcg/day | SC infusion (6–7 days) | Rat (tumour-bearing) | Lowered glucose + insulin; synergized with insulin for weight gain | PMID 8053901 |
| ~1–100 ng/mL | Cell-culture media | In vitro (CHO, fibroblasts) | Potent growth supplement — its actual intended use | Sigma-Aldrich I1271 |
| Local IM infusion | Intramuscular (native IGF-1) | Rat (single muscle) | Localized hypertrophy — the basis cited for "site injection" (but native IGF-1, not LR3) | PMID 9572822 |
| Plasma clearance | IV (PK) | Rat | LR3 cleared ~10× FASTER than native IGF-1 — debunks "long half-life" | PMID 7693845 |
Quick answers
Frequently asked
What is IGF-1 LR3?
It is a long-acting synthetic analog of IGF-1 — native IGF-1 with an arginine swap at position 3 and a 13–amino-acid N-terminal extension (83 amino acids total) that let it escape the IGF-binding proteins. It is sold as a cell-culture growth reagent, not as a medicine.
Is IGF-1 LR3 an approved drug?
No. It has no approved human therapeutic use anywhere and has never been tested in humans as a therapy. It is a research reagent, and it is prohibited in sport by WADA (Section S2.3, "IGF-1 and its analogues"). This page presents research literature only and makes no medical claims.
Does IGF-1 LR3 really have a 20–30 hour half-life?
That figure has no primary source — it is repeated by vendors but traces to nothing measured. There is no human PK study at all. The only primary data are in rats, where LR3 was cleared faster than native IGF-1, not slower. Its longer action comes from escaping the binding proteins (more free peptide), not from a long blood half-life.
How is IGF-1 LR3 commonly dosed?
No human trial has set a dose. In the user community the common pattern is roughly 20–50 mcg per day by subcutaneous injection, run for about 4–6 weeks. Treat that as convention extrapolated from animal research, not a recommendation — see the Dosing & Protocol section above.
What is the difference between IGF-1 LR3 and IGF-1 DES?
Opposite designs. LR3 is extended (83 AA) and built for prolonged, systemic action. IGF-1 DES is truncated — it is missing the first three amino acids (67 AA) — and is more potent but much shorter-acting, which is why it is used for short, timed, claimed-localized effects. Both escape the binding proteins; LR3 is the long one, DES is the strong-but-brief one.
Why does IGF-1 LR3 lower blood sugar, and what should I do about it?
IGF-1 and insulin receptors are closely related — IGF-1 can partially activate the insulin receptor, which drives glucose into cells and lowers blood sugar. This is a real, mechanism-driven effect, not a remote possibility. The practical response: always inject with a carbohydrate-containing meal nearby (not fasted), keep fast-acting carbs on hand during early cycles, and never combine LR3 with exogenous insulin.
Primary sources
References
- Sigma-Aldrich I1271MilliporeSigma I1271 (Long R3 IGF-1 datasheet)
- PMID 1378742Francis et al. 1992 (J Mol Endocrinol)
- PMID 7693845Bastian et al. 1993 (clearance)
- PMID 11472075Tomas et al. (food-restricted rat)
- PMID 8053901IGF/insulin in tumour-bearing rats
- PMID 9572822Local IGF-1 muscle hypertrophy (rat)
- PMID 39638246IGF-1 signaling landscape (review)
- UniProt P05019UniProt P05019 (native IGF-1)
- WADA S2.3WADA Prohibited List S2.3
Research use only · Not medical advice · Updated 2026-06-01