IGF-1 LR3 Dosage Chart.

It depends entirely on your mix, so read the number off the calculator rather than copying someone else’s. On the standard basis used here (a 1 mg vial reconstituted with 2 mL of bacteriostatic water, giving 500 mcg/mL), one unit on a U-100 syringe is 5 mcg. So 20 mcg is 4 units, 30 mcg is 6 units and 40 mcg is 8 units. If you mix that same 1 mg vial into only 1 mL you double the concentration and halve the units, which puts 20 mcg at 2 units. That is a very short draw with a lot of room for error, which is why 2 mL is the better default.

There is no evidence for that number, and the measurements that do exist point the other way. Nobody has ever measured LR3 half-life in a human. In rats, Bastian and colleagues found a metabolic clearance rate of 9.84 ml/min/kg for LR3IGF-I versus 0.90 ml/min/kg for IGF-I, roughly ten times faster. Ballard’s group put it plainly: LR3IGF-I "was removed from the plasma much more rapidly than was IGF-I". A third rat study, on transport into wound fluid, again found LR3IGF-I cleared from the circulation more rapidly. The reason is the whole point of the molecule: native IGF-1 lingers because it is bound into a 150 kDa complex with IGFBP-3, and LR3 was engineered to have about 1000-fold lower affinity for that binding protein. Escaping the reservoir means leaving the bloodstream faster, not slower.

Because nothing better has ever been tested. Once-daily dosing was inherited from the 20 to 30 hour figure this page rejects, and no alternative interval for IGF-1 LR3 has been studied in a human at any dose. We have kept it because it is what the reported protocols use and because inventing a split-dose schedule to fit rat clearance data would be substituting one unmeasured guess for another. What the clearance data does change is the expectation: do not assume a dose is still working on you a day later, and do not add a second daily injection on the theory that it must have worn off; that would raise exposure on a compound whose only documented dose-limiting toxicity is hypoglycaemia.

Yes, and this is the single most evidence-backed instruction on the page. The Increlex label requires the dose be given "shortly before or after (± 20 minutes) a meal or snack", and states that if the patient cannot eat, "that dose of INCRELEX should be withheld". The reason is in the trial data: 30 of 71 patients (42%) reported hypoglycaemia at least once, 5 had severe episodes requiring assistance, and 4 had hypoglycaemic seizures or lost consciousness. Those were higher doses in children, and the mechanism is the same one LR3 acts through.

No. A 2026 Frontiers in Endocrinology review of performance-enhancing peptides that modulate the GH-IGF-1 axis assessed IGF-1 LR3 and graded it Tier D ("no peer-reviewed human studies"), noting the compound rests entirely on "preclinical extrapolation and grey-literature user narratives", with half-life "not documented" in humans. Everything on this page that concerns dosing comes from either those user reports, rat pharmacokinetics, or the FDA label of a different IGF-1 molecule. There is no trial to point you at, and any page that offers you one is worth checking.

No study has ever tested whether injecting IGF-1 LR3 into a specific muscle grows that muscle, and the compound’s own design argues against it. LR3 exists precisely because it does not bind the IGF binding proteins, which points toward systemic distribution rather than staying put; Bastian’s 2000 study measured LR3IGF-I moving from blood into extracellular wound fluid and found its flux across the endothelial barrier was unaffected by binding proteins, unlike IGF-I. Note that the distribution data we have comes from intravenous dosing in rats, so it cannot speak to an injection site either way. Site-injection theory is bodybuilding folklore, and following it mostly gets you repeated injections into one spot, which is how lipohypertrophy develops.

Bacteriostatic water is the convention: add it slowly down the inside wall of the vial, swirl rather than shake, and give it a couple of minutes to dissolve. The ~28 day fridge window people quote comes from the benzyl alcohol preservative in bacteriostatic water, not from any published LR3 stability study. No such study exists. The closest regulator-reviewed reference point is the Increlex label, where the multi-dose vial is "stable for 30 days after initial vial entry when stored refrigerated at 2° to 8°C". Keep the unmixed powder cold and dark, and treat 28 days as a discard date, not a target.

The honest answer is that nobody knows for IGF-1 LR3, and the surrounding evidence is not reassuring. Malignant neoplasia or a history of malignancy is an outright contraindication on the Increlex label, which also carries post-marketing reports of malignant neoplasms in treated paediatric patients. The 2026 review flags "theoretical mitogenic potential based on IGF-1/IGF-1R signalling biology" for LR3 specifically, while noting that long-term cancer risk cannot be inferred from short-term exposure in either direction. That is genuinely unresolved, but it is why the cycle breaks matter and why anyone with a cancer history should not touch this.

You largely do not, and there is a documented case that makes the point sharply. In 2010, Kohler and colleagues analysed a seized black-market injection vial sold as Long-R3-IGF-I and identified the protein as Long-R3-IGF-I carrying a His6 purification tag on the C-terminus via a Leu-Glu linker (a laboratory artefact that is normally enzymatically removed, and only can be when the tag sits at the N-terminus). Their conclusion was that the effects of His-tagged Long-R3-IGF-I in humans "have not been elucidated or described" and that the product "may rather be a by-product from biochemical studies than synthesized for injection purposes". A certificate of analysis showing purity by HPLC does not rule this out, because a tagged protein can be perfectly pure.