Growth hormone axis
IGF-1 LR3
Long-acting IGF-1 analog used mainly in cell-culture research.
Where the evidence comes from
10 verified records from 4 countries. The number of studies or countries is not proof that IGF-1 LR3 works or is safe.
Animal study: 10
What is known
Editorial summary not yet written.
What remains uncertain
Editorial summary not yet written.
Conflicting findings
Editorial summary not yet written.
U.S. regulatory status (FDA)
Compound
Product or formulation
FDA status
FDA-approved branded drug
Approved indication
Metara availability (compounded formulation)
Research material (research use only)
Source
Last verified
Notes
Approval applies only to the exact finished drug, formulation and indication. A shared active ingredient does not make a compounded version, blend or other use FDA-approved. Pharmacy or research-material availability is not FDA approval.
International regulatory status
Kept separate from U.S. status. The regulator's country is not the same as where studies took place.
No sourced international decisions recorded yet.
Continue your research
These are two different pathways, not two ways to get the same thing. Neither changes the FDA status shown above.
Clinical care
Available through Metara Health
Explore clinician-guided care and available pharmacy options.
EXPLORE METARA HEALTH →Limitations
No human clinical trials of IGF-1 LR3.
Human clinical evidence (0)
No verified human studies listed yet.
Systematic & narrative reviews (0)
No verified reviews listed yet.
Laboratory, animal & other research (10)
N-Linked Glycosylation in Chinese Hamster Ovary Cells Is Critical for Insulin-like Growth Factor 1 Signaling.
Salvi R, Kumar C, Brahmbhatt K, Subedi R, Idicula-Thomas S, Madan T, Biswas B · International journal of molecular sciences · DOI 10.3390/ijms232314952
This lab study examined how attaching sugars to proteins affects IGF-1 signaling in cultured Chinese hamster ovary cells. Cells with defective sugar attachment had fewer IGF-1 receptors and weaker activation of ERK signaling proteins after IGF-1 LR3 stimulation. The findings suggest that proper sugar attachment is essential for this signaling pathway.
Reduced glucose-stimulated insulin secretion following a 1-wk IGF-1 infusion in late gestation fetal sheep is due to an intrinsic islet defect.
White A, Stremming J, Boehmer BH, Chang EI, Jonker SS, Wesolowski SR, Brown LD, Rozance PJ · American journal of physiology. Endocrinology and metabolism · DOI 10.1152/ajpendo.00623.2020
This animal and lab study examined IGF-1 LR3 in fetal sheep during late pregnancy and in pancreatic islets isolated from them. IGF-1 LR3 lowered circulating insulin and glucose and reduced insulin release in response to glucose. Reduced insulin release persisted in isolated islets, indicating a defect within the insulin-producing tissue itself.
IGF-1 infusion to fetal sheep increases organ growth but not by stimulating nutrient transfer to the fetus.
Stremming J, Heard S, White A, Chang EI, Shaw SC, Wesolowski SR, Jonker SS, Rozance PJ, Brown LD · American journal of physiology. Endocrinology and metabolism · DOI 10.1152/ajpendo.00453.2020
This animal study examined LR3 IGF-1 in fetal sheep during late pregnancy. It increased heart, adrenal gland, and spleen weights without significantly changing overall fetal weight, placental blood flow, or fetal protein turnover. Amino acid transfer to the fetus decreased, leading the researchers to speculate that organ growth reflected efficient use of available nutrients rather than increased nutrient delivery.
Coronary vascular growth matches IGF-1-stimulated cardiac growth in fetal sheep.
Jonker SS, Giraud GD, Chang EI, Elman MR, Louey S · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · DOI 10.1096/fj.202000215R
This animal study examined whether blood vessels supplying the heart kept pace with IGF-1 LR3-stimulated heart growth in fetal sheep. Heart growth was accompanied by appropriate growth and function of these vessels, with similar blood-flow responses to low oxygen in treated and control animals.
Inhibition of activin-like kinase 4/5 attenuates cancer cachexia associated muscle wasting.
Levolger S, Wiemer EAC, van Vugt JLA, Huisman SA, van Vledder MG, van Damme-van Engel S, Ambagtsheer G, IJzermans JNM, de Bruin RWF · Scientific reports · DOI 10.1038/s41598-019-46178-9
This laboratory and animal study tested ALK4/5 blockers and IGF-I LR3 in muscle cells and mice with cancer-related muscle wasting. GW788388 was more effective than SB431542 at limiting losses in body weight, grip strength, and muscle weight. IGF-I LR3 limited muscle loss but also accelerated tumor growth.
Enhancement of maternal lactation performance during prolonged lactation in the mouse by mouse GH and long-R3-IGF-I is linked to changes in mammary signaling and gene expression.
Hadsell DL, Parlow AF, Torres D, George J, Olea W · The Journal of endocrinology · DOI 10.1677/JOE-07-0556
This animal study compared growth hormone, prolactin, and IGF-I LR3 in mice during prolonged lactation. Growth hormone increased lactation capacity, measured through offspring weight gain, while IGF-I LR3 produced a modest increase and prolactin did not. IGF-I LR3 also increased mammary Akt signaling and activity of the SOCS3 gene.
Insulin-like growth factor-I and analogues increase growth in artificially-reared neonatal pigs.
Dunshea FR, Chung CS, Owens PC, Ballard JF, Walton PE · The British journal of nutrition · DOI 10.1079/BJNBJN2002574
This animal study tested IGF-I and LR3 IGF-I in artificially reared newborn pigs under restricted or unrestricted milk feeding. Neither peptide improved weight gain with restricted feeding. With unrestricted feeding, LR3 IGF-I increased weight gain during the later study period, while both growth factors increased milk intake.
Long [R3] insulin-like growth factor-I reduces growth, plasma growth hormone, IGF binding protein-3 and endogenous IGF-I concentrations in pigs.
Dunaiski V, Dunshea FR, Walton PE, Goddard C · The Journal of endocrinology · DOI 10.1677/joe.0.1550559
This animal study examined IGF-I and its LR3 analogue, alone or with growth hormone, in pigs nearing market weight. LR3 IGF-I reduced weight gain, food intake, and several circulating hormones and binding proteins; ordinary IGF-I did not change weight gain or food intake. Both peptides suppressed growth hormone, which may contribute to LR3 IGF-I's growth-inhibiting effects.
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Profile last reviewed September 26, 2026. Educational content only. Not medical advice, a dosing protocol or a treatment recommendation.