Long [Arg3] Insulin-like Growth Factor-1 (Long R3 IGF-1)
No human clinical trials have been conducted. All evidence comes from animal or laboratory studies.
A modified version of IGF-1 (a natural growth-promoting hormone) engineered to stay active in the body longer than the natural form. All published evidence comes from animal and laboratory studies showing tissue growth effects; no human clinical data exists for this specific version.
This entry is a cited research summary, not an established treatment reference. Dosing language is included as source context, not as medical instruction.
IGF-1 LR3 (Long R3 IGF-1) is preclinical or hypothesis-only.
No human clinical trials have been conducted. All evidence comes from animal or laboratory studies.
Controlled human safety data for IGF-1 LR3 are absent. In fetal sheep, LR3-IGF-1 lowered plasma insulin and glucose after 1 week and reduced in vivo glucose-stimulated insulin secretion; acute infusion also suppressed insulin during a hyperglycemic clamp (PMID 33938236, PMID 37114757). In growth-restricted fetal sheep, circulating amino acids fell during treatment without a growth benefit PMID 39679943. By contrast, local controlled release in a rat sciatic-nerve conduit study did not produce systemic toxicity PMID 41015370. Community sources consistently report hypoglycemia as the primary practical concern, with users maintaining carbohydrate intake during use. The AACE/ACE guidelines for GH deficiency note that IGF-1 levels should be kept within age-related physiological range to minimize side effects PMID 31760824. All frequency and severity ratings above are extrapolated and community reports; no controlled human safety data exists for LR3.
If real-world use or exposure is being considered, review potential interactions, contraindications, and monitoring needs with a licensed clinician rather than relying on summary copy alone.
Every claim on this page links to one of the 16 sources below. Identifiers are PubMed (PMID), ClinicalTrials.gov (NCT), or DOI; click through to the source of record before acting on a claim.