IGF-1 LR3

Areas of active research — not promised effects

Each tag links to other compounds with research into that goal. Research use only: these are areas of study, not human-use claims.

Related by research scope · open each to compare

IGF-1 LR3 has no FDA-approved drug application (NDA or BLA), no active IND on public record, and has never been designated a licensed therapeutic. It is not listed on the FDA 503A bulks list and cannot be lawfully compounded for human administration by 503A or 503B pharmacies. A physician cannot legally prescribe it for human use.

Transparent blend · bci-1.0 · never paid-placement

Primary name

IGF-1 LR3

Length

195 aa

Origin

IGF-1 LR3 (Long R3 IGF-1) is a fully synthetic 83-amino-acid analog of human insulin-like growth factor-1 (IGF-1, UniProt P05019). Two structural modifications distinguish it from the mature endogenous peptide: glutamic acid at position 3 is replaced by arginine, and a 13-residue N-terminal extension is prepended. Both changes substantially reduce affinity for the six circulating IGF-binding proteins (IGFBPs), particularly IGFBP-3, which normally sequesters ~75–90% of endogenous IGF-1 in the bloodstream. The result is a largely unbound, biologically active peptide with an extended plasma half-life. It is produced by recombinant protein expression (e.g., Pichia pastoris and CHO-based systems) and is sold strictly as a research-use-only (RUO) reagent; it has no approved therapeutic indication in any jurisdiction.

Appearance

White to off-white lyophilized powder

Solubility

Soluble in dilute acetic acid (0.1–1% v/v); limited solubility in water alone at…

Sequence · one-letter

Stability: Susceptible to protease degradation in biological fluids; maintain cold chain throughout storage and handling. Avoid exposure to oxidizing agents and prolonged

Vial sizes

1 mg · 0.1 mg

Purity grades

≥95% HPLC / ≥98% HPLC

Salt forms

Free base (primary)

• GHS hazard class on file
• PPE & spill response
• Disposal guidance
• Not-for-human-consumption posture

How much research exists, and of what maturity — never a verdict on whether it works.

Mechanism of action

• IGF-1 LR3 acts as a full agonist of the IGF-1 receptor (IGF-1R), a receptor tyrosine kinase widely expressed on skeletal muscle, cardiac muscle, bone, adipose, liver, and neural tissue
• Ligand binding triggers receptor autophosphorylation and initiates two principal downstream cascades: PI3K/AKT/mTOR, which drives protein synthesis, glucose uptake, and cell survival; and MAPK/ERK1-2, which promotes cellular proliferation and differentiation
• Because the structural modifications dramatically lower IGFBP binding affinity, a far greater fraction of administered peptide reaches IGF-1R in target tissues compared to equimolar native IGF-1, conferring approximately three-fold greater in vitro potency
• In fetal sheep models, infusion of LR3 IGF-1 promoted cardiac and skeletal muscle hyperplasia via ERK and PI3K signaling, increased organ weights, and stimulated myoblast proliferation, while also producing reductions in circulating branched-chain amino acids and insulin secretory capacity at supraphysiologic exposures, underscoring complex metabolic feedback through this axis

Pharmacokinetics (ADME)

Half-life

~20–30 hours (plasma, inferred from IGFBP-independent clearance kinetics); elimination half-life reported as approximately 56–72 hours in some reference tables

Clearance

Proteolytic clearance; IGFBP-independent elimination. Subcutaneous bioavailability estimated at ~70–80% with Tmax ~4–6 hours in non-clinical models. No validated human PK data available.

PK–PD note: PK figures are extrapolated from animal studies and manufacturer characterization data; no published controlled human pharmacokinetic trials exist. Contrast with native IGF-1 (plasma t½ ~10 min unboun…

Reading the evidence

• Evidence quality and gaps vary by application — see the cited grades above.
• Indexed-article counts span all evidence tiers, not only completed human trials.
• No first-party human-dosing, efficacy, or benefit claims are made here.

Key reviews & evidence-gap sources

• Bailes J, Soloviev M. Insulin-Like Growth Factor-1 (IGF-1) and Its Monitoring in Medical Diagnostic and in Sports. Biomolecules. 2021;11(2):217. — Umbrella review of IGF-1 network, IGFBPs, recombinant IGF-1 and derivatives; covers IGF-1R signaling (PI3K/Akt, Raf/MEK/ERK) and doping context. Not LR3-specific.
• Philippou A, Barton ER. Optimizing IGF-I for skeletal muscle therapeutics. Growth Horm IGF Res. 2014;24(5):157-163. — Review of IGF-I isoforms, signaling, and clinical trials of recombinant IGF-I (not LR3) for muscle therapy; tabulates human RCTs of rhIGF-I.
• Hakuno F, Takahashi S. IGF1 receptor signaling pathways. J Mol Endocrinol. 2018;61(1):T69-T86. — Mechanistic review of IGF1R → IRS/SHC → PI3K and Ras-MAPK cascades underpinning proliferation, differentiation, survival.
• Dominikowski A, et al. The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis. Front Endocrinol. 2026;17:1822475. — Recent review bridging clinical evidence and patient self-administration of GH-IGF1 axis peptides; addresses IGF-1 LR3 among performance-enhancing peptides.

No registered human trials found for this compound.

Status

No registered trials found

Summary (literature)

No controlled human safety data exist for IGF-1 LR3; zero registered clinical trials were identified in clinicaltrials.gov as of data capture. Anticipated risks, extrapolated from its pharmacological class, include: hypoglycemia from insulin-receptor cross-activation and enhanced…

WADA status

Prohibited — WADA 2026 Prohibited List Section S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics), prohibited at all times, both in- and out…

Dominant research route: Subcutaneous (SC) injection or continuous SC infusion in rat models (Tomas et al., 1996, J Endocrinol, PMID 8708565) is the dominant and best-cited research route for the LR3 analogue.

In vivo rat (Sprague-Dawley, normal and dexamethasone-catabolic); LR3IGF-I delivered SC for 7 days via osmotic pumps (continuous infusion) and by once- or twice-daily SC injection at 320–400 µg/day

Bioavailability: LR3IGF-I has very low affinity for rat IGF-binding proteins and is cleared from circulation more quickly than IGF-I; despite faster clearance, injected LR3IGF-I retained superior potency to injected IGF-I for several actions (e.g., body-weight gain, visceral organ weights, feed efficiency), though potency was reduced vs continuous infusion

Primary animal study (Tomas et al., 1996, J Endocrinol) directly compared SC infusion vs SC injection of LR3IGF-I in rats; this is the foundational route-of-administration evidence for the LR3 analogue. Not a human protocol.

No primary LR3-specific IM pharmacokinetic study located; community/secondary aggregator sources describe IM as a research route for localized muscle effects

Bioavailability: Community sources assert IM delivery provides higher local muscle concentration vs systemic SC distribution; no cited PK measurement for LR3 via IM was located in primary literature

IM route for LR3 appears in aggregator/community guidance rather than peer-reviewed LR3-specific PK data; de-identified aggregate only. Wikipedia lists 'Injection' generically without distinguishing IM vs SC.

Mentioned in secondary aggregator sources as a rodent-model research route (e.g., 0.1–1.0 mg/kg SC or IP in rodent models); no LR3-specific IP PK primary study located

Bioavailability: No primary PK characterization of LR3 via IP retrieved; route referenced only in aggregate rodent-protocol descriptions

IP appears in community/aggregator rodent-protocol summaries; not corroborated by a retrieved primary LR3 IP study. De-identified aggregate.

Continuous 'infusion' in Tomas 1996 was subcutaneous via osmotic pumps, not IV; no LR3-specific IV bolus/infusion PK study located. Native rhIGF-I IV/subcutaneous PK studies exist but are not LR3.

Bioavailability: No LR3-specific IV bioavailability data retrieved; native IGF-I PK (e.g., hemodialysis patients, SC 50–100 µg/kg) is not directly transferable to the LR3 analogue

IV route not established for LR3 in retrieved primary literature; the Tomas 1996 'infusion' arm was SC osmotic pump. Native IGF-I human PK studies (PubMed 7752586) used SC, not LR3.

No oral LR3 formulation studied; aggregator sources state there is no oral or topical version in research use

Bioavailability: Not studied. As an 83-amino-acid peptide/protein, LR3 would be subject to gastrointestinal proteolysis; no oral bioavailability figure exists for LR3

Oral stability ≠ oral absorption: the peptide is expected to be proteolytically degraded in the GI tract, but no LR3 oral absorption/PK study was retrieved. Aggregator sources confirm no oral research form exists.

Animal & human figures are kept visibly separate so studied animal doses are never misread as human guidance.

Sorted A–Z by vendor — never by price

Weekly median $/mg from the live vendor crawl.

Researched storefront prices, bucketed

p25 $87.50 · median $94.99 · p75 $147.50 · 6 researched vendors

Legit, COA-backed band: $50.00–$120.00/mg.

Value rule: don't just buy the cheapest — a price under $3/mg is a red flag. Pair price with COA and independent-test grade.

Estimated cost of research (10 mg)

Vial (best researched price)

$800

Bacteriostatic water (generic estimate)

$6

Syringes / supplies (generic estimate)

$12

What each test proves — general guidance, plus this compound's researched purity data

Independent labs cited for this compound

Buyer red-flag checklist

• No COA / in-house only
• Price < ~$3/mg
• Crypto-only payment
• No contact info
• No reship policy
• Old or photoshopped COA (> 6 mo)

GMP vs research-grade: the chemistry (SPPS + HPLC + MS) is identical — the difference is the quality system.

• An RUO label is not an import exemption — CBP judges actual intended use.
• Lyophilized powder is ambient-stable in transit; temperature control needed for > 7-day transit.
• US-warehouse vendors dodge import scrutiny — they cost more but ship more reliably.

Every item dated & sourced

Prohibited at all times (in- and out-of-competition). IGF-1 is included on the WADA Prohibited List under the class of peptide hormones, growth factors and related substances (S2). All forms of exogenous IGF-1 are prohibited at all times; any substance containing any form of exogenous IGF-1 should be considered prohibited.

No granted patents identified in current seed. Composition-of-matter coverage is limited given the peptide's synthetic origin.

• IACUC / IRB research context
• RUO buyer responsibilities & documentation
• Veterinary / alternative-use where lawful
• Jurisdiction-aware "who may lawfully obtain"

What people discuss

Reported concerns — discussion, not established effects

Reading caveats

• self-experimentation community
• bodybuilding-adjacent discourse
• survivorship bias toward responders
• vendor-affiliated aggregator pages present
• anecdotal logs unverified

Manually researched from reddit, youtube, x— theme weights are research estimates, not live counts; aggregated & de-identified. No individual posts, quotes, or usernames are ever shown.

Relative research / market volume — populated once the activity stream is wired

Inline tooltips for lyophilized, RUO, EU/mg, SPPS, 503A and more.

Toggle plain-language ↔ scientific in the header.

• How to read a COA
• Free base vs acetate
• Understanding evidence grades

Engineered 83-aa IGF-1 analog with Arg3 substitution and 13-aa N-terminal extension; markedly reduced IGFBP binding and extended half-life vs. native IGF-1. Approximately 10 articles are indexed (literature last scanned 2026-05-29). US regulatory status: Research use only; not FDA-approved; not compoundable. Research use only.

Emitted as JSON-LD: ChemicalSubstance · BreadcrumbList · FAQPage.

• Price-drop & back-in-stock alerts
• Regulatory-change email digest
• Print / share this datasheet