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Hormone signaling · Compound guide
Explore the mechanisms, study findings and evidence limits behind this research topic.
Product artwork identifies the SRP listing. It does not demonstrate safety or clinical benefit. The evidence guide and its sources follow below.
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IGF-1 LR3 (Long R3 IGF-1 / Long-[Arg3]IGF-I / LR3IGF-I) is an 83-amino-acid recombinant analog of mature human insulin-like growth factor I: a 13-residue N-terminal extension plus the 70-residue IGF-I chain with Arg substituted for Glu at position 3. It is not endogenous somatomedin C, not recombinant human IGF-1 / mecasermin (Increlex), not mecasermin rinfabate (IPLEX), not [Arg3]IGF-I without the Long extension, and not IGF-1 DES(1-3). Opened evidence is cell-culture and animal-reagent work. No opened ClinicalTrials.gov study names Long R3 / IGF-1 LR3 as an intervention. Human efficacy of a research-market 1 mg vial is not established. Research use only. Not medical advice. Not for human use.
Educational information only. This page describes an investigational laboratory research protein analog. It is not medical advice. Simple Research Peptides (SRP) materials are for laboratory research only and are not for human or veterinary use, consumption, administration, diagnosis, treatment, or therapeutic application. The opened SRP listing is a 1 mg lyophilized research compound in a 3 mL research vial. Sequence, CAS, UNII, molecular formula, and a public COA were not printed on the fetched SRP page. No human dosing, reconstitution, or administration protocol appears on this page. Historical animal µg/day and mg/kg figures are study conditions from opened papers, not instructions.
SRP product and index pages do not print a sequence, CAS, UNII, molecular formula, or a public COA. Identity below is taken only from opened public registries and primary papers that name Long-[Arg3]IGF-I, Long R3 IGF-I, LR3IGF-I, or IGF-1 LR3.
One-sentence identity: IGF-1 LR3 is an 83-amino-acid recombinant analog of mature human IGF-I (13-residue N-terminal extension plus the 70-residue IGF-I chain with Arg substituted for Glu at position 3). It is not endogenous somatomedin C, not mecasermin / Increlex, not mecasermin rinfabate / IPLEX, not [Arg3]IGF-I without the Long extension, and not IGF-1 DES(1-3). This is a defined literature / registry object, not a sequence printed on the SRP vial page.
| Identifier | Value on opened page | Source opened |
|---|---|---|
| Trade / development names | Long-(Arg3)insulin-like growth factor-I; Long R3 insulin-like growth factor-I; IGF-1 LR3; insulin-like growth factor long chain R3; Long-[Arg3]IGF-I; LR3IGF-I; Long R3 IGF-I | NCATS UNII M9L22Y19H9; Francis 1992 PMID 1378742; Tomas 1992 PMID 1371669 (full PDF); BMRB 4494 |
| Systematic / CAS-style name on NCATS | 1-13-somatotropin (swine reduced), 1-L-methionine-12-L-valine-, (13→1′)-protein with 3-L-arginine insulin-like growth factor I (human) | NCATS M9L22Y19H9 |
| SRP listing name | IGF-1 LR3 (1 mg Vial); page also prints “IGF-1 LR3 (1 mg / 3 mL Vial)” | SRP product page |
| SRP also-known-as line | Insulin-Like Growth Factor-1 Long R3, Long R3 IGF-1 | SRP product page |
| SRP listed strength / format | 1 mg lyophilized research compound in a 3 mL research vial | SRP product page |
| SRP SKU | Not printed on the fetched product page | SRP product page |
| SRP store / research category | Growth / Recovery Research | SRP product page (store taxonomy, not a clinical indication) |
| SRP index listing | “IGF-1 LR3 (1 mg Vial)” under Growth; “Evidence profile”; evidence tag Laboratory reagent evidence; field Growth-factor research | SRP compound-research-guides index |
| Chemical class | Recombinant single-chain IGF-I analog (protein, not a short linear peptide) | NCATS substance class protein; Francis 1992; Laajoki 2000 |
| Residue count | 83 | NCATS subunit length 83; BMRB 4494 “83 residues”; Laajoki 2000 (13-aa extension + Glu3→Arg) |
| Sequence printed on opened pages | MFPAMPLSSLFVNGPRTLCGAELVDALQFVCGDRGFYFNKPTGYGSSSRRAPQTGIVDECCFRSCDLRRLEMYCAPLKPAKSA | NCATS M9L22Y19H9 subunit; BMRB 4494 FASTA (same string) |
| N-terminal extension (as printed) | Met-Phe-Pro-Ala-Met-Pro-Leu-Ser-Ser-Leu-Phe-Val-Asn (13 aa). Francis 1992: first 11 residues of methionyl porcine GH plus Val-Asn. Tomas 1992 PDF: “N-terminal extension Met-Phe-Pro-Ala-Met-Pro-Leu-Ser-Ser-Leu-Phe-Val-Asn.” | Tomas 1992 full PDF; Francis 1992 abstract; BMRB vector p[MET1]pGH(1-11)-VAL-ASN-[ARG3]-IGF-I |
| Position-3 substitution | Glu-3 of the human IGF-I sequence replaced by Arg. On the 83-aa numbering the IGF-I domain starts at residue 14 (Gly), so Arg is residue 16. | Francis 1992; Laajoki 2000; NCATS sequence GPR… after the 13-aa leader |
| Disulfide links (NCATS 83-aa numbering) | 19–61, 31–74, 60–65 (three intramolecular bridges) | NCATS API _disulfideLinks shorthand |
| Native mature IGF-I (for comparison; not this analog) | GPETLCGAELVDALQFVCGDRGFYFNKPTGYGSSSRRAPQTGIVDECCFRSCDLRRLEMYCAPLKPAKSA (70 aa). UniProt P05019 chain 49–118. Rinderknecht 1978: 70 residues, calculated MW 7649. Increlex label: “70 amino acids… molecular weight of 7649 Da… sequence identical to endogenous human IGF-1.” | UniProt P05019; NCATS mecasermin 7GR9I2683O; PMID 632300; DailyMed Increlex. NOT the SRP vial. |
| UniProt for endogenous IGF-1 (not LR3) | P05019 (IGF1_HUMAN). Reviewed Swiss-Prot. 195-aa precursor; mature chain 49–118. Gene IGF1 / GeneID 3479. MIM 147440 (gene), 608747 (IGF1 deficiency). | UniProt REST JSON + FASTA, opened 16 August 2026 |
| PubChem compound CID for IGF-1 LR3 / Long R3 IGF-1 / Long Arg3 IGF-I | None. Name lookups returned HTTP 404 / PUGREST.NotFound. CAS 143045-27-6 xref/RN also 404 (no CID). | PubChem PUG REST, opened 16 August 2026 |
| PubChem substance SID (GSRS deposit) | SID 375085922 (source id M9L22Y19H9; synonyms include IGF-1 LR3, 143045-27-6, LONG R3 INSULIN-LIKE GROWTH FACTOR-I). SID 381123731 also returned on the name lookup; not re-opened as a second identity. | PubChem substance JSON |
| CAS printed for Long-(Arg3)IGF-I | 143045-27-6 (NCATS PRIMARY; PubChem SID 375085922 RN) | NCATS M9L22Y19H9; PubChem SID |
| Marketplace CAS 946870-92-4 | PubChem xref/RN resolved to CID 168009904, title a C80H154N4O6S2 lipid/amine (InChIKey CRZOPHSORDIMRX-UHFFFAOYSA-N). Rejected. Not used. | PubChem PUG REST + compound page |
| UNII | M9L22Y19H9. Display name LONG-(ARG3)INSULIN-LIKE GROWTH FACTOR-I. Approval Year Unknown. Development status Other. Record status “approved” is a GSRS record flag, not an FDA drug approval. | https://drugs.ncats.io/drug/M9L22Y19H9 |
| NCATS name search LONG R3 IGF-1 (quoted) | total 0. The hit required LONG ARG3. | NCATS API |
| IUPHAR / GtoPdb ligand for Long R3 / IGF-1 LR3 | No ligand. Search Long R3 returned HTTP 404. | IUPHAR services, opened 16 August 2026 |
| IUPHAR ligand for native / recombinant IGF-1 (not LR3) | Ligand 4971, name insulin-like growth factor 1, INN mecasermin, approved true, FDA (2005), species Human, gene IGF1, precursor prepro-insulin-like growth factor I. NOT the SRP vial. | IUPHAR HTML + services |
| ClinicalTrials.gov (LR3 / Long R3 / Long Arg3 / LR3IGF / IGF-1 LR3) | 0 studies | CT.gov API v2, opened 16 August 2026 |
| ClinicalTrials.gov query.intr=mecasermin | Studies exist for rhIGF-1 / Increlex / rhIGF-1/rhIGFBP-3, not for Long R3. Examples opened: NCT00764699, NCT01406444, NCT02386839, NCT00572156, NCT01588093. Not the SRP vial. | CT.gov API v2 |
| NCT01767909 (seen as a data citation on Engel 2025) | SNIFF trial of intranasal insulin (Humulin R), not LR3. Unused as LR3 evidence. | CT.gov API v2 |
| openFDA / Drugs@FDA | INCRELEX / mecasermin = BLA021839, approved 2005-08-30, UNII 7GR9I2683O. No Long R3 / IGF-1 LR3 application. NOT the SRP vial. | openFDA Drugs@FDA JSON |
| FDA-approved Long R3 / IGF-1 LR3 product | None on the opened NCATS / openFDA / IUPHAR / CT.gov pages | NCATS Approval Year Unknown; IUPHAR no ligand; CT.gov 0 |
What the molecule actually is. Francis, Ross, Ballard, Wallace and colleagues (1992, PMID 1378742) expressed E. coli fusion peptides built from the first 11 amino acids of methionyl porcine GH plus Val-Asn fused to human IGF-I, including the Glu-3→Arg variant they named Long [Arg3]-IGF-I. Tomas et al. 1992 (PMID 1371669; full PDF opened) print the same chemistry as “arginine replacing glutamate at position 3 of human IGF-I and the N-terminal extension Met-Phe-Pro-Ala-Met-Pro-Leu-Ser-Ser-Leu-Phe-Val-Asn,” supplied as recombinant human LR3IGF-I by GroPep. BMRB entry 4494 and NCATS UNII M9L22Y19H9 store the matching 83-residue FASTA. Laajoki et al. 2000 (PMID 10744677) determined the NMR solution structure and attributed reduced IGFBP affinity to reorientation of the N-terminal three residues of the IGF-I domain. A research vial labeled “IGF-1 LR3” is not chemically identified until that 83-aa Long-[Arg3] sequence, fold, and disulfide pairing are confirmed analytically.
Naming that must not be collapsed.
Registry chaos that must not be collapsed.
Not printed on SRP pages and therefore not claimed as SRP-verified: amino-acid sequence, CAS, UNII, disulfide pairing, folding, endotoxin, bioactivity, or a public COA file. The product page prints “COA (Certificate of Analysis) available for batch verification” as a catalog bullet. That bullet is not an opened analytical package.
This page is Long-[Arg3]IGF-I / IGF-1 LR3 only. Catalog “IGF-1” or “growth peptide” language is a nickname, not a chemical identity.
| Identity | What opened sources actually describe | Length | Typical literature role |
|---|---|---|---|
| Endogenous IGF-1 / somatomedin C | UniProt P05019 mature chain 49–118; Rinderknecht 1978 (PMID 632300): 70 aa, MW 7649, three disulfides, proinsulin homology. Woods 1996 (PMID 8857020): human IGF1 gene deletion → IUGR and postnatal growth failure. | 70 aa | Circulating GH-axis effector. Not the analog. |
| Mecasermin / Increlex (NOT the SRP vial) | NCATS UNII 7GR9I2683O; sequence identical to mature human IGF-1; CAS 68562-41-4 (PRIMARY) / 67763-96-6 (family); DrugBank DB01277; IUPHAR 4971; BLA 021839; FDA 2005. DailyMed: 70 aa, 7649 Da, E. coli rhIGF-1. | 70 aa | Approved pediatric rhIGF-1 for severe primary IGFD / GH-gene-deletion neutralizing antibodies. Not Long R3. NOT the SRP vial. |
| Mecasermin rinfabate / IPLEX (NOT the SRP vial) | NCATS UNII NZ8M50KKRG; two subunits (264-aa IGFBP-3 + 70-aa IGF-1); CAS 478166-15-3; DrugBank DB14751. CT.gov NCT02386839 used rhIGF-1/rhIGFBP-3. | Complex | Co-formulated IGF-1 + IGFBP-3. Opposite of an IGFBP-resistant analog. NOT the SRP vial. |
| [Arg3]IGF-I or [Gly3]IGF-I (no Long) | King 1992 (PMID 1311930): 70-aa peptides after cleavage of a pGH(1-46)-Val-Asn fusion. Poor bovine IGFBP-2 binding; slightly lower type-1 receptor binding; more potent than IGF-I on L6 myoblasts. | 70 aa | Position-3 point mutants. Not the 83-aa Long form. |
| des(1-3)IGF-I / IGF-1 DES | Ballard 1996 (PMID 8930132): Gly-Pro-Glu removed from the N-terminus; isolated from bovine colostrum, human brain, porcine uterus; ~10-fold more potent in culture because Glu-3 is gone. | 67 aa | Truncated analog. Francis 1992 compared it with Long [Arg3]; they are not interchangeable. |
| Long IGF-I (Glu-3 retained) | Francis 1992: [Met1]-pGH(1-11)-Val-Asn-IGF-I. More potent than IGF-I in IGFBP-secreting cells, less potent than Long [Arg3] or des(1-3). | 83 aa | Extension-only analog. Not R3. |
| Mechano growth factor / IGF-1Eb | UniProt alternative name on P05019; splice/E-peptide biology. UniProt alternative-name / splice-product biology; not opened as an LR3 paper. | Different product | Not Long R3. |
| IGF-1 LR3 / Long-[Arg3]IGF-I (this page) | 13-aa pGH-derived extension + E3R; 83 aa; UNII M9L22Y19H9; CAS 143045-27-6; BMRB 4494 | 83 aa | Cell-culture / animal reagent; no opened human trial |
Native IGF-1 is a 70-aa serum peptide that spends most of its circulating life in an IGFBP-3 / ALS ternary complex (Increlex label §12.3: “>80% bound as a complex with IGFBP-3 and an acid-labile subunit”). Long R3 was built so that IGFBP binding is poor (Francis 1992; Tomas 1992; Laajoki 2000). Using somatomedin-C physiology as if it were LR3 pharmacology is a category error.
Increlex is 70-aa rhIGF-1 whose sequence “is identical to that of endogenous human IGF-1” (DailyMed description). NCATS, IUPHAR, openFDA, and the Increlex label do not list an Arg3 substitution or a 13-aa leader. Chernausek 2007 (PMID 17192294) and the Increlex pooled pediatric program are mecasermin data. They are labeled on this page as NOT the SRP vial.
DES removes the first three residues. Long R3 adds thirteen residues and replaces residue 3. Francis 1992 ranked Long [Arg3] with des(1-3) in IGFBP-secreting cells and below native IGF-I in chicken embryo fibroblasts that do not secrete detectable IGFBPs — the opposite of a potency-always-higher story.
King 1992 (PMID 1311930) made the 70-aa E3R/G3R peptides by cleaving a longer fusion. Those reagents share the Arg3 idea and the IGFBP-resistance logic; they do not contain the Long leader that Laajoki showed reorients the IGF-I N-terminus. NCATS Approval Year is Unknown. IUPHAR has no Long R3 ligand. ClinicalTrials.gov returned zero Long R3 studies. openFDA’s Increlex record is mecasermin.
Opened primary papers support a working laboratory model. It is not a treatment claim for an SRP vial. Observed means a measurement on the opened paper or registry. Proposed means a mechanistic inference the authors or this page mark as such. Class / adjacent means distinction biology (mecasermin, native IGF-1). Not shown means absent from the opened record.
UniProt P05019: IGF-1 binds the IGF1R α-subunit, activates the receptor tyrosine kinase, and initiates PI3K–AKT and Ras–MAPK cascades; it also binds integrins and can form ternary complexes with IGF1R. Increlex label §12.1: Type 1 IGF-1 receptor activation stimulates processes that result in statural growth and has insulin-like effects on glucose, fatty-acid, and amino-acid uptake. Those sentences describe IGF-1 / mecasermin, not a research-market LR3 lot. NOT the SRP vial.
Francis 1992: N-terminal analogs show increased biological potency in IGFBP-secreting cells because of changed IGFBP interactions, not higher receptor affinity. In chicken embryo fibroblasts that do not secrete detectable IGFBPs, Long [Arg3]-IGF-I was less potent than IGF-I. King 1992 (the 70-aa Arg3/Gly3 pair): both analogs “bound very poorly to bovine IGF-binding protein-2 and slightly less well than IGF-I to the type-1 receptor.” Tomas 1992 PDF: LR3IGF-I “binds 3-fold less well than IGF-I to the type 1 IGF receptor” yet was ~2.5-fold more potent than IGF-I in dexamethasone-treated rats; the authors attribute that to poor IGFBP binding and faster blood-to-tissue transfer. (PMID 1378742; PMID 1371669; PMID 1311930.)
Laajoki 1997 (PMID 9450557) and 2000 (PMID 10744677): the IGF-I domain fold is largely retained; the major change is reorientation of the N-terminal three residues of the IGF-I domain; the 13-aa extension is flexible (negative heteronuclear NOEs) with some transitory structure. The authors interpret those N-terminal changes as the structural basis for lower IGFBP affinity. BMRB 4494 stores the 83-aa sequence used here.
In L6 myoblasts and other IGFBP-secreting lines, Long [Arg3] stimulated protein and DNA synthesis and inhibited protein breakdown more potently than IGF-I (Francis 1992). In dexamethasone-treated rats, LR3IGF-I improved body-weight change and nitrogen retention ~2.5-fold more potently than IGF-I and increased gut weight by up to 45% (Tomas 1992). In streptozotocin-diabetic rats, variants restored growth without restoring insulin-like control of glucosuria or Nτ-methyl-histidine excretion (Tomas 1993). In guinea pigs, LR3IGF-I increased fractional weights of adrenals, gut, kidneys, and spleen without increasing body-weight gain (Conlon 1995). In finisher pigs, LR3IGF-I decreased average daily gain, food intake, plasma GH, IGFBP-3, IGF-I, and insulin (Dunaiski 1997). Those are species- and model-specific reagent findings, not a human indication.
That a lyophilized 1 mg catalog protein is the folded 83-aa Long-[Arg3] chain with the three NCATS disulfides, low endotoxin, and the IGFBP-resistant pharmacology of GroPep / CSIRO material. That marketplace “20–30 hour half-life” figures (common on unopened vendor pages) apply to any lot. No opened paper printed a human LR3 half-life. Increlex’s labeled terminal t½ of 5.8 hours is mecasermin, and even that value is IGFBP-3–dependent (DailyMed §12.3). NOT the SRP vial.
A cloned “LR3 receptor” distinct from IGF1R / insulin receptor; human PK of an SRP vial; proof that research-market material is Long-[Arg3] rather than native IGF-1, [Arg3]IGF-I, DES, aggregated chain, or a mislabeled peptide; an FDA-approved LR3 drug; interchangeability with Increlex. IUPHAR has no Long R3 ligand. ClinicalTrials.gov returned 0 LR3 studies.
70 aa, three disulfides, calculated MW 7649, proinsulin homology. Used only so the 70-aa chain is not collapsed into the 83-aa analog. PMID 632300.
Extension = pGH(1-11) + Val-Asn. In IGFBP-secreting lines, potency order Long [Arg3] ≈ des(1-3) > Long [Gly3] > Long IGF-I > IGF-I. In CEF (no detectable secreted IGFBPs), Long [Arg3] was less potent than IGF-I. PMID 1378742.
Fusion leader cleaved off. Poor bovine IGFBP-2 binding. Not the Long analog. PMID 1311930.
Sequence printed; ~2.5× IGF-I potency; receptor 3-fold less well; gut +45%. Rat osmotic pumps. PMID 1371669. PMC 1130894.
Conlon 1995 (PMID 7561636): organ growth, no body-weight gain. Dunaiski 1997 (PMID 9488001): pigs decreased ADG and suppressed GH.
Solution structure of Long-[Arg3]IGF-I. BMRB 4494 stores the 83-aa sequence. PMID 10744677.
70-aa rhIGF-1. UNII 7GR9I2683O. NOT the SRP vial. PMID 17192294.
Intranasal LR3-IGF-1 in 5XFAD mice. Data citation NCT01767909 is the SNIFF insulin trial, not LR3. PMID 39610283.
Not shown on an opened page: a cloned “LR3 receptor” distinct from IGF1R; human PK of an SRP vial; proof that research-market material is the folded 83-aa Long-[Arg3] chain; a human LR3 half-life; an FDA-approved LR3 drug; interchangeability with Increlex. Marketplace “20–30 hour half-life” figures were not taken from an opened primary paper.
Label every row. LR3 ≠ native IGF-1 ≠ mecasermin / Increlex ≠ DES(1-3) ≠ [Arg3]IGF-I ≠ SRP vial. Human mecasermin numbers are historical facts about a different molecule. Historical µg/day and mg/kg figures from animal papers are facts from opened records, not reconstitution or dosing instructions for an SRP vial.
Francis et al. 1992, PMID 1378742: Long [Arg3]-IGF-I named; potency order in IGFBP-secreting lines; less potent than IGF-I in CEF. King 1992, PMID 1311930: 70-aa [Arg3]/[Gly3] after cleavage — not Long. Laajoki 2000, PMID 10744677: NMR; BMRB 4494. Xi 2004, PMID 15254966: rpIGFBP-3 still restrains LR3 proliferation. Cell systems. Not a vial COA. Not human.
Tomas 1992, PMID 1371669 (full PDF): dex-treated rats; ~2.5× IGF-I; gut +45%. Tomas 1993, PMID 7683875: diabetic rats; growth without insulin-like metabolism. Steeb 1995, PMID 8549937: 3-day rat gut. Conlon 1995, PMID 7561636: guinea-pig organs without body growth. Dunaiski 1997, PMID 9488001: pigs decreased ADG. Engel 2025, PMID 39610283: 5XFAD mice; plaque remodeling, no cognitive preservation. Usually GroPep / CSIRO material, not an SRP 1 mg vial.
DailyMed INCRELEX (mecasermin) label; openFDA BLA 021839; UNII 7GR9I2683O; CAS 68562-41-4; IUPHAR 4971; UniProt P05019. Chernausek 2007, PMID 17192294: rhIGF-I in children. Woods 1996, PMID 8857020: IGF1 gene deletion. CT.gov mecasermin NCTs exist; zero Long R3 NCTs. Every row in this block is NOT the SRP vial and is not Long R3.
CT.gov API v2 queries for IGF-1 LR3 / Long R3 / Long-R3 / Long Arg3 / LR3IGF each returned {"studies":[]}. NCATS Approval Year Unknown. IUPHAR: no Long R3 ligand. openFDA Increlex is mecasermin. Do not invent NCTs.
Native 70-aa IGF-1: PMID 632300; UniProt P05019. DES: Ballard 1996, PMID 8930132. Cleaved [Arg3]: King 1992, PMID 1311930. IPLEX / mecasermin rinfabate: UNII NZ8M50KKRG. Marketplace CAS 946870-92-4 / CID 168009904 rejected. Vendor PMID 1280101 is a pancreatic-acini paper, not Francis 1992.
Opened SRP page: IGF-1 LR3 (1 mg Vial); Growth / Recovery Research; 1 mg / 3 mL; also-known-as Long R3 IGF-1; research use only. Sequence, CAS, UNII, molecular formula, SKU, and a public COA were not printed. Index tag: Laboratory reagent evidence. Product page.
Read the “what it did not show” column. Published study designs are historical facts from those papers. They are not a protocol. Animal µg/day and mg/kg figures are study conditions, not instructions for an SRP research vial. Evidence snapshot date: 16 August 2026, America/Indianapolis.
| Study | Species / model | What was tested | Actual finding (from the opened record) | What it did not show |
|---|---|---|---|---|
| Rinderknecht & Humbel, 1978 PMID 632300. DOI 10.1016/s0021-9258(17)40889-1. Opened abstract. Distinction only. |
Human serum IGF-I | Native sequence | Defines mature IGF-1, not LR3. 70 aa, three disulfides, calculated MW 7649, proinsulin homology. Used only so the 70-aa chain is not collapsed into the 83-aa analog. | Anything about Long R3. An SRP-vial identity. A human LR3 trial. |
| King et al., 1992 PMID 1311930. DOI 10.1677/jme.0.0080029. Opened abstract. Distinction: [Arg3] not Long. |
E. coli fusion → cleaved [Gly3]-IGF-I and [Arg3]-IGF-I (70 aa); rat L6 myoblasts; bovine IGFBP-2 | Position-3 point mutants without the Long leader | Both analogs more potent than IGF-I on protein/DNA synthesis and protein-breakdown inhibition. Bound very poorly to bovine IGFBP-2 and slightly less well than IGF-I to the L6 type-1 receptor. Authors: reduced IGFBP binding, not increased receptor binding, explains potency. Not Long R3. | The 83-aa Long analog. An SRP vial. Human data. |
| Francis et al., 1992 PMID 1378742. DOI 10.1677/jme.0.0080213. Opened abstract. Defines Long [Arg3]. |
E. coli Long IGF-I, Long [Gly3]-IGF-I, Long [Arg3]-IGF-I; L6 myoblasts; H35 hepatoma; chicken embryo fibroblasts | Defines the Long [Arg3] name | Extension = pGH(1-11) + Val-Asn. In IGFBP-secreting lines, potency order Long [Arg3] ≈ des(1-3) > Long [Gly3] > Long IGF-I > IGF-I. In CEF (no detectable secreted IGFBPs), Long [Arg3] was less potent than IGF-I. Receptor/IGFBP association “reinforced… increased biological potency due to changes in the degree of their IGFBP interactions.” Not a vial COA. Not human. | Human data. A public COA for a research-market vial. Proof that an SRP lot is GroPep material. |
| Laajoki et al., 1997 PMID 9450557. DOI 10.1016/s0014-5793(97)01496-8. Opened Europe PMC core abstract. |
15N-labelled Long-[Arg-3]-IGF-I NMR | Secondary structure | IGF-I domain “almost identical” to IGF-I; N-terminal seven extension residues have few medium/long-range NOEs; next five form a turn near helix 1. Interpreted as increased potency and decreased IGFBP binding. | Human PK. An SRP-vial fold confirmation. A crystal structure of a marketplace lot. |
| Laajoki et al., 2000 PMID 10744677. DOI 10.1074/jbc.275.14.10009. Opened abstract. |
15N Long-[Arg3]IGF-I NMR + dynamics | Solution structure | Helix backbone RMSD 0.82 ± 0.28 Å. Major change vs IGF-I: reorientation of the N-terminal three residues of the IGF-I domain, interpreted as lower IGFBP affinity. Extension flexible (negative hetNOEs) with some transitory structure. BMRB 4494 stores the 83-aa sequence used here. | Human data. Proof a catalog vial matches this NMR construct. |
| Gajanandana et al., 1998 PMID 9582496. DOI 10.1677/joe.0.1560407. Opened abstract. |
LR3IGF-I ELISA vs IGF-I/II; cow plasma after LR3 treatment | Analog-specific assay | Detected 50 pg / 100 µl; native IGF-I and -II <0.01% cross-reactivity; IGFBPs did not affect the ELISA. Used to measure LR3 in cows given a “pharmacologically active dose.” Animal assay paper, not human PK. | Human PK of an SRP vial. A clinical immunoassay claim. |
| Xi et al., 2004 PMID 15254966. DOI 10.1002/jcp.20068. Opened abstract. |
L6 myoblasts; recombinant porcine IGFBP-3 vs IGF-I and Long-R3-IGF-I | Does IGFBP-3 still restrain LR3? | rpIGFBP-3 suppressed both IGF-I- and Long-R3-stimulated proliferation (IGF-dependent and IGF-independent). It suppressed IGF-I-stimulated differentiation but not Long-R3-stimulated differentiation. Cell line. Not a vial bioassay. | Human muscle. An SRP-lot bioassay. A treatment claim. |
| NCATS M9L22Y19H9 + BMRB 4494 + UniProt P05019 | Human reference sequences | Identity map | 83-aa Long-(Arg3) record with CAS 143045-27-6 and UNII M9L22Y19H9; native precursor P05019 / 70-aa mature chain. PubChem CID not found. | An FDA approval for Long R3. A CID. An SRP COA. |
These rows test infused or added Long R3 / LR3IGF-I, usually GroPep / CSIRO recombinant material, not an SRP 1 mg vial. Historical µg/day and mg/kg figures are study conditions, not instructions.
| Study | Species / model | What was tested | Actual finding (from the opened record) | What it did not show |
|---|---|---|---|---|
| Tomas et al., 1992 PMID 1371669. PMC 1130894. DOI 10.1042/bj2820091. Opened full PDF. |
150 g male Hooded Wistar rats; dexamethasone 20 µg/day; osmotic-pump IGF-I, des(1-3)IGF-I, or LR3IGF-I | Catabolic-rat anabolism | Dex-only: −19 g / 7 days. IGF-I 695 µg/day: +6 g. des(1-3) and LR3 ~2.5-fold more potent than IGF-I on weight and nitrogen retention. LR3 binds type-1 receptor 3-fold less well than IGF-I. Gut weight up to +45%. Fractional carcass weight stayed low; carcass gain was nitrogen, not fat. 3MH excretion fell; muscle Ks only partly restored (highest Ks still ~60% of pair-fed). Thymus atrophy not reversed. Rat osmotic pumps. Historical µg/day figures are not vial instructions. | Human anabolism. An SRP-vial protocol. Reversal of all catabolic features. |
| Tomas et al., 1993 PMID 7683875. PMC 1132436. DOI 10.1042/bj2910781. Opened abstract. |
Streptozotocin-diabetic ~160 g rats; IGF-I, des(1-3), LR3-IGF-I; insulin 30 IU/day reference | Growth vs insulin-like metabolism | IGF-I 695 µg/day: +48.1 ± 1.7 g / 7 days vs +11.0 ± 2.8 g vehicle. Variants 2.5–3× more potent than IGF-I. Insulin gained more weight, but the extra gain was fat. IGFs did not decrease glucosuria or Nτ-MH excretion; insulin did. Authors: IGFs restore growth without restoring all insulin-dependent liver/muscle/adipose processes. Diabetic rat. Not human diabetes. | Human diabetes treatment. Insulin replacement. An SRP-vial indication. |
| Steeb, Trahair, Read, 1995 PMID 8549937. PMC 1382866. DOI 10.1136/gut.37.5.630. Opened abstract. |
Female rats ~110 g; 3-day infusion IGF-I or LR3IGF-I 2.5 mg/kg/day | Short-term gut mitogenesis | LR3IGF-I, not IGF-I, increased body weight and small- and large-intestine wet weight +20%. Duodenal/ileal crypt length +13% / +22% with LR3 only. Both peptides raised thymidine labelling (up to 14%); only LR3 enlarged the crypt compartment. Authors: LR3 more potent and faster. 3-day rat infusion. | Human gut growth. A chronic program. An SRP-vial instruction (2.5 mg/kg/day is a historical rat exposure). |
| Conlon et al., 1995 PMID 7561636. DOI 10.1677/joe.0.1460247. Opened abstract. |
Female guinea pigs ~350 g; 7-day IGF-I, IGF-II, or LR3IGF-I 120 µg/day (IGFs also 360 µg/day) | Species with circulating IGF-I and IGF-II | No significant effect on body-weight gain, feed intake, feed conversion, or carcass composition. High-dose IGF-I increased adrenal fractional weight only. LR3IGF-I increased fractional weight of adrenals, gut, kidneys, and spleen without stimulating overall growth. IGF-I and IGF-II infusions did not raise total circulating IGF; LR3 still grew selected organs. Guinea pig. Organ growth ≠ body growth. | A simple “more IGF = more growth” claim. Human organ-growth safety. An SRP-vial protocol. |
| Dunaiski, Dunshea, Walton, Goddard, 1997 PMID 9488001. DOI 10.1677/joe.0.1550559. Opened abstract. |
Finisher pigs; 4-day LR3IGF-I 180 µg/kg/day ± pGH 30 µg/kg/day; IGF-I comparator | Livestock growth | LR3IGF-I decreased average daily gain, food intake, plasma IGFBP-3, IGF-I, and insulin. Mean plasma GH −23%; area under GH peaks −60%. pGH co-administration did not restore those suppressions. IGF-I decreased insulin and mean GH but did not significantly change IGFBP-3, ADG, or feed intake. Plasma glucose unchanged. Authors: GH suppression may explain the inhibitory effect of LR3 on pig growth. Opposite of a simple “more IGF = more growth” claim. | Human muscle gain. Transferability to people. An SRP-vial livestock or bodybuilding protocol. |
| Engel et al., 2025 PMID 39610283. PMC 12617435. DOI 10.1177/13872877241299056. Opened abstract. |
Male wild-type and 5XFAD mice; 7 months (ages 3–10) intranasal LR3-IGF-1 vs vehicle; n = 19–27/group | Alzheimer-model cognition / Aβ | Improved body composition. Did not significantly alter cognitive symptoms on multiple assays. Cortex: fewer filamentous plaques, more inert plaques, lower low-MW Aβ oligomers. In vitro, LR3 enhanced BV2 uptake of Aβ1-42 and actin-remodeling / endocytosis gene pathways. Authors: does not support LR3 as monotherapy; plaque remodeling without preserved cognition. Mouse IN study. Not a human AD trial. The paper’s CT.gov data citation NCT01767909 is the SNIFF insulin trial, not LR3. | A human Alzheimer trial of LR3. Cognitive benefit. An SRP-vial CNS protocol. |
These rows are historical facts about mecasermin / Increlex / endogenous IGF-1. They are not Long R3 evidence and they are not the SRP vial.
| Study / record | What was tested | Actual finding (from the opened record) | Why it is not the SRP vial |
|---|---|---|---|
| DailyMed INCRELEX (mecasermin) label setid a8b27a1b-a611-4f91-ad22-76d4b390c3ae, revised 07/2025. Opened HTML. NOT the SRP vial. |
70-aa rhIGF-1, BLA 021839 | Pediatric indication: growth failure in patients ≥2 y with severe primary IGF-1 deficiency (height SDS ≤ −3.0, basal IGF-1 SDS ≤ −3.0, normal/elevated GH) or GH-gene deletion with neutralizing GH antibodies. 70 aa, 7649 Da, sequence identical to endogenous IGF-1. Warnings include hypoglycemia, hypersensitivity, intracranial hypertension, lymphoid hypertrophy, SCFE, scoliosis progression, malignant neoplasia, benzyl-alcohol risk in infants. Pooled 71-subject program: year-1 height velocity 2.8 → 8.0 cm/yr. Terminal t½ after 0.12 mg/kg SC in n=3: 5.8 h. | Mecasermin, not Long R3. NOT the SRP vial. Label never names Arg3 or an 83-aa extension. UNII 7GR9I2683O; CAS 68562-41-4; BLA 021839. |
| openFDA Drugs@FDA INCRELEX / BLA021839 Opened JSON. NOT the SRP vial. |
Regulatory file | Priority NME, orphan, approved 2005-08-30; UNII 7GR9I2683O. | Same: approved 70-aa product. NOT the SRP vial. |
| Chernausek et al., 2007 PMID 17192294. DOI 10.1210/jc.2006-1610. Opened Europe PMC core abstract. Mecasermin-class. NOT the SRP vial. |
rhIGF-I in 76 children with GH-insensitivity IGF-I deficiency; up to 12 y | Height velocity 2.8 → 8.0 cm/yr in year 1 (P < 0.0001); remained above baseline up to 8 y. Hypoglycemia 49%; lipohypertrophy 32%; tonsillar/adenoidal hypertrophy 22%. | rhIGF-I / mecasermin-class. Not Long R3. NOT the SRP vial. |
| Woods et al., 1996 PMID 8857020. DOI 10.1056/nejm199610313351805. Opened page (no abstract text). Distinction only. |
Human IGF1 gene deletion | Title: intrauterine growth retardation and postnatal growth failure associated with deletion of the IGF-I gene. UniProt cites this for IGF1 deficiency (MIM 608747). | Endogenous-gene human biology. Not LR3. NOT the SRP vial. |
| CT.gov query.intr=mecasermin (opened 16 August 2026) NOT the SRP vial. |
Increlex / rhIGF-1 / rhIGF-1+IGFBP-3 | NCT00764699 (Increlex, Crohn, terminated); NCT01406444 (rhIGF-1, anorexia, completed); NCT02386839 (rhIGF-1/rhIGFBP-3, ROP follow-up, completed); NCT00572156 (Increlex + somatropin, terminated); NCT01588093 (Increlex, muscle glucose, completed). | Mecasermin or IGF-1/IGFBP-3. NOT the SRP vial. Zero Long R3 NCTs on the LR3-term query. |
| Question | Opened-record answer |
|---|---|
| Is IGF-1 LR3 a defined molecule? | Yes, as a literature / registry object. 83-aa Long-[Arg3]IGF-I; sequence concordant on NCATS M9L22Y19H9, BMRB 4494, and Tomas 1992. |
| Did SRP print that sequence? | No. 1 mg / 3 mL vial; no sequence, CAS, UNII, or public COA. |
| Is there a UNII / CAS? | UNII M9L22Y19H9; CAS 143045-27-6. Marketplace CAS 946870-92-4 rejected (CID 168009904). |
| PubChem CID? | Not found. |
| IUPHAR ligand? | Not found for Long R3. Ligand 4971 is IGF-1 / mecasermin. NOT the SRP vial. |
| Human LR3 trial? | None on opened CT.gov LR3 queries. No LR3 NCT. |
| Strongest LR3-specific evidence? | Francis 1992 (defines the analog); Tomas 1992/1993 (rat anabolism, with important limits); Steeb 1995 (gut); Conlon 1995 (guinea-pig organs without body growth); Dunaiski 1997 (pigs: growth down); Laajoki 2000 (structure); Engel 2025 (mice: plaque remodeling, no cognitive preservation). |
| Does that equal human efficacy of a 1 mg vial? | No. |
| Is Increlex evidence transferable? | No. Different sequence, IGFBP binding, and regulatory object. NOT the SRP vial. |
| Popular claim | Status after this review |
|---|---|
| “IGF-1 LR3 is the same as IGF-1 / somatomedin C” | False identity. 83-aa analog vs 70-aa native chain. |
| “It is Increlex / mecasermin” | False. Increlex is 70-aa rhIGF-1 (UNII 7GR9I2683O; BLA 021839; CAS 68562-41-4). NOT the SRP vial. |
| “It is IPLEX / mecasermin rinfabate” | False. That product adds IGFBP-3. LR3 was built to avoid IGFBPs. NOT the SRP vial. |
| “It is IGF-1 DES / des(1-3)” | False. DES is a 67-aa truncation (PMID 8930132). |
| “CAS 946870-92-4 identifies Long R3” | Not used. PubChem mapped that RN to an unrelated lipid (CID 168009904). |
| “PMID 1280101 is the Francis Long R3 paper” | False. Opened 1280101 is a pancreatic-acini paper. Use 1378742. |
| “Human trials proved research-market LR3 builds muscle” | Unsupported. 0 LR3 NCTs. Mecasermin trials are a different molecule. |
| “Pigs and rats both grew on LR3, so people will” | False reading. Dunaiski 1997 pigs reduced gain; Conlon 1995 guinea pigs grew organs without body-weight gain. |
| “Increlex dosing can be copied onto an LR3 vial” | False and out of scope. Different molecule; SRP material is RUO only. This page does not provide dosing. |
| “There is an FDA-approved IGF-1 LR3 drug” | False on opened NCATS / openFDA / IUPHAR / CT.gov. |
| Research vial = GroPep / CSIRO study lot | Not established. No sequence/CAS/public COA on the SRP page. |
ClinicalTrials.gov returned 0 studies for IGF-1 LR3 / Long R3 / Long Arg3 / LR3IGF. Mecasermin NCTs are a different molecule and are labeled NOT the SRP vial.
PubChem compound CID not found. CAS 143045-27-6 has no CID. Marketplace 946870-92-4 maps to CID 168009904, an unrelated C80 lipid. Not used.
Rats retained nitrogen and grew gut. Guinea pigs grew organs without body-weight gain. Pigs lost gain and suppressed GH. 5XFAD mice remodeled plaques without preserving cognition.
Opened product page prints no sequence, CAS, UNII, or public COA. A catalog 1 mg lyophilizate is not established as the folded 83-aa BMRB 4494 chain.
Each card is a single opened record. Historical animal exposures are study conditions, not instructions. No LR3 NCT is attached because ClinicalTrials.gov returned 0 studies. Mecasermin cards are labeled NOT the SRP vial.
Novel recombinant fusion protein analogues of insulin-like growth factor (IGF)-I indicate the relative importance of IGF-binding protein and receptor binding for enhanced biological potency. Defines Long [Arg3]-IGF-I as [Met1]-pGH(1-11)-Val-Asn-[Arg3]-IGF-I. In IGFBP-secreting lines, potency order Long [Arg3] ≈ des(1-3) > Long [Gly3] > Long IGF-I > IGF-I. In chicken embryo fibroblasts that do not secrete detectable IGFBPs, Long [Arg3] was less potent than IGF-I. Not a vial COA. Not human. PMID 1378742. DOI 10.1677/jme.0.0080213.
Production and characterization of recombinant IGF-I and potent analogues with Gly or Arg substituted for Glu3, following expression in E. coli as fusion proteins. 70-aa [Arg3]/[Gly3] after cleavage of a pGH(1-46)-Val-Asn fusion. Bound very poorly to bovine IGFBP-2 and slightly less well than IGF-I to the type-1 receptor. Not the 83-aa Long analog. PMID 1311930. DOI 10.1677/jme.0.0080029.
IGF-I and especially IGF-I variants are anabolic in dexamethasone-treated rats. Prints the LR3IGF-I chemistry (Arg replacing Glu at position 3 plus the 13-aa Met-Phe-Pro-Ala-Met-Pro-Leu-Ser-Ser-Leu-Phe-Val-Asn extension); GroPep recombinant human LR3IGF-I. ~2.5-fold more potent than IGF-I on weight and nitrogen retention; binds type-1 receptor 3-fold less well; gut weight up to +45%. Rat osmotic pumps. Historical µg/day figures are not vial instructions. PMID 1371669. DOI 10.1042/bj2820091. PMC 1130894.
IGF-I and more potent variants restore growth of diabetic rats without inducing all characteristic insulin effects. Streptozotocin-diabetic rats. Variants 2.5–3× more potent than IGF-I. IGFs did not decrease glucosuria or Nτ-MH excretion; insulin did. Not human diabetes. PMID 7683875. DOI 10.1042/bj2910781. PMC 1132436.
Administration of IGF-I peptides for three days stimulates proliferation of the small intestinal epithelium in rats. LR3IGF-I, not IGF-I, increased body weight and small- and large-intestine wet weight +20%. Only LR3 enlarged the crypt compartment. 3-day rat infusion. Historical 2.5 mg/kg/day is a study condition, not an instruction. PMID 8549937. DOI 10.1136/gut.37.5.630. PMC 1382866.
Long R3 IGF-I infusion stimulates organ growth but reduces plasma IGF-I, IGF-II and IGF binding protein concentrations in the guinea pig. No significant effect on body-weight gain, feed intake, feed conversion, or carcass composition. LR3IGF-I increased fractional weight of adrenals, gut, kidneys, and spleen without stimulating overall growth. Organ growth ≠ body growth. PMID 7561636. DOI 10.1677/joe.0.1460247.
Long [R3] IGF-I reduces growth, plasma growth hormone, IGF binding protein-3 and endogenous IGF-I concentrations in pigs. LR3IGF-I decreased average daily gain, food intake, plasma IGFBP-3, IGF-I, and insulin. Mean plasma GH −23%; area under GH peaks −60%. Opposite of a simple “more IGF = more growth” claim. PMID 9488001. DOI 10.1677/joe.0.1550559.
Secondary structure determination of 15N-labelled human Long-[Arg-3]-insulin-like growth factor 1 by multidimensional NMR spectroscopy. IGF-I domain almost identical to IGF-I; N-terminal seven extension residues have few medium/long-range NOEs. Europe PMC core JSON opened. PMID 9450557. DOI 10.1016/s0014-5793(97)01496-8.
Solution structure and backbone dynamics of long-[Arg(3)]insulin-like growth factor-I. Major change vs IGF-I: reorientation of the N-terminal three residues of the IGF-I domain, interpreted as lower IGFBP affinity. Extension flexible. BMRB 4494 stores the 83-aa sequence. PMID 10744677. DOI 10.1074/jbc.275.14.10009.
Measurement of an analog of IGF-I in blood plasma using a novel ELISA. Detected LR3 with native IGF-I and -II <0.01% cross-reactivity. Animal assay paper, not human PK. PMID 9582496. DOI 10.1677/joe.0.1560407.
Effect of recombinant porcine IGFBP-3 on IGF-I and long-R3-IGF-I-stimulated proliferation and differentiation of L6 myogenic cells. rpIGFBP-3 suppressed both IGF-I- and Long-R3-stimulated proliferation. It suppressed IGF-I-stimulated differentiation but not Long-R3-stimulated differentiation. Cell line. Not a vial bioassay. PMID 15254966. DOI 10.1002/jcp.20068.
Des(1-3)IGF-I: a truncated form of insulin-like growth factor-I. Gly-Pro-Glu removed; 67 aa. Different analog. Francis 1992 compared it with Long [Arg3]; they are not interchangeable. PMID 8930132. DOI 10.1016/1357-2725(96)00056-8.
Intranasal long R3 insulin-like growth factor-1 treatment promotes amyloid plaque remodeling in cerebral cortex but fails to preserve cognitive function in male 5XFAD mice. Did not significantly alter cognitive symptoms. Authors: does not support LR3 as monotherapy. Mouse IN study. Not a human AD trial. Data citation NCT01767909 is the SNIFF insulin trial, not LR3. PMID 39610283. DOI 10.1177/13872877241299056. PMC 12617435.
The amino acid sequence of human insulin-like growth factor I and its structural homology with proinsulin. 70 aa, MW 7649. Defines mature IGF-1, not LR3. PMID 632300. DOI 10.1016/s0021-9258(17)40889-1.
Intrauterine growth retardation and postnatal growth failure associated with deletion of the insulin-like growth factor I gene. Endogenous-gene human biology. Not LR3. Page opened (no abstract text). PMID 8857020. DOI 10.1056/nejm199610313351805.
Long-term treatment with recombinant IGF-I in children with severe IGF-I deficiency due to growth hormone insensitivity. Height velocity 2.8 → 8.0 cm/yr in year 1. rhIGF-I / mecasermin-class. Not Long R3. NOT the SRP vial. Europe PMC core opened. PMID 17192294. DOI 10.1210/jc.2006-1610.
IGF-1 LR3 / Long-[Arg3]IGF-I is an investigational laboratory research protein analog. It is not an FDA-approved drug for human use. This page is educational. It does not provide dosing, reconstitution, administration, or any human-use instructions.
Simple Research Peptides (SRP) materials are for laboratory research only and are not for human or veterinary use, consumption, administration, diagnosis, treatment, or therapeutic application.
Laboratory identity is the first practical issue. Opened papers, NCATS UNII M9L22Y19H9, and BMRB 4494 describe the 83-aa analog MFPAMPLSSLFVNGPRTLCGAELVDALQFVCGDRGFYFNKPTGYGSSSRRAPQTGIVDECCFRSCDLRRLEMYCAPLKPAKSA (CAS 143045-27-6; disulfides 19–61, 31–74, 60–65 on 83-aa numbering). PubChem compound CID was not found. Marketplace CAS 946870-92-4 resolved to CID 168009904, an unrelated C80 lipid, and is rejected. Mecasermin / Increlex (UNII 7GR9I2683O; CAS 68562-41-4; BLA 021839; IUPHAR 4971; UniProt P05019) is 70-aa rhIGF-1 — NOT the SRP vial. [Arg3]IGF-I without the Long leader (PMID 1311930) and DES(1-3) (PMID 8930132) are different analogs. SRP product pages do not print sequence, CAS, UNII, formula, or a public COA. A method written for Increlex, native IGF-1, DES, or cleaved [Arg3]IGF-I is not automatically valid for this 83-aa analog.
Confirm the 83-aa Long-[Arg3] sequence, disulfide pairing, and fold before treating a vial as the literature article. Independently sourced research proteins are not established as equivalent to GroPep / CSIRO LR3IGF-I used in the 1990s papers. Historical animal µg/day and mg/kg figures are study conditions from those papers. They are not a reconstitution scheme and they are not a use guide for an SRP 1 mg / 3 mL research vial.
Biological inference has the same problem. The opened record is strong on analog identity and IGFBP-resistance biochemistry, real but model-dependent on animal growth/organ effects (rats up, pigs down, guinea-pig organs without body growth), empty on human LR3 trials (0 NCTs), and not transferable from mecasermin. That is a laboratory-reagent evidence profile, which matches the live SRP index card.
Yes, as a 1992 CSIRO / GroPep recombinant protein. Francis 1992 named Long [Arg3]-IGF-I. Tomas 1992, BMRB 4494, and NCATS M9L22Y19H9 print the same 83-aa idea (13-aa extension + Arg3). Sequence: MFPAMPLSSLFVNGPRTLCGAELVDALQFVCGDRGFYFNKPTGYGSSSRRAPQTGIVDECCFRSCDLRRLEMYCAPLKPAKSA. Whether a given research vial is that folded chain is not established without analytical identity testing. PMID 1378742.
Opened product page: 1 mg lyophilized material in a 3 mL research vial; also-known-as “Insulin-Like Growth Factor-1 Long R3, Long R3 IGF-1”; Growth / Recovery Research; RUO. No sequence. http://simpleresearchpeptides.com/product/igf-1-lr3-1-mg-vial/
No. Endogenous IGF-1 is the 70-aa somatomedin-C chain (P05019 residues 49–118; Rinderknecht 1978, PMID 632300).
No. Increlex is recombinant 70-aa human IGF-1 (UNII 7GR9I2683O; CAS 68562-41-4; BLA 021839; IUPHAR 4971; UniProt P05019; FDA 2005) for a narrow pediatric IGFD indication. That label and Chernausek 2007 (PMID 17192294) are not Long R3 evidence and are NOT the SRP vial.
No. DES(1-3) lacks the first three residues (Ballard 1996, PMID 8930132). Long R3 adds a 13-aa leader and substitutes Arg at position 3.
No. King 1992 (PMID 1311930) made 70-aa E3R/G3R peptides by cleaving a longer fusion. Those reagents do not contain the Long leader.
Not on the opened ClinicalTrials.gov queries (0 studies). No LR3 NCT. Human PK, efficacy, and safety of research-market LR3 are not established.
Not shown. Tomas 1992 used GroPep recombinant human LR3IGF-I in osmotic pumps. SRP does not print sequence, CAS, or a public COA. Historical animal exposures are not instructions.
Opened record is mixed by species and endpoint. Rats: more nitrogen retention and gut growth (Tomas 1992; Steeb 1995). Guinea pigs: organ growth without body-weight gain (Conlon 1995, PMID 7561636). Pigs: less gain and suppressed GH (Dunaiski 1997, PMID 9488001). 5XFAD mice: plaque remodeling without cognitive preservation (Engel 2025, PMID 39610283). Francis 1992 already showed Long [Arg3] can be less potent than IGF-I when IGFBPs are absent.
UNII M9L22Y19H9 and CAS 143045-27-6 on opened NCATS / PubChem SID pages. Do not use 946870-92-4 (CID 168009904). PubChem CID not found.
No. SRP listings are for laboratory research only and are not for human or animal use. This page does not provide reconstitution, administration, or dosing instructions. Increlex is a different molecule. NOT the SRP vial.
Yes. The opened record is strong on analog identity and IGFBP-resistance biochemistry, real but model-dependent on animal growth/organ effects, empty on human LR3 trials, and not transferable from mecasermin. That is a laboratory-reagent evidence profile, which matches the live SRP index card.
No. There is no human dosing, reconstitution, or administration protocol on this page. Historical animal µg/day and mg/kg figures are study conditions, not instructions. Research use only. Not medical advice. Not for human use.
Sources actually opened for this draft. Do not add PMIDs or NCTs that are not on the allowed list. ClinicalTrials.gov returned 0 Long R3 studies; no LR3 NCT is listed as an intervention.
query.intr=mecasermin (NCT00764699, NCT01406444, NCT02386839, NCT00572156, NCT01588093); NCT01767909 (insulin SNIFF; unused). Opened 16 August 2026. No LR3 NCT. Do not invent one.Long R3 = no ligand. Opened 16 August 2026. NOT the SRP vial.Allowed PMID list used on this page (Long R3 named): 1378742, 1371669, 7683875, 8549937, 7561636, 9488001, 9450557, 10744677, 9582496, 15254966, 39610283. Distinction PMIDs (do not cite as LR3-vial efficacy): 1311930 ([Arg3] not Long), 8930132 (DES), 632300 (native), 8857020 (IGF1 deletion), 17192294 (mecasermin-class). PMID opened only to reject a bad citation: 1280101. NCT: none for Long R3 / IGF-1 LR3. Adjacent unused IDs (mecasermin or insulin, not LR3): NCT00764699, NCT01406444, NCT02386839, NCT00572156, NCT01588093, NCT01767909. Opened PMC: PMC1130894, PMC1132436, PMC1382866, PMC12617435. UniProt P05019 (endogenous IGF-1, not the analog). UNII/CAS used: M9L22Y19H9 / 143045-27-6 (Long R3); 7GR9I2683O (mecasermin, distinction); NZ8M50KKRG (mecasermin rinfabate, distinction). CAS rejected: 946870-92-4 (CID 168009904). No other PMIDs were added. No LR3 NCT was invented.
Educational information only. IGF-1 LR3 (Long R3 IGF-1 / Long-[Arg3]IGF-I / LR3IGF-I) is an 83-amino-acid recombinant analog of mature human IGF-I: a 13-residue N-terminal extension plus the 70-residue IGF-I chain with Arg substituted for Glu at position 3. Opened sequence (BMRB 4494 / NCATS M9L22Y19H9): MFPAMPLSSLFVNGPRTLCGAELVDALQFVCGDRGFYFNKPTGYGSSSRRAPQTGIVDECCFRSCDLRRLEMYCAPLKPAKSA. CAS 143045-27-6. UNII M9L22Y19H9. PubChem CID not found. Marketplace CAS 946870-92-4 / CID 168009904 rejected. It is not endogenous somatomedin C (UniProt P05019; PMID 632300), not mecasermin / Increlex (UNII 7GR9I2683O; CAS 68562-41-4; BLA 021839; IUPHAR 4971) — NOT the SRP vial, not mecasermin rinfabate / IPLEX, not [Arg3]IGF-I without the Long extension (PMID 1311930), and not IGF-1 DES(1-3) (PMID 8930132). Francis 1992 (PMID 1378742) defines the analog. Tomas 1992 (PMID 1371669) printed the sequence. Laajoki 2000 (PMID 10744677) determined the NMR structure. Conlon 1995 (PMID 7561636) and Dunaiski 1997 (PMID 9488001) show species-dependent limits. Engel 2025 (PMID 39610283) remodeled plaques without preserving cognition. Chernausek 2007 (PMID 17192294) is mecasermin-class — NOT the SRP vial. Not FDA-approved as Long R3. ClinicalTrials.gov returned 0 Long R3 studies; no LR3 NCT. Historical animal µg/day and mg/kg figures are study conditions, not instructions. Laboratory research use only; not for human or animal use. Not medical advice. Not for human use. No human dosing protocol. Last source review: 16 August 2026 (America/Indianapolis). Locked draft converted to HTML the same day. For laboratory research only. Not for human or veterinary use.
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