Both are sold to the same reader under the same three letters, and they are not the same molecule. Increlex (mecasermin) is human IGF-1 made by bacteria, an approved prescription drug for a rare childhood growth disorder. IGF-1 LR3 is an engineered analogue sold as a research chemical. This page puts the two records side by side so the difference is a table, not an impression.
What LR3's own literature contains, paper by paper, is on our IGF-1 LR3 dosage page; the harms record, and the one black-market vial that was analysed, on our IGF-1 LR3 side effects page. What IGF-1 is as a hormone is in Peptide Lexicon's IGF-1 entry. Nothing here is a recommendation.
The two molecules
| Increlex (mecasermin) | IGF-1 LR3 | |
|---|---|---|
| What it is | Recombinant human IGF-1 | Engineered IGF-1 analogue ("Long R3 IGF-I") |
| Length | 70 amino acids | 83 amino acids |
| Sequence | Identical to the body's IGF-1 | Arg replaces Glu at position 3, plus a 13-residue N-terminal extension |
| Mass | 7,649 Da (label) | ~9,111 Da (our calculation from the sequence) |
| Made in | E. coli (label) | E. coli, as first described (Francis 1992) |
| Designed for | Replacing a missing hormone | Cell culture: escaping the binding proteins cells secrete |
| Approval | FDA, 30 August 2005 (BLA021839) | None |
| Registered trials | 40 (ClinicalTrials.gov, "mecasermin") | 0 |
The label states the first column. The second comes from the papers that introduced the analogue, read on 22 October 2026: Francis and colleagues at CSIRO in Adelaide described it in 1992 as methionine, the first ten residues of porcine growth hormone and the dipeptide Val-Asn fused to human IGF-1 with arginine at position 3 (J Mol Endocrinol 1992;8:213). The extension was added partly because it helped the protein fold correctly during manufacture.
The mass figure is ours. Summing the residues of the two published sequences, with three disulfide bridges each, gives 7,648.7 Da for IGF-1 — matching the label's 7,649 — and 9,111.5 Da for LR3. Per microgram, LR3 therefore carries about 16% fewer molecules than IGF-1. Any figure carried over from one molecule to the other by weight is already off by that much before biology enters.
Why the analogue exists
More than 80% of IGF-1 in blood travels bound to IGFBP-3 and an acid-labile subunit, the Increlex label says, and that binding governs how much reaches tissue. LR3 was built to slip that leash. In the 1992 cell work, it was the most potent of the variants tested in cells that secrete binding proteins — but less potent than IGF-1 in chicken fibroblasts that secrete none. The potency is the binding-protein escape, not a stronger signal.
The CSIRO team gave it to rats made catabolic with dexamethasone for seven days by osmotic pump (Tomas 1992, Biochem J). LR3 and des(1-3)IGF-I were about 2.5 times as potent as IGF-1, although LR3 binds the IGF-1 receptor about three times less well. A companion paper found the gut was among the most responsive tissues: the highest IGF-1 dose raised total gut weight by up to 60%, and the analogues were "consistently severalfold more potent" (Read 1992, J Endocrinol). Those are the founding data; they are rat data.
What Increlex is approved for, and what it did
The current label (Eton Pharmaceuticals, DailyMed, effective 18 May 2026, read 22 October 2026) approves Increlex for growth failure in children aged two and older with:
- Severe primary IGF-1 deficiency — height and basal IGF-1 both at or below −3.0 standard deviations, with normal or raised growth hormone. Laron syndrome, where the growth-hormone receptor does not work, is the classic cause.
- Growth hormone gene deletion in children who have developed neutralising antibodies to growth hormone.
The label adds two limits: it is "not a substitute" for growth hormone in growth hormone's own indications, and it is not for IGF-1 deficiency that follows growth hormone deficiency, malnutrition, hypothyroidism or long-term steroid treatment. It is contraindicated once the growth plates have closed — the point at which an adult body has nothing left for it to lengthen.
The efficacy record is the label's pooled trial table. Children entered at a mean age of 6.7 years and a height of −6.7 standard deviations; 87% had Laron syndrome.
| Year of treatment | Children followed | Height velocity, cm/yr (mean) | Height SDS change from baseline |
|---|---|---|---|
| Before treatment | 58 | 2.8 | — |
| 1 | 58 | 8.0 | +0.8 |
| 2 | 48 | 5.8 | +1.2 |
| 3 | 38 | 5.5 | +1.4 |
| 5 | 21 | 4.7 | +1.4 |
| 8 | 13 | 4.3 | +1.5 |
Growth nearly tripled in the first year and settled near 4–6 cm a year after that; the children finished well short of average height. The trials were uncontrolled, each child compared with their own pre-treatment rate, and the number followed falls from 58 to 13. Bone age advanced 5.3 years over 4.9 years of treatment in the 49 children analysed for it.
The label's regimen, reported as label text: 0.04–0.08 mg/kg twice daily by subcutaneous injection, raised by 0.04 mg/kg per dose after at least a week if tolerated, to a maximum of 0.12 mg/kg twice daily, given within 20 minutes of a meal or snack, supervised by a paediatric growth specialist. Our dosage page sets that shape against the flat microgram figures that circulate for LR3.
The harms that come with the approved one
The approved molecule is the only IGF-1 with a human harms record, and it is not short. In 71 children treated for a mean 3.9 years (274 patient-years), the label reports hypoglycaemia in 30 (42%), severe in five, with seizures or loss of consciousness in four. Its warnings add anaphylaxis, intracranial hypertension, tonsil and adenoid enlargement, slipped capital femoral epiphysis, progression of scoliosis and malignant neoplasia: "several cases" in treated children, and a contraindication in any child with a cancer or a history of one. The vial is preserved with 9 mg/mL benzyl alcohol, which is why the label advises against use in infants. Our peptides and cancer page covers what is and is not known about growth-axis peptides and tumours.
None of that is IGF-1 LR3's record. It is the record of a hormone identical to the body's own, given to children whose bodies lacked it, under glucose monitoring. A molecule engineered to stay unbound in blood has no record at all; whether it would cause more or less hypoglycaemia is not established.
Who holds Increlex
Drugs@FDA lists one mecasermin application, BLA021839, sponsor Ipsen, approved 30 August 2005 and marketed by prescription (openFDA data of 20 October 2026). DailyMed carries two current-format Increlex labels: Ipsen's (version 21, published 7 August 2025) and a newer one naming Eton Pharmaceuticals with a manufacturing chain of Hospira, Simtra Deutschland and Tjoapack Netherlands (version 5, published 20 May 2026). The supply is a single 40 mg/4 mL multiple-dose vial, refrigerated, discarded 30 days after first use.
A second IGF-1 drug existed. Iplex (mecasermin rinfabate — IGF-1 bound to its carrier protein IGFBP-3), from Insmed, was approved on 12 December 2005 under application 021884; Drugs@FDA lists it as discontinued. Both applications were moved from drug to biologic status on 23 March 2020, the same transition that changed compounding of hCG.
What does not exist for LR3
- No approval and no label, so no indication, dose, maximum or reviewed warning.
- No registered trial. ClinicalTrials.gov returned zero studies for "IGF-1 LR3", "LR3-IGF-I" and "long R3 IGF" on 22 October 2026, against 40 for mecasermin.
- No human study. PubMed returned 105 records for the analogue's names; filtered to clinical trials in humans, none. The three records indexed to humans at all are a 2026 narrative review placing LR3 in the "complete absence of human studies" tier (Front Endocrinol 2026), a 1999 wound-clearance study, and the 2010 Cologne analysis of a black-market vial that contained His-tagged LR3, a laboratory reagent form (Growth Horm IGF Res 2010).
- No route to a prescription. With no approved product, there is nothing for a physician to prescribe as LR3; what US prescribing and compounding cover is on our 503A vs 503B page and in the list of FDA-approved peptides.
What does not transfer
The temptation in this comparison is to borrow the approved drug's record for the analogue. Three reasons it does not carry over: the molecules differ in mass by 19%, so equal weights are unequal doses; LR3's whole design changes the binding-protein step that governs IGF-1's exposure and clearance, so the label's 5.8-hour half-life in deficient children does not describe it; and Increlex's benefit was measured only in children with open growth plates and missing IGF-1, a population with nothing in common with an adult buying a research vial. What muscle, fat-loss and recovery claims for LR3 rest on is the rodent work above.
Reproducing the census
- ClinicalTrials.gov API v2,
query.term=mecasermin(40),IGF-1 LR3,LR3-IGF-I,long R3 IGF(0 each), 22 October 2026. - PubMed:
"IGF-1 LR3"[tiab] OR "LR3-IGF-I"[tiab] OR "long R3 IGF-I"[tiab] OR "Long R3-IGF-I"[tiab](105);AND humans[mh] AND clinical trial[pt](0), 22 October 2026. - openFDA Drugs@FDA,
openfda.generic_name:mecaserminandproducts.brand_name:IPLEX, data of 20 October 2026.
Sources and dates
- Increlex (mecasermin) label, Eton Pharmaceuticals, DailyMed set d5b2b0e1-c523-468d-9a0b-4ae4e4a8dbce, version 5, effective 18 May 2026 — read 22 October 2026. Ipsen label, set a8b27a1b-a611-4f91-ad22-76d4b390c3ae, version 21, published 7 August 2025 — listed.
- Drugs@FDA via openFDA: BLA021839 (Increlex, Ipsen, original approval 2005-08-30) and BLA021884 (Iplex, Insmed, approved 2005-12-12, discontinued; deemed a BLA 2020-03-23) — data of 20 October 2026.
- Francis GL et al. J Mol Endocrinol 1992;8(3):213–23 (PMID 1378742); Tomas FM et al. Biochem J 1992;282:91–7 (PMID 1371669); Read LC et al. J Endocrinol 1992;133(3):421–31 (PMID 1613443); King R et al. J Mol Endocrinol 1992;8(1):29–41 (PMID 1311930) — abstracts read 22 October 2026.
- Kohler M et al. Growth Horm IGF Res 2010;20(5):386–90 (PMID 20675162); Dominikowski A et al. Front Endocrinol 2026;17:1822475 (PMID 42395176).
- UniProt P05019 (human IGF-1 precursor; mature chain residues 49–118) — read 22 October 2026, for the mass calculation.