IGF DES
Des(1-3)IGF-1 — ≠ LR3 ≠ MGF ≠ PEG-MGF; CID/CAS TBD; rodent potency only.
Editorial review:Evidence snapshot
This drawer marks papers. It is not a plan, a dose, or a source. A paper is a bounded report. It is not a protocol. Grades name the object. They are not a safety rating.
Identity lock — not LR3, not MGF, not PEG-MGF. Des(1-3)IGF-1 (des-(1-3)-IGF-I) is native human IGF-1 lacking the N-terminal tripeptide Gly-Pro-Glu. Truncation reduces IGF-binding-protein affinity and increases biologic potency in many in-vitro/in-vivo models relative to intact IGF-1. It is an IGF-1 variant protein, not a GHRH/GHRP secretagogue. PubChem lacks a clean, collision-free CID lock in this pass → identity fields To be confirmed; do not invent CAS. ≠ IGF-1 LR3 (Long-Arg3 analog with N-terminal extension). ≠ MGF / IGF-1 Ec (splice-variant / E-peptide object). ≠ PEG-MGF (next-batch object). No approved human therapeutic indication in this pack. This drawer marks papers. It is not use advice.
Bottom line
Ballard/Francis-line biochemistry established des(1-3)IGF-I as a naturally occurring truncated IGF-1 with reduced IGFBP binding and enhanced potency in rodent growth and tissue models. Controlled human clinical efficacy trials for Des(1-3)IGF-1 administration are absent from this Selected sources set. Do not borrow LR3 or MGF papers as DES proof.
Papers
Foundational truncated-IGF biochemistry
PMID 8930132 — Ballard 1996
Tested: focused review of des(1-3)IGF-I as a truncated form of IGF-I (identity, potency, IGFBP relationships).
Does not show: a human clinical approval package.
PMID 3390164 — Francis 1988
Tested: sequences and biologic activities of IGFs in bovine colostrum compared with a potent truncated form (early truncated-IGF identity work).
Does not show: human DES therapeutic use.
PMID 2539101 — Ross 1989
Tested: IGF-binding proteins inhibit IGF-1 and IGF-2 activities but not des-(1-3)-IGF-1 — classic IGFBP-escape mechanism paper.
Does not show: human outcome trials.
PMID 1883485 — McKinnon 1991
Tested: expression/purification/characterization of recombinant human IGF-I and the potent variant des(1-3)IGF-I.
Does not show: clinical dosing evidence (and this drawer never provides dosing).
Rodent potency / anabolic models (preclinical)
PMID 2280209 — Gillespie 1990
Tested: enhanced potency of des(1-3)IGF-I relative to IGF-I in lit/lit mice.
Does not show: human growth-disorder therapy proof for DES.
PMID 1996625 — Lemmey 1991
Tested: IGF-I and des-(1-3)IGF-I enhancing growth in rats after gut resection.
Does not show: human short-bowel clinical DES indication.
PMID 1928375 — Martin 1991
Tested: IGF-I and des-(1-3)IGF-I enhancing growth in rats with reduced renal mass.
Does not show: human CKD therapy for DES.
PMID 2005410 — Ballard 1991
Tested: plasma clearance and tissue distribution of labelled IGF-I, IGF-II, and des(1-3)IGF-I in rats.
Does not show: human PK as a labeled drug product.
PMID 7683875 — Tomas 1993
Tested: IGF-I and more potent variants (including truncated/analog framing) restoring growth of diabetic rats without all characteristic insulin effects.
Does not show: identity match to IGF-1 LR3; do not merge DES and LR3 grades.
PMID 9415072 — Tomas 1997
Tested: IGF-I variants that bind poorly to IGFBPs showing more potent/prolonged hypoglycaemic action in rats.
Does not show: a human hypoglycemia-therapy license for DES.
What is not established
Human clinical efficacy for Des(1-3)IGF-1 administration. Equivalence to IGF-1 LR3, MGF/IGF-1 Ec, PEG-MGF, or intact mecasermin-class IGF-1 products. Bodybuilding or recovery claims from forums. Product identity for unregulated “IGF DES” preparations. This drawer does not provide use advice, schedules, or sourcing.
Selected sources
8930132 3390164 2539101 1883485 2280209 1996625 1928375 2005410 7683875 9415072
Reported experiences
Reported topics are not established benefits.Risks and unknowns
Compare experiences with care.
Join the discussion
Verified members can contribute to compound conversations.