IGF-1 DES
What do these badges mean?
Evidence tier
- AHuman-validated — Human trials showing positive results and good safety.
- BAnimal-grade — No human trials yet, but solid animal/preclinical evidence of effect and safety.
- CAnecdotal — No human or animal trials — only anecdotal/observational reports.
- DInsufficient evidence — No or insufficient evidence (encyclopedia only — never recommended by the builder).
Safety light
- 🟢 Green — Only mild, manageable side effects; reasonable safety data.
- 🟡 Yellow — Needs active management, has a meaningful contraindication/interaction, or has thin long-term data.
- 🔴 Red — Risk of a hospital-level event — treat with serious caution.
Browse-only — not on the protocol builder's curated shortlist, so the builder won't recommend it.
What is it?
IGF-1 DES is native IGF-1 with its first three N-terminal amino acids removed (“Des(1-3)” = deletion of residues 1–3). That tiny truncation does one big thing: it slashes the molecule’s affinity for the IGF-binding proteins (IGFBPs) that normally sequester ~99% of circulating IGF-1. The result is a variant that binds the IGF-1 receptor at full affinity but stays free and active far more than native IGF-1 — peptidelist and the FAQ describe it as roughly 10× more potent than intact IGF-1 for this reason.
It belongs to the same directly-administered IGF-axis family as IGF-1 LR3 (see IGF-1 LR3 and MGF — the IGF-1 axis muscle cluster). The two solve the same problem — escaping the IGFBP brake — by different edits: LR3 uses an arginine substitution plus a 13-aa N-terminal extension; DES uses an N-terminal truncation. Both end up as high-free-fraction IGF-1 signals. This article cross-links rather than re-deriving the shared IGF-1-axis biology, which IGF-1 LR3 and MGF — the IGF-1 axis muscle cluster covers in full (PI3K/Akt/mTOR for synthesis, MAPK/ERK for proliferation, and the cancer epidemiology that is the class’s central safety story).
What does it do in my body?
The N-terminal pentapeptide of IGF-1 is functionally important for IGFBP binding — remove the first three residues and you knock out most of that binding while preserving receptor activity. Bagley CJ et al. 1989 (Biochem J, 2730580,) characterized exactly this “key functional role for the IGF-1 N-terminal pentapeptide,” and Ballard FJ et al. 1989 (Biochem Soc Symp, 2559737,) examined why some IGF molecular variants are more potent — the mechanistic basis for DES’s enhanced activity.
How can it help me?
- Where the science stands: **** — 6 preclinical studies, 0 human trials
The full evidence — every human, animal, and lab study, graded — is one tap away: use the See the deeper science → toggle at the top.
Is it dangerous? What are the side effects?
The IGF-1-axis class concerns apply: hypoglycemia from the insulin-crossover effect (keep fast-acting carbs on hand — the same rule detailed for LR3 in IGF-1 LR3 and MGF — the IGF-1 axis muscle cluster), and the theoretical tumor-signaling concern at chronic supraphysiologic exposure. There is no human safety record to draw on.
Contraindications across the IGF-axis class: active cancer or cancer history (mitogenic concern), pregnancy/breastfeeding, uncontrolled diabetes.
Regulatory status: Not FDA-approved; research-chemical; not eligible for compounding; WADA-banned. Unlike Somatropin (HGH) — which is an approved prescription drug — IGF-1 DES has no approval pathway and no human clinical dossier behind it.
Typical dosing
Educational context only — talk to a licensed medical provider before any protocol. What follows describes the doses and schedules most commonly reported in the research and by practitioners, shared so you can have an informed conversation. These compounds are sold for research use only, are not FDA-approved drugs, and this is not medical advice.
Animal-model dosing in the literature is in the low-microgram range, but there is no validated human protocol — DES has no human trials at all. The community frames it the way LR3 is framed (a directly-injected, high-potency IGF-1 signal, post-workout, with the same hypoglycemia and IGF-axis cautions), but anyone treating DES dosing as established is extrapolating from animal data and from the LR3 community playbook, not from human evidence.
What should I avoid combining — and what's synergistic?
IGF-1 DES doesn't have a dedicated stacking protocol in our notes — the interactions that matter most are in the safety section above. For how people combine it with other peptides, the deeper-science view has the full detail.
Where do people source this?
OHM does not sell or handle any compound. Research-use-only material is sold by third-party vendors; our vetting notes and disclosures are on the Where to buy page. If you'd rather have a physician in the loop, see the telehealth option. Whatever the route, the supply chain is the real risk: only consider vendors that publish batch-level third-party Certificates of Analysis.
IGF-1 DES is native IGF-1 with its first three N-terminal amino acids truncated — an edit that slashes its affinity for the binding proteins that normally sequester most circulating IGF-1, making it a far more potent, “free” signal at the tissue level. It is a research chemical, not FDA-approved, with zero human trials — the evidence base here is entirely animal/in-vitro, and this article is honest about that gap throughout.
| Class | Des(1-3)IGF-1 — native IGF-1 truncated by its first 3 N-terminal amino acids |
| Mechanism (one line) | Binds IGF-1R at full affinity, but ~10× more potent than intact IGF-1 because it barely binds IGFBPs — more free signal reaches tissue |
| Evidence base | **** — 6 preclinical studies, 0 human trials |
| Safety record | No human safety record; IGF-axis class concerns (hypoglycemia, theoretical tumor-signaling at chronic supraphysiologic exposure) |
| Regulatory status | Not FDA-approved; research-chemical; not eligible for compounding; WADA-banned |
What it is
IGF-1 DES is native IGF-1 with its first three N-terminal amino acids removed (“Des(1-3)” = deletion of residues 1–3). That tiny truncation does one big thing: it slashes the molecule’s affinity for the IGF-binding proteins (IGFBPs) that normally sequester ~99% of circulating IGF-1. The result is a variant that binds the IGF-1 receptor at full affinity but stays free and active far more than native IGF-1 — peptidelist and the FAQ describe it as roughly 10× more potent than intact IGF-1 for this reason.
It belongs to the same directly-administered IGF-axis family as IGF-1 LR3 (see IGF-1 LR3 and MGF — the IGF-1 axis muscle cluster). The two solve the same problem — escaping the IGFBP brake — by different edits: LR3 uses an arginine substitution plus a 13-aa N-terminal extension; DES uses an N-terminal truncation. Both end up as high-free-fraction IGF-1 signals. This article cross-links rather than re-deriving the shared IGF-1-axis biology, which IGF-1 LR3 and MGF — the IGF-1 axis muscle cluster covers in full (PI3K/Akt/mTOR for synthesis, MAPK/ERK for proliferation, and the cancer epidemiology that is the class’s central safety story).
How it works
The N-terminal pentapeptide of IGF-1 is functionally important for IGFBP binding — remove the first three residues and you knock out most of that binding while preserving receptor activity. Bagley CJ et al. 1989 (Biochem J, 2730580,) characterized exactly this “key functional role for the IGF-1 N-terminal pentapeptide,” and Ballard FJ et al. 1989 (Biochem Soc Symp, 2559737,) examined why some IGF molecular variants are more potent — the mechanistic basis for DES’s enhanced activity.
What the research shows
Peptidelist grades IGF-1 DES Emerging: 6 studies, 0 human trials. Its own summary is blunt: “No human studies or randomized controlled trials have been conducted on IGF-1 DES; the 6 available studies are limited to in vitro and animal models… Clinical evidence for IGF-1 DES in humans does not currently exist.” OHM grades it Tier C / Safety Yellow, PRIMARY muscle — preclinical hypertrophy + small PK studies, no human efficacy trials.
The preclinical anchors (all):
- Kaplan-Lefko PJ et al. 2008 Oncogene — epithelial IGF-1 expression promotes prostate hyperplasia. 18026134
- Guan J et al. 1996 Endocrinology — IGF-1, IGF-2, and des-IGF-1 reduce neuronal loss after hypoxic-ischemic brain injury in rats. 8603600
- Hill DJ et al. 1997 J Endocrinol — IGF-1’s dual effect on insulin release from isolated rat islets. 9135565
- McGrath MF et al. 1991 Endocrinology — IGFs stimulate bovine mammary-cell proliferation. 1713160
Two of those four are worth naming honestly: the prostate-hyperplasia (Kaplan-Lefko) and mammary-cell-proliferation (McGrath) findings are exactly the tissue-proliferation signals that make IGF-axis exposure an oncology-watch class. Same story as LR3 — see IGF-1 LR3 and MGF — the IGF-1 axis muscle cluster for the full epidemiology.
Real-world protocol
The information here is educational only. IGF-1 DES is a research chemical, not an FDA-approved drug, and has no established human dosing protocol. This is not medical advice.
Animal-model dosing in the literature is in the low-microgram range, but there is no validated human protocol — DES has no human trials at all. The community frames it the way LR3 is framed (a directly-injected, high-potency IGF-1 signal, post-workout, with the same hypoglycemia and IGF-axis cautions), but anyone treating DES dosing as established is extrapolating from animal data and from the LR3 community playbook, not from human evidence.
Side effects & management
The IGF-1-axis class concerns apply: hypoglycemia from the insulin-crossover effect (keep fast-acting carbs on hand — the same rule detailed for LR3 in IGF-1 LR3 and MGF — the IGF-1 axis muscle cluster), and the theoretical tumor-signaling concern at chronic supraphysiologic exposure. There is no human safety record to draw on.
Contraindications across the IGF-axis class: active cancer or cancer history (mitogenic concern), pregnancy/breastfeeding, uncontrolled diabetes.
Regulatory status
Not FDA-approved; research-chemical; not eligible for compounding; WADA-banned. Unlike Somatropin (HGH) — which is an approved prescription drug — IGF-1 DES has no approval pathway and no human clinical dossier behind it.
Sources
- — thepeptidelist.com IGF-1 DES profile: Des(1-3) structure, ~10× potency, 6 preclinical studies / 0 human, named animal/in-vitro PMIDs (all), research-only status.
- — grading: IGF-1 DES Tier C/Yellow (lines 232–240); the supraphysiologic-dose + cancer-signaling safety framing.
- Named anchors (all): Kaplan-Lefko 2008 18026134; Guan 1996 8603600; Hill 1997 9135565; McGrath 1991 1713160; Bagley 1989 2730580; Ballard 1989 2559737.
Content migrated from gh-igf-reference-cluster.md (2026-06-10 build) per the 2026-07-16 cluster-elimination directive — no facts added or removed from the source article’s IGF-1 DES section.
See also: Somatropin (HGH), PEG-MGF, IGF-1 LR3 and MGF — the IGF-1 axis muscle cluster, CJC-1295, Ipamorelin, Sermorelin, Tesamorelin, MK-677 (Ibutamoren).
Sources & references
- — thepeptidelist.com IGF-1 DES profile: Des(1-3) structure, ~10× potency, 6 preclinical studies / 0 human, named animal/in-vitro PMIDs (all), research-only status.
- — grading: IGF-1 DES Tier C/Yellow (lines 232–240); the supraphysiologic-dose + cancer-signaling safety framing.
- Named anchors (all): Kaplan-Lefko 2008 18026134; Guan 1996 8603600; Hill 1997 9135565; McGrath 1991 1713160; Bagley 1989 2730580; Ballard 1989 2559737.
Content migrated from gh-igf-reference-cluster.md (2026-06-10 build) per the 2026-07-16 cluster-elimination directive — no facts added or removed from the source article’s IGF-1 DES section.
See also: Somatropin (HGH), PEG-MGF, IGF-1 LR3 and MGF — the IGF-1 axis muscle cluster, CJC-1295, Ipamorelin, Sermorelin, Tesamorelin, MK-677 (Ibutamoren).