IGF-1 DES
Dosage Protocol
IGF-1 DES (Des(1-3)IGF-1) is a truncated form of IGF-1 lacking the first three N-terminal amino acids. This truncation eliminates the primary IGFBP-binding domain, producing a peptide that cannot be sequestered by binding proteins. The result is dramatically increased potency at the IGF-1 receptor — approximately 10× greater than native IGF-1 — with a primarily local, site-specific action profile.
What is IGF-1 DES?
IGF-1 DES was first identified as a naturally occurring form of IGF-1 in human brain and blood, generated by proteolytic cleavage of the N-terminus. Its lack of IGFBP affinity means that unlike native IGF-1 or even IGF-1 LR3, it does not distribute widely through the body — instead producing intense, localized IGF-1 receptor activation in the tissue adjacent to the injection site.
This localized action profile is its key differentiating feature from IGF-1 LR3. Researchers use IGF-1 DES for site-specific muscle hyperplasia research — injecting directly into the muscle intended to receive growth stimulus. Its approximately 10× greater potency at IGF1R compared to native IGF-1 means lower doses are required, but hypoglycemia risk remains relevant at higher doses.
Dosing Schedule
Parameters documented in published preclinical and clinical research.
| Phase | Dose | Frequency | Duration | Notes |
|---|---|---|---|---|
| Start | 50 mcg per site | Post-workout SubQ | Days 1–7 | Inject near target muscle. Eat with or after to manage glucose. |
| Working dose | 50–100 mcg per site | Post-workout | Weeks 1–6 | SubQ into subcutaneous fat adjacent to target muscle belly. |
| Advanced | 100–150 mcg per site | Post-workout | Weeks 1–6 | Higher doses — hypoglycemia risk. Multiple site injections possible. |
| Off cycle | — | — | 4 weeks | Equal on/off cycling recommended. |
Safety & Side Effects
Academic References
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[1]
Hümpel M, et al. (1992). Human insulin-like growth factor binding protein-1 (IGFBP-1): production in heterologous systems. Regul Pept. 39(2-3):133–44. PubMed ↗
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[2]
Szabo L, et al. (1988). Isolation of brain insulin-like growth factor. Biochem J. 256(3):781–6. PubMed ↗
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[3]
Ballard FJ, et al. (1987). Reduced inhibition of protein degradation by insulin-like growth factor-1 (IGF-1) and truncated IGF-1 in cells lacking IGF binding proteins. Biochem J. 249(3):765–72. PubMed ↗
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[4]
Heding A, et al. (1996). Properties of des(1-3)IGF-I compared to IGF-I. Growth Regul. 6(2):65–70. PubMed ↗