IGF-1 DES

A naturally occurring truncated form of IGF-1 missing the three N-terminal amino acids (Gly-Pro-Glu). It has been isolated from bovine colostrum, human brain, and porcine uterus, likely produced by post-translational cleavage. Removal of the N-terminal tripeptide reduces IGFBP binding affinity to approximately 1% of native IGF-1 while retaining full IGF-1 receptor affinity, making it roughly 10× more potent in stimulating cell proliferation in vitro.

In GH-deficient lit/lit mice, 3 mcg/day of des(1-3) IGF-1 matched the anabolic effects of 30 mcg/day native IGF-1 (Tomas et al., 1990). The very short half-life (~20-30 minutes) has led community users to favor site-specific intramuscular injection protocols. No human clinical trials have been conducted with this compound.

Des(1-3) IGF-1 was first characterized in the late 1980s by Ballard, Francis, and colleagues at CSIRO in Australia. Key animal studies demonstrated 10× greater potency than native IGF-1 in GH-deficient mice (Tomas et al., 1990) and more pronounced hypoglycemia in pigs and marmosets (Ballard et al., 1998). A comprehensive 1996 review (Ballard et al.) explicitly noted that clinical opportunities had not been evaluated — this remains true as of March 2026.

No registered clinical trials exist on ClinicalTrials.gov. Community dosing ranges are extrapolated from animal potency data and are not clinically validated.