Either documented serious adverse events in humans, or effectively no retrievable evidence base. Dosing figures circulating for these compounds have no scientific foundation.
No human pharmacokinetic half-life located. The commonly cited "20-30 minute half-life" could not be traced to any retrievable primary source and is not reported. Animal anti-doping data only: in rats, Des(1-3)-IGF-I remained detectable until 24 hours after administration, LONGER than LongR3-IGF-I which disappeared rapidly after 4 hours. This directly contradicts the community claim that DES is the shorter-acting variant. These are detection windows, not half-lives.
No human dosing data. Sold as a research reagent. Community protocols are anecdotal with no published human basis.
SERIOUS RISK. Des(1-3)IGF-I lacks the N-terminal tripeptide, reducing IGFBP-3 affinity roughly 25-fold and yielding about 10-fold greater in-vivo potency than native IGF-1. That potency gain is a direct consequence of escaping IGF-binding-protein buffering, which is precisely what makes it dangerous: hypoglycaemia risk is amplified relative to native IGF-1, and mitogenic IGF-1R signalling is unopposed. Potency data are from in-vitro and animal systems. No human safety or dosing data exist.
- Detection of LongR3-IGF-I, Des(1-3)-IGF-I, and R3-IGF-I using immunopurification and high resolution mass spectrometry for antidoping purposes · pubmed
- The effects of IGF-I, IGF-II and des(1-3)IGF-I on growth hormone and IGF-binding protein secretion from cultured rat anterior pituitary cells · pubmed