Evidence Grade E — Very limited evidence. 6 published studies. 0 registered clinical trials.
Medically reviewed by a licensed medical professional
IGF-1 DES is a naturally occurring shortened form of IGF-1, missing its first three amino acids. This small change nearly eliminates binding to regulatory proteins, making it approximately 10 times more potent than normal IGF-1. It was identified in human brain tissue and bovine colostrum. No human clinical trials have been conducted and it has no regulatory approval.
IGF-1 DES is also known by these brand and alternate names:
6 published studies: 1 human, 5 animal, 1 in-vitro, 0 reviews
IGF-1 DES has no marketing authorisation. No human clinical trials have been conducted. Animal studies demonstrated approximately 10-fold greater potency than native IGF-1 in growth-promoting assays.
Like IGF-1 LR3, this compound bypasses normal IGF-1 regulation, making standard safety data inapplicable. Products available through unregulated channels lack pharmaceutical quality assurance. The combination of high potency and absent regulatory protein binding creates an unpredictable pharmacological profile for uncontrolled human use.
Research indicates IGF-1 DES activates the IGF-1 receptor through the same signalling pathways as native IGF-1. The removal of the first three amino acids eliminates the primary binding site for IGF binding proteins, meaning the compound is almost entirely 'free' and bioactive. Its short half-life (estimated 20–30 minutes) and high potency create a rapid, intense but brief IGF-1 receptor activation pulse.
Research in animal models from the 1990s established the approximately 10-fold greater potency compared to native IGF-1. Key safety concerns include organ enlargement at low doses (heart, kidney, and gut enlargement observed in animals), hypoglycaemia risk, and theoretical cancer concerns from sustained IGF-1 receptor activation. No human data of any kind exist. Most foundational studies are now over 25 years old, with limited recent research activity. The narrow margin between effective and harmful doses (due to the high potency) makes uncontrolled use particularly risky. Products from unregulated channels lack pharmaceutical quality assurance.
PeptideTrace tracks 0 registered clinical trials for IGF-1 DES sourced from ClinicalTrials.gov.
No trials registered on ClinicalTrials.gov for this compound.
Des(1-3)IGF-1 is a naturally occurring truncated IGF-1 analogue consisting of 67 amino acids, missing the first three N-terminal residues (Gly-Pro-Glu). Molecular weight is approximately 7,372 Da. Unlike IGF-1 LR3, this variant has been isolated from bovine colostrum, human brain, and porcine uterus, and research suggests it results from post-translational enzymatic cleavage. Removal of the N-terminal tripeptide, particularly Glu3, reduces IGFBP binding affinity to approximately 1% of native IGF-1 while retaining full receptor affinity. This results in approximately 10-fold enhanced potency in cell proliferation and hypertrophy assays. The half-life is very short at approximately 20-30 minutes, making it a rapid-acting, predominantly local agent. Research administration routes include subcutaneous and intramuscular injection.
IGF-1 DES signals through the same IGF-1R/PI3K/Akt and MAPK/ERK pathways as native IGF-1. The critical mechanistic distinction is near-complete bypass of IGFBP regulation, meaning virtually all administered compound is immediately bioavailable at the receptor. The short half-life and IGFBP evasion suggest predominantly autocrine/paracrine action at the injection site. Research indicates satellite cell activation and proliferation, myoblast differentiation stimulation, and localized protein synthesis enhancement. In brain tissue, where Des(1-3)IGF-1 is naturally produced, research suggests it may function as a local growth factor independent of circulating IGF-1.
Gillespie et al. (1990) demonstrated in GH-deficient mice that 3 ug/day of des(1-3)IGF-I produced equivalent effects to 30 ug/day of native IGF-I, confirming approximately 10x potency in vivo. The lower dose increased kidney and heart weights, while higher doses increased liver, lung, and stomach weights. Simes et al. (1991) showed IC50 values of approximately 1 ug/L for des(1-3)IGF-I versus approximately 20 ug/L for IGF-I (approximately 20-fold potency difference) in GH secretion inhibition assays. Tomas et al. (1992) confirmed approximately 2.5x greater potency than native IGF-I in dexamethasone-treated rats. No human clinical trials have been conducted. Ballard et al. (1996) reviewed the compound and noted that clinical opportunities were 'not yet evaluated.' The compound is not approved by any regulatory agency.
The information on this page is provided for educational and research reference purposes only. This is not medical advice. Always consult a qualified healthcare professional before making any health-related decisions.
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Somatrogon is marketed as Ngenla (approved June 2023) for paediatric growth hormone deficiency in children aged 3 years and older. In the pivotal trial, once-weekly somatrogon produced growth rates equivalent to daily somatropin injections (10.1 cm/year versus 9.8 cm/year), confirming that reducing injection frequency does not compromise growth outcomes. Ngenla represents a meaningful advance for paediatric patients and their families, reducing injections from 365 to 52 per year. Treatment adherence has been a persistent challenge with daily growth hormone, and weekly dosing is expected to improve long-term outcomes through better compliance. Somatrogon competes directly with somapacitan (Sogroya), the other approved weekly growth hormone, creating a new generation of less burdensome treatment options.
MGF has no marketing authorisation. No human clinical trials have been conducted. The evidence base consists of animal studies and cell culture experiments. A single mouse study reported increased muscle fibre size after intramuscular injection. The compound's very short half-life (estimated minutes) in its native form has led to the development of PEGylated versions (PEG-MGF, #105) in unregulated channels, though this creates a pharmacologically distinct molecule. Products available through unregulated channels lack pharmaceutical quality assurance.
Tesamorelin is marketed as Egrifta SV (approved November 2010) for the reduction of excess abdominal fat in HIV-infected patients with lipodystrophy. In clinical trials, it reduced visceral fat by approximately 15% compared to a 5% increase with placebo, and this reduction was sustained with continued treatment. Tesamorelin occupies a unique niche — it is the only approved GHRH analogue and the only medication specifically approved for HIV-associated lipodystrophy. Beyond its approved indication, it has attracted research interest for potential effects on liver fat, cognitive function, and peripheral neuropathy. Fat reduction reverses when treatment stops, and it is not approved for general weight loss or body composition purposes.
This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making decisions about your health.
