Source comparison
Comparison: IGF-1 LR3 vs Endogenous IGF-1 vs Growth Hormone
Half-Life 12–15 hours (bound to IGFBPs) 20–30 hours (evades IGFBPs) 2–4 hours (pulsatile release) IGF-1 LR3's extended half-life removes natural regulatory feedback Receptor Specificity Primarily IGF-1R, regulated by IGFBPs IGF-1R with minimal IGFBP interferen
This comparison does not assign a generated winner or score.
- Half-Life
- 12–15 hours (bound to IGFBPs)
- 20–30 hours (evades IGFBPs)
- 2–4 hours (pulsatile release)
- IGF-1 LR3's extended half-life removes natural regulatory feedback
- Receptor Specificity
- Primarily IGF-1R, regulated by IGFBPs
- IGF-1R with minimal IGFBP interference
- Indirect via hepatic IGF-1 synthesis
- Direct receptor agonism bypasses growth hormone's hepatic control
- Tissue Selectivity
- Controlled by local IGFBP expression
- Systemic. All IGF-1R-expressing tissues
- Broad metabolic effects beyond IGF-1
- Lack of tissue selectivity raises multi-organ risk
- Long-Term Human Data
- Decades of observational studies
- None beyond 8–12 weeks
- FDA-approved for specific deficiencies with monitoring
- Absence of long-term human trials is the critical gap
- Hypoglycaemia Risk
- Low (physiologic regulation)
- Moderate to high (dose-dependent)
- Low (indirect glucose effects)
- Acute hypoglycaemia is documented. Chronic glucose dysregulation is plausible
- Tumour Promotion Concern
- Elevated endogenous levels correlate with increased cancer risk in some cohorts
- Theoretical amplification due to sustained receptor activation
- Similar concerns with supraphysiological dosing
- Mechanism suggests risk. Epidemiological data in humans does not exist