Source comparison
MK-677 IGF-1 LR3 for Growth Factor Research: Compound Comparison
Mechanism Ghrelin receptor agonist → endogenous GH secretion Modified IGF-1 analog → direct IGF-1R activation MK-677 preserves pulsatile GH physiology; IGF-1 LR3 isolates receptor-level effects without upstream signalling Bioavailability Oral, 62–68% absorptio
This comparison does not assign a generated winner or score.
- Mechanism
- Ghrelin receptor agonist → endogenous GH secretion
- Modified IGF-1 analog → direct IGF-1R activation
- MK-677 preserves pulsatile GH physiology; IGF-1 LR3 isolates receptor-level effects without upstream signalling
- Bioavailability
- Oral, 62–68% absorption
- Subcutaneous/IM injection, ~100% systemic
- Oral dosing simplifies chronic protocols; injection allows tissue-specific targeting
- Half-Life
- 4–6 hours (pharmacokinetic); 18–24 hours (pharmacodynamic GH elevation)
- 20–30 hours (extended by reduced IGFBP binding)
- IGF-1 LR3 requires less frequent dosing but lacks the metabolic breadth of sustained GH
- Primary Research Applications
- Metabolic studies (lipolysis, glucose homeostasis), bone density, nitrogen retention
- Anabolic signalling studies, muscle hypertrophy models, connective tissue repair
- Use MK-677 when GH's metabolic effects are the variable; use IGF-1 LR3 for IGF-1R-specific investigations
- Purity Standard (Research-Grade)
- ≥98% HPLC, <5 EU/mg endotoxin
- ≥98% HPLC, <5 EU/mg endotoxin, sequence-verified
- Both require equivalent analytical rigor. Avoid suppliers without third-party COAs
- Storage (Lyophilised)
- −20°C, stable 24+ months
- Ambient temperature tolerance is <48 hours for both
- MK-677 and IGF-1 LR3 serve complementary but non-overlapping experimental niches. Laboratories investigating growth hormone's systemic metabolic effects. Lipolytic activity, hepatic IGF-1 synthesis, glucose disposal. Should use MK-677 to preserve endogenous signalling architecture. Studies isolating IGF-1 receptor activation in target tissues, particularly muscle or cartilage, benefit from IGF-1 LR3's extended half-life and reduced binding protein interference.