IGF1-LR3

IGF-1 LR3 is a synthetic analog of insulin-like growth factor-1 engineered to extend biological activity by reducing binding to IGF-binding proteins. In research settings, IGF-1 LR3 is studied for its role in cellular growth signaling, protein synthesis pathways, tissue repair models, and metabolic regulation through IGF-1 receptor activation. For research use only.

1MG | PHYSICIAN USE ONLY

$127.50

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Research Profile

At a Glance

  • Type: Synthetic IGF-1 Analog Peptide
  • Also Known As: Long Arg3 IGF-1; LR3-IGF-1
  • Sequence: Modified IGF-1 with arginine substitution at position 3 and N-terminal extension
  • Molecular Weight: ~9,111 Da
  • Primary Target: Insulin-Like Growth Factor-1 Receptor (IGF-1R)
  • Research Focus: Cell growth signaling, protein synthesis pathways, tissue repair models, metabolic regulation, anabolic signaling
  • Regulatory Status: RUO (Research Use Only); not FDA-approved
  • Categories: Hormone Research; Recovery & Repair; Metabolic Research; Anti-Aging Research

What Research Shows

  • Demonstrates prolonged IGF-1 signaling activity compared to native IGF-1 due to reduced affinity for IGF-binding proteins (IGFBPs), resulting in extended receptor engagement in experimental systems.
  • Activates IGF-1 receptor–mediated anabolic pathways, including PI3K/Akt and MAPK signaling cascades involved in cellular growth, differentiation, and survival.
  • Supports protein synthesis and cellular hypertrophy research, as IGF-1 signaling is a central regulator of muscle cell growth and satellite cell activation in preclinical models.
  • Plays a role in tissue repair and regeneration models, with IGF-1 pathways associated with wound healing, connective tissue remodeling, and cellular recovery following injury.
  • Influences metabolic signaling pathways, including glucose uptake and nutrient partitioning, reflecting IGF-1’s close relationship with insulin signaling in experimental contexts.
  • Demonstrates anti-apoptotic signaling effects in cell culture and animal models, as IGF-1R activation promotes cell survival under stress conditions.

Mechanistic Notes

IGF-1 LR3 exerts its biological effects through sustained activation of IGF-1 receptor signaling pathways:

  • Reduced IGFBP binding: Structural modifications decrease sequestration by IGF-binding proteins, increasing bioavailability and receptor interaction time.
  • IGF-1R activation: Binding to IGF-1 receptors triggers downstream PI3K/Akt and MAPK pathways involved in growth, metabolism, and survival signaling.
  • Anabolic signaling: Activation of mTOR-related pathways supports protein synthesis and cellular hypertrophy in muscle and connective tissue models.
  • Cell survival modulation: IGF-1 signaling inhibits pro-apoptotic pathways and supports cellular resilience during metabolic or mechanical stress.
  • Crosstalk with insulin signaling: Overlapping pathways influence glucose transport, nutrient utilization, and metabolic efficiency in research systems.

What Remains Unknown

  • Lack of controlled human clinical trials evaluating IGF-1 LR3 specifically
  • Long-term safety and tissue-specific effects remain uncharacterized
  • Optimal timing and exposure patterns for different tissue models are not standardized
  • Potential differential effects across cell types and developmental stages require further study