Side by side

1. 1.Binds the IGF-1 receptor, which drives cell growth, division and survival.
2. 2.Because it escapes IGF-binding proteins, it reaches tissues at far higher free concentrations than natural IGF-1.
3. 3.Its extended half-life means sustained rather than pulsatile signalling.
4. 4.In animal models it increases protein synthesis and glucose uptake in muscle, and also drives connective-tissue and organ growth.
5. 5.It suppresses the body's own growth-hormone output through negative feedback.

• Animal and cell-culture models of muscle growth
• IGF signalling research in cancer biology
• Tissue-engineering and repair models
• Human therapeutic use has been studied only for the approved analogue, not for LR3

• Increased lean tissue in animal models
• Hypoglycaemia — IGF-1 acts like insulin
• Fluid retention, joint pain and carpal-tunnel symptoms seen in the IGF-1 drug class
• Growth of existing tumours is a theoretically and experimentally supported risk

• Hypoglycaemia, occasionally severe
• Jaw and joint pain, carpal tunnel syndrome
• Swelling and fluid retention
• Headache and injection-site reactions
• Possible promotion of existing cancers

Research context only — no human protocol exists for LR3. There are no published human dose-ranging studies; schedules circulating online, such as 20–50 micrograms per day with weekly increases, are entirely anecdotal. Any dose carries a real risk of hypoglycaemia.

Research context only