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While endogenous IGF-1 is produced in the liver in response to growth hormone (GH), LR3 is engineered for enhanced performance with a half-life of 2030 hours compared to IGF-1s natural 2030 minutes

Elevated intracellular GSH levels represent both a barrier to conventional therapies and an opportunity to design redox-responsive drug delivery systems

The Arg3 substitution and N-terminal extension substantially reduce IGFBP-3 and IGFBP-5 binding affinity, making IGF-1 LR3 a preferred research tool over native IGF-1 for long-duration cell culture experiments where IGFBP-mediated sequestration would otherwise limit bioavailability

However, it is unclear how tirzepatide increases potency and what role GIP receptor agonism plays [80]