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The consequence that actually shows up on a bench is this: in a serum-containing medium, the free fraction of added IGF-1 LR3 is much higher than the free fraction of an equal mass of native IGF-1, and it is far less buffered, because the binding-protein reservoir that would normally absorb an excess and release it slowly is largely not engaging with this molecule
The next generation of studies is, in that sense, as much a test of trial design and molecular delivery as of the hypothesis itself
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