in green, period 2 in magenta, period 3, the baseline is dropping, despite the fact that it's more than 7 weeks since that last dose. So we've affected the kinetics of endogenous T4 by giving those very large doses.
Well, the biology of T4 is very, very complex and this is a schematic that sort of is a testimony to that complexity. I'm not going to go through that schematic, but I want to make a point that Dale mentioned.
In the discussion of bioequivalence, there's talk about rate and extent of absorption and appearance of the active principle in the biophase. Well, what we're talking about here as the biophase is the tissue compartment and the active component probably is more T3 than it is T4. It's much more active in binding the thyroid receptor. Well, of course, we can't measure T3 within cells, but we have a very good surrogate of that, and as has been spoken to before, that surrogate is TSH.
A thing that I have to make a point about is that all of these pathways in this diagram, all of those arrows are controlled by the levels of T3 and TSH. As a result, the half-life of T4 can be as small as 4 days in hyperthyroidism, as much as 9 days in hypothyroidism. So