range, you really have no sensitivity or no ability to tell the difference between them simply because when you're on the plateau with a maximal response, you really can have tens or hundreds of times difference in the bioavailability and not see any difference in the response.
So it's critical, if you're going to use this type of response to test the difference between formulations, that you do it at the proper dosing range where you're on the steep, sensitive part of the curve. So that's one of the considerations for doing equivalence testing between products using a pharmacodynamic or clinical response.
How does this situation change? I mean, it seemed a fairly simple, straightforward, beginning to end process, but how have I changed that to look at endogenous drug substances, such as hormones?
Obviously we have now a substance that -- if we try and measure it in blood. In the previous drugs I described, the only source of that drug appearing in blood is from the dosage form that you actually gave. Now, it's not quite so simple. We have not only that dosage form that we gave supplying drug that appears in the blood and