I find that a hollow claim. The literature has many examples of AAG being up in various disease and inflammation states (RA, prostate cancer, Crohn's) and that the relationship isn't necessarily linear. I'm not of the impression that these proteins in the serum go up and down in idiopathic fashion. If AAG does not correlate to patient health / biology of disease in some way, then why would you even consider stratifying patients based on it? What would be the biological rationale?*
Perhaps the relationship here is related to its ability to bind drugs? Perhaps use it as a dosing indicator where: patient with high AAG = higher expected drug binding, therefore dose that patient more intensively. This would also explain why high AAG did less well... they didn't get as much free drug?
For the trial I'd put my money on your first scenario. If you have a deep pocketed partner then let them try the stratification.
* The other question for these biomarker data: how many other ones did they measure / test to come up with AAG? I see this type of data presentation very often, and it's usually because the investigator had serum samples and data mined the cr*p out of it. That's why, quite often, the quartile cut offs that they report for a given protein across various little trials never match, making it hard to work off the data prospectively.
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