>>a good bet that the placebo arm with baseline HbA1C>8 started a lot more additional diabetes drugs during the 1 year trial than the equivalent 1067 arm. Thereby shrinking the apparent benefit of 1067 in the HbA1C>8 subpopulation.<<
The protocol for the ANDES trial isn't on clincialtrials.gov or centerwatch. What's up with that? Is "AGI-1067" not the right keyword? It got me the ARISE trial, obviously listed as no longer recruiting . . .
Your digging and deduction wrt to the patient population in ARISE -- thanks, by the way -- are interesting, indeed. And I saw your Ihub post regarding the cardiologist who dissed the data presented today, but made no comment on the patient populations, either.
Anyhow, the PR announcing the first enrollment for ANDES said that patients could be on one diabetes medication or none. That criterion seems to address the issues you raise reasonably well, I guess, so if your speculation is correct, perhaps AGIX will surprise the bears yet.
While VCAM levels do tend to be elevated in T2 diabetes patients, my search for the causal relationship with glucose control for half an hour or so turned up correlation, but not cause and effect. For example:
care.diabetesjournals.org
"Because HbA1c levels in insulin-sensitive and -resistant patients were comparable, the significant elevation of sVCAM-1 and sE-selectin in insulin-resistant patients may be independent of the plasma glucose level."
That is to say, I can't find the mechanism of action by which VCAM inhibition via AGI-1067 should work. But it's late, I've had some wine, and maybe I'm not researching/thinking well. I invite those with more interest to prove me wrong, I'm not sufficiently motivated to spends hours at it.
Whatever; I no longer have a position, but will be watching.
Cheers, Tuck |
