I'm not disputing that they show difference levels of desmosine reduction in their lab experiments. What I'm suggesting, however, is that the validity of the method of action in the *clinic* needs to show some impact on its mechanistic correlates.
But no matter, let's accept the premise there are different amounts of desmosine reduction in the clinic.
If true, then why is there no difference in relative change in lumen diametre, fistula blood flow or hemodynamically significant stenosis at 3 months for either the 10 or 30 ug doses versus placebo? Shouldn't different extents of desmosine removal show some impact on those three mechanistic surrogates?
Note that the primary patency plots in the phase 2 for 30 ug had seemingly diverged from placebo or 10 ug at the 3 month point.
Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.