DMOAD is basically "disease modifying", so if the treatment groups cluster differently to placebo and these clusters are tight then it represents a modification to the underlying disease, otherwise there's no other reason for why they would cluster differently. Of course it would need to be interpreted in conjunction with the 6 month data, which is vast and complex.
The real picture of how iPPS acts in vivo will come with the autopsy results from the canine study and cross sections of the joint area. This will allow us to see what is happening to ARGS, COMP, CTX etc in the joint. The reality is we don't know how iPPS improves pain and function scores, but we will soon find out. If we see ARGS being built up or retained, then that's disease modifying. You don't need to see a reduction of all biomarkers or the joint returned to its youthful state, that will simply never happen.
PAR doesn't know precisely how iPPS acts in vivo, hence the reason why 002 is exploratory. We have already met the primary endpoint, so all other endpoints are essentially free shots at goal. PAR have an idea of how iPPS works from previous studies, but we now need to show 1) how iPPS improves pain and function scores in vivo (for approval) and 2) whether or not iPPS halts the disease process (for the DMOAD label).
For CTX-II, IL-b and C2C, I presume either they couldn't really detect these proteins in enough of the synovial fluid samples to generate meaningful results or they were only present in very low quantities. PAR previously identified CTX-II reduced in the serum of trial participants and in the canine study, so we should expect to see it as part of the 6 month data release.
PAR Price at posting:
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