Thank you for he response, I wonder if you could tell me if my reasoning of the following is correct. In the announcement on the 13th November the following statement was made
• Pre-clinical models suggest that addressing the underlying cause of PKD (the way
that PYC’s drug candidate works) could arrest the course of the disease in
humans, enabling damaged kidneys to regenerate and restore function
My understanding is that "the way that PYC’s drug candidate works" is in reference to our ability to target specific cells effectively. having said that and knowing that the results were in vivo. Unlike the eye candidate where you can't remove someones eye and then test the drug we were able to achieve this with kidneys. The second part to my thoughts is that with the eye candidate there is no way of obtaining definitive results quickly because its just a wait and see game (no pun Intended) but on the other hand with PKD its a bio marker test to see the efficacy.
So the only obstacle with PKD is that of treating patients ie human trials. But as I see it we are in someways further ahead in scientific terms / results with PKD that we are with the eye candidate, in the sense that the data that would be required by BP would be more definitive and resilient than that of the eye candidate.
I am still not sure I have explained myself properly but hope you get the gist of what i am trying to get a grip on
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