ICPT OCA is a FXR agonist and is a direct competitor of Novartis FXR agonist. They are both targeting earlier fibrosis stages trying to prevent progression to Cirrhosis.
CNAT is also in ph2 in NASH Fibrosis but its not their focus and might be used in combination with NVS FXR agonist, hence resulting more effective than ICPT OCA monotherapy.
CNAT is focussing on NASH Liver Cirrhosis instead,where it has already given efficacy signs and I think it will expand to other Liver Cirrhosis etiologies, where it has proved to be as effective as in NASH Cirrhosis. So any news about ICPT OCA I would say it is almost irrelevant for CNAT.
the LC segment is made of patients who need treatment most and only current treatmnt is Transplant, for a tiny % of patients, due to costs, risks, lack of donours. Decompensated patients have a 1 year death risk ranging from 20% to 57%. No other drugs has ever proved effective in improving High Portal Vein Pressure or MELD/Child Pugh score as Emricasan, and other companies developing NASH LC drugs are GALT (whose drug has already failed its NASH stage 3 fibrosis trial), whilst GILD Simutuzumab NASH Cirrhosis trial has been discontinued. Basically Emricasan success, at least based on current scenario, will entirely depend on how effective is at controlling/reversing Liver Cirrhosis hence allowing natural Liver healing and function improvement. So far it has shown that it is capable to do that.
All in all, also considering CNAT and NVS agreement, Emricasan is in much better shape than OCA, in both NASH Fibrosis (as combo therapy if needed) and NASH Cirrhosis, which is a much more lucrative segment than NASH Fibrosis, in addition to also the other LC Etiologies, 4 times bigger market than NASH Cirrhosis. In fact CNAT should be trading in the USD Billions now, not ICPT. The issue with CNAT Emricasan is that it treats something that has never been treated, but nevertheless claims 1.3M lives each year. It is grossly overlooked
