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Re: DewDiligence post# 697

Friday, 11/14/2014 8:27:05 AM

Friday, November 14, 2014 8:27:05 AM

Post# of 2958
I think another reason I confused the compounds was that Luly was commenting that Novartis also had a cyclophilin inhibitor, Deb-025 and that it might give a preview of what could be attained w/ another DAA (not that it would make any sense to combine two cyclophilin inhibitors)

So what would the Enanta cyclophilin inhibitor look like? Here is what a short snapshot of Deb-025.

http://www.medscape.com/viewarticle/756591_11

It looks interesting. The question would be if the compound could be partnered with drugs to maximize genotype/sub-genotype/resistant subspecies coverage, if the size of dose could be brought down, if once a day dosing was possible, and what of the issue of (increased risk of) hyperbilirubinemia?
That is a number of ifs. : )

Since it is essentially a second generation drug, the Enanta iteration of the same type of inhibitor could be superior in a few ways. I recall an acquaintance taking Deb-025 in trials in summer 2008. So when Novartis resumed trials this past summer in 2014, it was 6 years later, and we now can see that Novartis decided it was not worth pursuing. This is one reason I had some reservations about the likelihood that Deb-025 would suddenly become a player in the HCV space.

An improved version of the drug could however, and given that some of the harder to treat types of patients are being given longer dosing periods a lower (and presumably safer) dose, the pan-genotypic aspect, and the likeihood of knocking down DAA resistance subspecies could hold some promise. It also may be a simple bolt on to almost any regimen if the safety and efficacy were promising.
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