Prurisol bioequivalence is great news, but we will have to wait for the Phase II/III study to see if it works in humans with psoriasis, and thus might achieve blockbuster status.
I mean, it was pretty much a given (in my mind, but alas, not the FDA's) that the abacavir acetate would convert to abacavir in humans like it did in animals, and similar to abacavir from abacavir sulfate (Ziagen, for HIV). I guess this trial was required to pursue the 505(b)2 pathway of FDA approval, since we're saying we just have a new form of the approved drug, abacavir, in a different delivery vehicle, so to speak.
What isn't so certain is if prurisol treats psoriasis in humans as well as it did in the humanized mouse model. I haven't even seen any plausible mechanism of action of prurisol in psoriasis, other than related to "the principle of PRINS reduction." How, exactly does abacavir reduce PRINS and treat psoriasis? Does it inhibit production of the PRINS lncRNA or its interactions?
I think the general concept of prurisol is that it is a prodrug of abacavir, and should have less toxicity due to the way it is metabolized into its apparent active metabolite, carbovir triphosphate (a nucleoside analog reverse transcriptase inhibitor against HIV). It's interesting that abacavir itself is a less toxic prodrug of carbovir.
The whole idea of a less-toxic prodrug for a toxic antiviral (or anti-inflammatory apparently here) nucleoside analog can be a lucrative one. Chimerix (CMRX) has shown some nice data for brincidofovir, prodrug of cidofovir, a much less toxic, but effective broad-spectrum antiviral against CMV, adenoviruses, and other viruses.
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