Abacavir is the active component of Prurisol. Prurisol is called abacavir acetate, it's the "acetate" that makes the difference, ha!

Anyway, one of the more knowledgeable poster in iHub posted his/her comment:-

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Unfortunately regarding oral bioavailability, the 25% number for prurisol from 2012 PR was before the Phase I bioequivalent trial in humans, and must have been an estimate for humans from the animal data.

If they say that 350 mg of Prurisol p.o is bioequivalent to 300 gm of Ziagen (Phase I detail recently reported), then the oral bioavailability of Prurisol in humans appears to be 83%*300/350 = 71%.

71% of 350 mg Prurisol ~= 250 mg abacavir into the circulation
83% of 300 mg Ziagen ~= 250 mg abacavir into the circulation

I'm still a little concerned that the active moiety abacavir (which gets converted into carbovir triphosphate for its antiviral effects) may not be any different and we may have generic competition. I don't think management ever really addressed this, even in Bertolino's interview responses.

One interesting thing from their latest presentation to partners (public version of dermatology overview from 7/8/16), was the notion of the potential MOA of abacavir (carbovir triphosphate) in psoriasis: some trigger causes release of human defensin (cathelicidin antimicrobial peptide) LL37, which forms a complex with RNA and DNA to activate dendritic cells and start the whole autoimmune / inflammatory cascade. Perhaps the abacavir (nucleoside analog) interrupts the formation of the LL37-DNA/RNA complex. Will have to read some more about it.

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