As ewave says, there is a huge difference between the two drugs: 4.4xlog(10)-1.5xlog(10)=2.9xlog(10)=>~1000. VPHM's drug as a single agent leaves about thousand hold greater viral counts after 2wks' dosing than the outcome of 950 dosing as a single agent.
On the other hand, if you were to superpose the two drugs for the same duration or sequentially, the resulting effect on viral counts would be additive (because polymerase inhibitor and protease inhibitor hit two independent targets). The resulting counts would be reduced by a factor of nearly one million:
(4.4 + 1.5) x log(10) = 5.9 x log(10).
The side effects would be additive also, but both drugs are well tolerated as single agents.
The above little exercise illustriates the hidden power in combining two different drugs even if one is inferior to the other.
If a pair of two targets interact favorably as in case of PI and IFNalpha, the combined therapy can result in an effect greater than the sum of the two separate effects -- call it synergistic. It can be antagonistic, if the two drugs interfere with each other.
I guess I didn't look at it that way, but would they still continue development of that drug even though there are other polymerase inhibitors out there with greater effects? I think one thing that is tough to factor in when doing assumptions, is that right now I think most assume 48 week tx for possible revenue from any drug, when in fact, it might not be by the time it is approved. Very hard to calculate value for any other partnered compound IMO.
Of course, I was referring to the Gilead's HIV drugs, not their HBV drugs. But, analogous ideas should be explored and exploited by all biotechs and pharmas. They should build corporate synergy on the basis of drug synergies.
The terminology sounds familiar, but the only thing I know about it that is important is that I have read it causes terrible sides. And, VRTX I think would prefer not to used it because the side profile would be better for them (and patients, too, of course) without it.