Replies to post #44758 on Biotech Values

[dewophile]

"Response for HCV is due to the virus' sensitivity to the drug"

but it is also due to the concentration of drug at target sites...the obvious example would be more efficient GI absorption and increased bioavailability of the drug..another could be due to improved target organ absorption from circulation, or increased binding in tissues, regardless of whether that tissue is the liver (which would translate to efficacy) or another tissue like the skin (rash)..another possibility is synergy with another agent in the cocktail - DD speculated some time ago that the rash may in fact be due to boosting of ribavirin, as rash is a common SE of ribavirin..who knows, but certainly it is at least plausible that efficacy and side effects could be linked

[gofishmarko]

Re : Rash as a surrogate marker for response

I haven't seen anything conclusive on this in the HCV area , but there are several cancer treatments that have shown an association between rash and response. In the case of MEDX' MDX-010 , rash ( and/or GI SEs ) is presumed to result from an abrupt reversal of immune tolerance , so one could imagine that reversing a longstanding tolerance to viral disease might have similar effects.

Here's a recent abstract on a proteasome inhibitor - Velcade - that might be doing something similar :

Drug-induced cutaneous vasculitis in patients with non-Hodgkin lymphoma treated with the novel proteasome inhibitor bortezomib: a possible surrogate marker of response?

http://tinyurl.com/336pb4