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anonymousone - 23 Mar 2007 03:49 GMT

Seriously, though - it's extremely unlikely that Vertex is going to do
a
Phase 2 on folks with advanced liver damage. Plus, in all clinical
trials so far, VX-950 still had to be combined with Interferon and
Riba,
it was generally given for just 10-14 days, and then treatment was
switched to the standard combo. It gets the viral load down pretty
quickly at the start of treatment, which is certainly a very good
thing,
but VX-950 is not the interferon replacement everyone has been
waiting
for. The virus quickly mutates and becomes resistant to it, so it has
to
be finished off with a (possibly shortened) regular treatment. Also,
P2
trials generally are still relatively risky, so you might be better
off
not attempting to "score" some VX-950 through back channels.

Thomas
*******************************************************************************

Thomas:

Just curious where you got this information:

"The virus quickly mutates and becomes resistant to it"

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Thomas Wagner - 23 Mar 2007 15:47 GMT

>Just curious where you got this information:
>
>"The virus quickly mutates and becomes resistant to it"

Here: http://www.natap.org/2006/AASLD/AASLD_17.htm

VX-950 HCV Protease Inhibitor Resistance Profile: combination therapy
suppresses drug resistance

Brief Summary: Tara Keiffer from Vertex presented an oral talk at AASLD
on VX-950 drug resistance and how to prevent resistance. She presented
an analysis of patients who received VX950 in a 14-day study. The goal
of this sub-study analysis was to identify VX950 resistant variants
(mutations) and the kinetics of their emergence (selection) in patients
dosed with VX950 or VX950+Pegasys. They used a highly sensitive clonal
method to characterize the mutations (viral variants), and they also did
a phenotypic analysis. VX-950 has demonstrated a rapid & profound viral
load reduction; drug resistance mutations can emerge when VX950 is given
alone (as monotherapy), as sequence changes (mutations) in the HCV
genome occur spontaneously & frequently as a natural result of the high
levels of replication of the HCV virus-pre-existing mutations are likely
present at a low level prior to drug treatment; but, resistant HIV and
wild-type HCV (non-resistant virus) were suppressed & became
undetectable with Pegasys added in combination therapy. With continued
use of Pegasys+Ribavirin, after VX950 was stopped in the short-term
study of VX950, wild-type & resistant HCV were suppressed & became or
remained undetectable. [...]

Thomas

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