Just a few notes...PNN355 is in Phase I clinical
trials. We haven't seen the results, but I assume that this is for
PN355 alone. It was shown to be effective and safe (give us the
results, please!).
Yes, PN355 will be the foundation for a combination of drugs. However,
Dr. Babish was not clear on where the other drug would come from.
It would be highly unusual for PRLN to add an investigational
drug to the PN355 in the Phase II trials. (Instead, for each
combination, they would have to start over again.) What I think they
intend to do is to try PN355 in combination with currently approved
drugs. Any comments on that one?
Also, if I understand correctly, the point of the c-mos discovery is
that this is a human component involved (publish the scientific paper
please!). Since HIV mutates rapidly, it can become resistant to
the protease inhibitors, and reverse transcriptase inhibitors,
which both target proteins FROM THE HIV. Since HIV mutates
rapidly, the inhibitors may become ineffective as their targets
mutate. However, c-mos does not mutate rapidly, and PN355 should
remain effective, regardless of HIV's mutations. (However, it is still
a grteat idea to target three pathways to inhibit HIV instead of
just one.)
I assume this is
also the basis for their claim that they can determinme "long-term"
survivors. Perhaps the long-term survivors have different c-mos
kinase? Any comments on this?
BTW, I have discussed this with my girlfriend, who is also a
medical student and used to work in an AIDS lab. She told me that
as part of her job she would take HIV and
infect T-cells from different people in the lab. There was one
guy whom she "couldn't get his cell infected." I asked her:
why didn't you patent this guy's T-cells?!!!
Rick |
