allotment, page-86

Maslow, let me give you the example of HBV. Just 3 or 4 years ago there were multiple drug companies involved in HBV treatment, each peddling drugs that were so so in the short term, but developed resistance with longer term use. Our viral hepatitis meetings were dominated by discussions about which combinations reduced the risk of resistance, and what to do for the patients with resistant virus. Then entecavir turned up as monotherapy with virtually no resistance, and shortly after tenofovir with no resistance issues at all. The majority of other companies in this field virtually disappeared overnight. Now our meetings are about whether we can actually cure HBV rather than just suppress it. HBV is now largely owned by Gilead and Roche.

HCV is similar, just a few years behind. Until last year it was whether a protease or polymerase inhibitor with interferon was going to be the best combination. We all knew that HCV got resistant to telaprevir pretty quick so we were going to have to use interferon in the protocol. Then all of a sudden a potent polymerase inhibitor with little/no resistance issues turns up which can cure some patients with ribavirin only. This has changed the playing field. Now everyone knows that resistance is not inevitable with HCV, and suitably engineered drugs can probably avoid it. Two such drugs taken in combination will almost certainly avoid it.

BIT225 potentially had a niche in the 'old world' up until last year, but frankly I don't see it now. As for all the other diseases you mention, there is no comparison with HCV. The latter has a series of defined known proteins that can be individually targeted. Cancers etc are our own cells behaving badly - identifying specific features of each which can be targeted without damaging the behaving cells in our body is dramatically more complex. This is an exciting area in itself because genomics may be opening a door for us here - we now have the ability to identify all the genes active in a specific tumour, and can compare those to the genes active in normal cells of that tissue. It might not be too far off when we can specifically silence the aberrant gene expression in tumours on a personalised basis.