Bristol’s Heir to Gleevec
Forbes Magazine writer Robert Langreth reported yesterday on late-breaking clinical results with Bristol-Myers Squibb’s new anticancer candidate BMS-354825, currently being investigated at UCLA in phase II studies on CML patients. According to Langreth’s account, the BMS compound is 500-times more potent than Gleevec, the current miracle drug for this kind of leukemia. In addition, BMS-354825 is active against 14 out of 15 CML strains resistant against Gleevec.
It’s great to read about these kinds of successes from the pharmaceutical industry, especially since they are so rare, comparatively speaking. Langreth pointed out that BMS initiated their CML-program in 2000, after finding that BMS-354825 works even better against CML cancer cell lines than the ones it was originally designed for. I guess you can call that a lucky break.
No, what struck me about the reporting was that it gave the impression that - as of 2004 - pharmaceutical companies have finally learned their game well enough to pump out new drugs within no time.
“The finding has broad implications beyond leukemia because it provides a paradigm for other researchers attempting to design targeted cancer drugs. This is an example of how to do mechanism-driven cancer drug development…”
What can I say? [a] Rarely do you have a mono-genetic disease such as CML, where jamming up a single kinase stops the cancer dead in its tracks. Most of the time, a given disease has multiple pathways that compensate for each other should you fiddle with individual parameters in the equation. [b] It’s great when you have structure-based drug design at your disposal, meaning you can get 3-D pictures of your compound bound to the protein. A picture is worth more than a thousand words - only problem is, what if your membrane-bound protein doesn’t form crystals ?
We should certainly celebrate our successes with the public, but at the same time we shouldn’t raise expectations that success is a routine matter in our industry.