A couple of years brought us to finally having the top line results of especially two large Phase III studies -the combination of ruxolitinib plus navitoclax versus ruxolitinib placebo, and then BET inhibitor pelabresib/ruxolitinib versus rux/placebo. So everybody is expecting those results, kind of like seeing excellent spleen responses but questionable symptoms, so we are all eagerly looking out for how this data will look, how are they going to fill in, and what’s going to happen to these drugs? That is really exciting...
A couple of years brought us to finally having the top line results of especially two large Phase III studies -the combination of ruxolitinib plus navitoclax versus ruxolitinib placebo, and then BET inhibitor pelabresib/ruxolitinib versus rux/placebo. So everybody is expecting those results, kind of like seeing excellent spleen responses but questionable symptoms, so we are all eagerly looking out for how this data will look, how are they going to fill in, and what’s going to happen to these drugs? That is really exciting.
And lots of novel compounds or novel preclinical ideas. The role of, for example, NF-kappaB, TGFbeta mutations or inhibitors, some newer drugs or pathways that we could block. And of course very exciting calreticulin, the calreticulin monoclonal antibody, which is the original, the naked one, as well as the the bispecific with the CD3, which is a poster at ASH, is really, really getting all of us into excitement where we may finally find calreticulin-directed therapy for ET and MF patients and hopefully, hopefully, which I keep saying, separate the calreticulin mutated versus the rest of the MPNs and completely shape the field into the near future.