So currently, as of now, we think that the patient population that will benefit most are those individuals with myelofibrosis who have been receiving a clinically approved JAK inhibitor for some time, but are now showing increasing signs of loss of response. So maybe their spleens are getting bigger, maybe their symptoms are worsening, maybe their white counts are going up...
So currently, as of now, we think that the patient population that will benefit most are those individuals with myelofibrosis who have been receiving a clinically approved JAK inhibitor for some time, but are now showing increasing signs of loss of response. So maybe their spleens are getting bigger, maybe their symptoms are worsening, maybe their white counts are going up. And so the goal of the Type II inhibitor is that these agents will replace these current inhibitors with the goal of seeing, again, can we further maximize treatment response or prolong treatment response, but maybe even best-case scenario, see these MPN cells go away or at least be reduced in the bone marrow of these treated patients. And then long-term, I think we’ll have to see, you know, if there is a response in this relapsed/refractory setting, whether or not there might be a role for these Type II inhibitors for patients who are newly diagnosed in an upfront setting. And so again, this will all sort of be borne out based on the results of this ongoing trial.
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