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Can New MPN Treatments in Development Decrease Fibrosis?

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Published on February 8, 2016

Transcript | Can New MPN Treatments in Development Decrease Fibrosis?

Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you.        

Andrew Schorr:      

I want to ask you, Dr. Verstovsek, Peppe here, one of the trials she’s on is on a trial that you’d been doing, if I get it right, PRM-151, did I get it right?

Dr. Verstovsek: 

That’s right. 

Andrew Schorr:                  

Okay. What is that?  Where does that fit in here? 

Dr. Verstovsek: 

So PRM-151 is one of the antifibrotic medications.

There were two in studies so far.  And the goal here is to tackle the other problem. It’s not about the genetic makeup or the transformation to acute leukemia that everybody worries about, because that’s very unfavorable for the patients.  It is about the fibrosis that affects the reduction of the blood cell count.  It may also affect, in fact, the quality of life as well as the spleen, but, particularly, the production of the bone marrow cells. So the idea here is to prevent fibrosis from renewing itself.  We identify the cells that lead to the fibrosis.  If it can interrupt that renewal of the fibrosis, then fibrotic cells should go away over time like any other cells in the body.

They die off.  And the PRM-151 is a natural product that is produced in the liver that now we can make as a medication and give it IV once a month in patients that have fibrosis and low blood cell count.

And with the decrease in fibrosis over time, we can improve the quality of life. We can improve the anemia, low platelets, and potentially, also shrink the spleen. So tackling all at once by tackling the process that is inevitable in patients, worsening of the fibrosis, stopping it, and maybe preventing it from even happening, or at least decreasing the fibrosis.  So it’s a different scope of work.  Rather than looking at the intra cellular or inside the cells, the signaling pathways, the JAK2 pathways, or genetic complexity, we are looking at the completely new biological entity.

How does fibrosis happen? What are the cells responsible for fibrosis?  Can we interrupt the fibrotic process? Can we decrease it? Can we prevent it? And that would lead to clinical benefit.  Like here, you mentioned we have patients on the study that are doing very well. And what I’m discovering that with good control of the not just signs and symptoms but the fibrotic process, it appears to be making people live longer.

Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you.

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