Published on August 26, 2014
Dr. David Snyder from City of Hope explains what immunomodulators and interferons are and their role in the treatment of MPNs. He describes what researchers know about how these types of treatments work and how they can be used in combination with other therapies to be more effective.
This event was produced in association with City of Hope and sponsored by Patient Empowerment Network through educational grants from Incyte Corporation and Geron Corporation.
Transcript | MPN Treatments in Development: Immunomodulators and Interferon
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Dr. Snyder, immunomodulators. What’s going on there? What is it, and what’s going on?
So besides the specific targeting of the JAK STAT pathway, we know there are other ways to impact the control of cell activity and cell growth. And there’s a class of drugs that are called immunomodulators, things like lenalidomide (Revlimid), thalidomide (Thalomid), pomalidomide (Pomalyst).
Frankly, I don’t think we know exactly at the molecular level how they do their job, but we do know that they’re often helpful in restoring balance to disregulated cell growth or cell activity, not just in these conditions, MDS, myelodysplastic syndrome, is another area.
Before the JAK inhibitors came along for MPNs the most effective combinations we had were combinations of immunomodulators, thalidomide or revlimid plus prednisone (Deltasone), which could control some of the inflammatory features of these diseases and sometimes improve cell counts and reduce spleen size. And I think there’s still, you know, a role for some of these drugs as we go forward.
Now, we mentioned interferon before. So is there more work going on there with the new interferons?
So Pegasys also has been used in these conditions, and, again, Pegasys is probably better tolerated than the standard interferon. By itself, it also has activity. It’s, you know, 25 percent, 30 percent of patients, in that range, will get some benefit in terms of improvement in blood counts and possibly constitutional symptoms.
Not a home run, and I think we talked about this earlier that the approach with the JAK STAT inhibitors is what is called targeted therapy. You identify a specific, unique genetic defect inside these abnormal cells and then try to develop a drug that can target that specific defect. It’s very elegant.
But, you know, what we’re learning is that maybe that’s not, you know, the whole story. I mean, maybe that’s not the best approach because there are multiple pathways within cells that control the cell growth, and there’s a lot of redundancy built in for any engineers here.
So that if you come in with a drug that’s very specific in where it acts, the cell is going to outsmart the drug and find a way to bypass it and still accomplish what it’s trying to do.
So the idea of combinations therapy of hitting the cell to at least two or more different targets is attractive as a way to help overcome this potential resistance that could emerge to a focused therapy.
So let me see if I understand. So I’m on one expensive medicine now. But you’re talking about there could be another pill, for example, I’ll take that you might recommend some day. Could you take two to control the activity, the malignant activity of the cell in two ways?
That’s correct and, as you said, it does add potential expense both in terms of financial expense and in terms of side effects. Anytime you have one drug with potential side effects and add another, that, you know, complicates the situation.
One approach perhaps is to study how each individual drug works and how it’s tolerated and then combine maybe slightly lower doses of each so that the side effects aren’t quite as severe, but the combination may be even more effective.