Skip to Navigation Skip to Search Skip to Content
Search All Centers

Novel CLL Drugs in Development

Read Transcript Download/Print Transcript

Published on January 5, 2018

What could be coming out of the CLL treatment pipeline in the near future? Leading CLL experts, Dr. Michael Keating, Dr. Stephen Spurgeon and Dr. Kathryn Kolibaba, join us to share exciting developments in cancer research that have led to changes in treatment methods. Watch now to discover the way modern therapies are designed and how they work to target CLL cells.

Provided by CLL Global Research Foundation, which received support from AbbVie Inc., Gilead Sciences, TG Therapeutics, Pharmacyclics LLC and Janssen Biotech, Inc., and Genentech. Produced by Patient Power in collaboration with The US Oncology Network, Compass Oncology, and Willamette Valley Cancer Institute and Research Center.

Featuring

What a wonderful time we had! We were excited like fans at a rock concert, but our rock stars were the medical experts.

— Lynn, CLL town meeting attendee

Partners

CLL Global Research Foundation Compass Oncology The US Oncology Network Willamette Valley Cancer Institute and Research Center

You might also like

Transcript | Novel CLL Drugs in Development

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.

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:

So let’s say that with one of these drugs that we’ve had around for even just a few years, you start to see that somebody’s progressing. You have trials trying to see what’s next, right? Some of these are combinations—a number of them are combinations, right? And we’ll meet some of your patients who are doing that.

So, for instance, he was mentioning earlier—Dr. Sharman mentioned SyK inhibitors, we talked about other BTKs—I know it’s alphabet soup. PI3K, and those Lin inhibitors. So what’s the big idea here? Trying to get at the cancer in a different way, or in a more targeted way, or if—he said the Pac-Man mouth, something changed there, you hit the Pac-Man in a different place?

Dr. Kolibaba:      

Yeah, the real exciting part about that signaling pathway is that it is like the signal hopping from one protein to the next, and so each one of those proteins is a potential target to block the signal moving into the cell. And so, we really do, then, need to see if it works and the only way to do that is in clinical trials, to see if that drug is better or not tolerated, to see if it works in people for whom ibrutinib (Imbruvica) has failed. So all of those are clinical trials that we’re glad to offer to patients.

Andrew Schorr:

So, Dr. Spurgeon, you do research at OHSU—they all do, all of you do research—so combination therapies. What’s the idea? I mean, when I had FCR with Dr. Keating—Dr. Keating, I’ll never forget you told me this. You said, “Well, the fludarabine is gonna hit the cell in the moth, and one’s gonna hit it in the knees, and one’s gonna hit it in the solar plexus.” Is that the idea – to try to surround the cell so it has no escape?

Dr. Keating:         

I cleaned up where they were gonna be

Dr. Spurgeon:     

I’ll have to remember that three-pronged approach there. So, I think the key thing about here is we’re trying to outsmart the cancer before it outsmarts us. I think that’s number one. I think you can apply that—some analogies would be how we think about treating tuberculosis or HIV. When HIV was first discovered, we had one drug. HIV quickly outsmarted that one drug, and now we treat it with multiple therapies at once. The same is for tuberculosis.

So when you get this mutation in BTK, or if someone’s on ibrutinib anyway, other pathways may be up-regulated, meaning that the cancer works on trying to find an escape route. Or, not all these cancer cells are exactly the same. They may have a little different genetics to them, and there may be even a portion that’s not responding well to that drug. So, the idea of the combination is just to—like you said, trap it from all sides.

The other thing that’s so relevant—and this has pharmaco-economic implications as well—is that if we could create a combination therapy, an oral combination of three drugs, let’s say—or maybe two drugs, three drugs and an antibody—that you could still get, like you did with chemotherapy, for six months, that fully eradicates the disease and then we can have another period of observation, I think we’d all aim for that due to long-term toxicity, whether it be financial or ongoing side effects.

So I think those are the key things to understand: can we outsmart the cancer, and can we suppress it so we don’t have to do prolonged therapy?

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. 

You might also like