Hematologic Oncology Update, Issue 3, 2016 (Video Program) - Video 18

DR TIBES: No, it just kills a lot of cancer cells. And it’s a direct mechanism, so you essentially take this Bcl-2 away. And the apoptotic escape — so the cell death escape — is just opened up. So you see cell deaths and tumor lysis.

DR LOVE: Do you think there’s something biologically also about tumor lysis in CLL and venetoclax, specifically, there’s some — I’m just curious why you see it so often.

DR TIBES: I think it’s just a very potent drug. It’s a very potent drug that has a direct on-target effect of taking the brake away, essentially. You take the brake away to cell death, and it just opens up the floodgate.

DR LOVE: That's fascinating. Fascinating.

DR TIBES: And that’s why this drug is given often at lower dosages the first couple of days a week. And then the dosage is increased. In the trials, you actually do observe the patients the first few days in the hospital for tumor lysis. So that’s very important. You have to monitor, because it’s a potent drug.

And we’ve seen tumor lysis with other drugs, as well. There’s the drug flavopiridol, which is not approved, or a CDK, so cyclin-dependent kinase inhibitors. We also have seen tumor lysis in CLL and other diseases. So it’s just being aware of managing them. And then we can prevent it, essentially.

Non-Hodgkin lymphoma (NHL), Hodgkin lymphoma and chronic lymphocytic leukemia (CLL)

Acute and chronic leukemias and myeloproliferative neoplasms

Multiple myeloma (MM)