Episode 346: Pharmacology 101: BTK Inhibitors


Episode Artwork
1.0x
0% played 00:00 00:00
Jan 17 2025 52 mins   5

"In B cell malignancies, BTKi inhibits that BTK enzyme which is very upstream. It tells NF-κB to stop signaling into the nucleus and then inhibits proliferation and survival of B cells," Puja Patel, PharmD, BCOP, clinical oncology pharmacist at Northwestern Medicine Cancer Center at Delnor Hospital in Geneva, IL, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about BTK inhibitors.

Music Credit: “Fireflies and Stardust” by Kevin MacLeod

Licensed under Creative Commons by Attribution 3.0

Earn 1.0 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by January 17, 2027. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center’s Commission on Accreditation.

Learning outcome: Learners will report an increase in knowledge related to the BTK inhibitor drug class.

Episode Notes

To discuss the information in this episode with other oncology nurses, visit the ONS Communities.

To find resources for creating an ONS Podcast Club in your chapter or nursing community, visit the ONS Podcast Library.

To provide feedback or otherwise reach ONS about the podcast, email [email protected].

Highlights From This Episode

“1952 we have the discovery by Colonel Ogden Bruton of that severe immunodeficiency due to lack of B-cell maturation, and next linked to e-gamma globular anemia. In 1993, we had Professor Vetrie and colleagues discover that this was actually due to mutation in a kinase, and they called that BTK. And then in 1993 was a discovery of our first BTKi inhibitor in the lab setting, and that’s called LFM-A13. It wasn’t until 2013, so that’s 20 years after BTK kinase was discovered, where ibrutinib was our first-in-class BTK inhibitor, and the success of ibrutinib really promoted the exploration of second- and third-generation BTKis.” TS 6:24

“It’s thought that BTK and other members in the pathway are constitutively phosphorylated, which just means they’re spontaneously on. This leads to this uncontrolled activation of NF- κB signaling and thus uncontrolled proliferation and suppression of apoptosis. So, these B cells are rapidly dividing, but they’re not functioning like they’re supposed to be, meaning they won’t differentiate, or, you know, they won’t grow up to be either a plasma cell, like we talked about, or a memory B cell. They’ve been hacked.” TS 10:11

“This class is generally called—if you have to think of an umbrella term—it’s just called targeted small molecule therapies. Now a subclass is BTKi or Bruton tyrosine kinase inhibitors. So, we’re really shifting away from the use of cytotoxic chemotherapy, which is kind of designed to indiscriminately destroy rapidly dividing cells, to a more precise approach of targeting cells based on specific molecular changes in tumor DNA.” TS 13:47

“Cardiac toxicity can manifest as atrial fibrillation. And here I’ll specifically talk about ibrutinib values because we have the most data with it, and the numbers actually get better with second- and third-generation BTKis. So frequency: Grade 1–2 atrial fibrillation was reported in 12%–15% of patients on Ibrutinib. And grade 3 AFib is 3%–5%. The onset, median onset is 8–13 months.” TS 20:23

“For nurses, they should really advise their patients that the caliber of headaches are easily managed and they will decrease over time over a period of four weeks. This is an upfront conversation reassuring the patient that this is not a long-term side effect.” TS 33:47

“One aspect that was being discussed at length was kind of identifying biases and then methods to neutralize those biases. So, I think first you have to identify what your bias could be toward BTK, maybe it’s age or comorbidities or side-effect profile. And then, how can we mitigate our own biases is kind of the solution part to that.” TS 46:26