Can Next-Generation PI3K Inhibitors Unlock the Full Potential of the Class in Patients With B-Cell Lymphoma?

Tycel J Phillips1, Jean-Marie Michot2, Vincent Ribrag2

  • 1Rogel Cancer Center, University of Michigan, Ann Arbor, MI.

Insights

Relapsed non-Hodgkin lymphoma (NHL) treatment is improving, but new therapies are needed. Phosphatidylinositol 3-kinase (PI3K) inhibitors show promise for relapsed or refractory NHL, with ongoing research focused on newer agents and combinations.

Area of Science:

  • Oncology
  • Hematology
  • Pharmacology

Background:

  • Outcomes for non-Hodgkin lymphoma (NHL) are improving, yet relapse remains a significant challenge.
  • Existing treatments for relapsed or refractory NHL have limited efficacy.
  • The phosphatidylinositol 3-kinase (PI3K) pathway is implicated in hematologic malignancies.

Purpose of the Study:

  • To review the current landscape of PI3K inhibitors in treating relapsed or refractory NHL.
  • To discuss the development and potential of newer PI3K inhibitors.
  • To explore strategies for improving therapeutic outcomes in NHL.

Main Methods:

  • Review of current literature on PI3K inhibitors for NHL.
  • Analysis of approved PI3K inhibitors (idelalisib, copanlisib, duvelisib) for follicular lymphoma.
  • Discussion of ongoing clinical development of novel PI3K inhibitors.

Main Results:

  • Three PI3K inhibitors are approved for relapsed/refractory follicular lymphoma, with response rates of 40-59%.
  • Toxicities associated with approved PI3K inhibitors necessitate careful risk/benefit assessment.
  • No PI3K inhibitors are currently approved for aggressive NHL.

Conclusions:

  • Newer PI3K inhibitors are in development to enhance treatment benefits for relapsed or refractory NHL.
  • Optimizing PI3K inhibitor therapy may involve developing agents with reduced toxicity.
  • Combination strategies involving novel PI3K inhibitors and other antitumor agents hold promise for improved NHL treatment outcomes.

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
4.9K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.4K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
8.2K