The CDK inhibitors in cancer research and therapy

Jonas Cicenas1, Mindaugas Valius

  • 1Department of Medicine, Institute of Anatomy, University of Fribourg, Rte. Albert- Gockel 1, 1700, Fribourg, Switzerland. j.cicenas@mapkinases.eu

Insights

This review discusses seventeen small-molecule cyclin-dependent kinase (CDK) inhibitors, detailing their targets, availability, and efficacy. It aids researchers in selecting appropriate CDK inhibitors for cancer research and therapeutic applications.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Kinase inhibitors are crucial tools for understanding mammalian cell biochemical processes.
  • Cyclin-dependent kinases (CDKs) regulate cell cycle and proliferation, with deregulation implicated in human tumors and various diseases.

Purpose of the Study:

  • To review seventeen small-molecule CDK inhibitors for their utility in cancer research and therapy.
  • To guide researchers in selecting the most suitable CDK inhibitor for their specific research needs.

Main Methods:

  • Compilation and discussion of seventeen CDK inhibitors.
  • Inclusion of inhibitor targets, commercial availability, and IC(50) values.
  • Overview of clinical studies involving selected CDK inhibitors.

Main Results:

  • Detailed information on seventeen CDK inhibitors is presented.
  • Data on targets, IC(50) values, and commercial availability are provided for each inhibitor.
  • Clinical study data for some inhibitors are summarized.

Conclusions:

  • The review provides a comprehensive resource for researchers investigating CDK inhibitors.
  • Informed selection of CDK inhibitors is facilitated for both research and therapeutic development.
  • Understanding inhibitor profiles aids in advancing cancer research and treatment strategies.

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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...
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...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...