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Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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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...
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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.
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Negative Regulator Molecules01:23

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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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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.
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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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Related Experiment Video

Updated: Jul 1, 2025

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors
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A Highly Anticipated Selective Therapeutic Agent against CDK2: INX-315.

Lotte P Watts1, Sabrina L Spencer1

  • 1Department of Biochemistry and BioFrontiers Institute, University of Colorado-Boulder, Boulder, Colorado.

Cancer Discovery
|March 1, 2024
PubMed
Summary

A new drug, INX-315, selectively inhibits CDK2, showing promise for treating CCNE1-amplified cancers. It also offers potential for breast cancers resistant to CDK4/6 inhibitors.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Cyclin-dependent kinases (CDKs) are crucial regulators of the cell cycle.
  • Dysregulation of CDKs, particularly CDK2, is implicated in various cancers.
  • Resistance to CDK4/6 inhibitors is a significant clinical challenge in breast cancer treatment.

Purpose of the Study:

  • To describe and characterize a novel selective inhibitor of CDK2, named INX-315.
  • To evaluate the therapeutic potential of INX-315 in specific cancer contexts.

Main Methods:

  • Characterization of INX-315 as a selective CDK2 inhibitor.
  • Assessment of INX-315 efficacy in preclinical cancer models, including those with CCNE1 amplification and CDK4/6 resistance.

Main Results:

  • INX-315 demonstrates potent and selective inhibition of CDK2.
  • The agent shows significant promise in preclinical models of CCNE1-amplified cancers.
  • INX-315 exhibits efficacy in breast cancer models that are resistant to existing CDK4/6 inhibitors.

Conclusions:

  • INX-315 represents a promising novel therapeutic agent targeting CDK2.
  • This inhibitor holds potential for treating specific subsets of cancer, including CCNE1-amplified tumors and CDK4/6 inhibitor-resistant breast cancers.