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Related Experiment Video

Updated: Mar 21, 2026

Characterization of the Effects of Migrastatic Inhibitors on 3D Tumor Spheroid Invasion by High-resolution Confocal Microscopy
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Development of MKI-3: A Potent and Selective MASTL Inhibitor with Improved Efficacy for Cancer Treatment.

Ji-In Kim1,2, Ye-Hyun Kim3,4, Navin Pandit1

  • 1Therapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Daejeon 34114, Republic of Korea.

Journal of Medicinal Chemistry
|March 20, 2026
PubMed
Summary
This summary is machine-generated.

We developed MASTL kinase inhibitor-3 (MKI-3), a potent drug that stops cancer cell growth by targeting the MASTL-ENSA-Aurora A pathway. MKI-3 shows promise for treating triple-negative breast cancer with no observed toxicity.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Microtubule-associated serine/threonine kinase-like (MASTL) is a key regulator of mitosis.
  • Dysregulation of MASTL is implicated in cancer development.
  • MASTL is a potential therapeutic target for cancer treatment.

Purpose of the Study:

  • To discover and optimize a potent and selective MASTL kinase inhibitor.
  • To evaluate the in vivo efficacy and safety of the inhibitor.
  • To elucidate the mechanism of action of the novel inhibitor.

Main Methods:

  • Structure-activity relationship studies were conducted to identify MKI-3.
  • In vitro kinase inhibition assays determined potency and selectivity.
  • Cell-based assays assessed antiproliferative effects and mechanism of action in breast cancer cell lines.
  • In vivo studies in a 4T1 triple-negative breast cancer model evaluated tumor growth inhibition and toxicity.

Main Results:

  • MKI-3, a quinazoline-based scaffold, demonstrated potent MASTL inhibition (IC50 = 5.72 nM) with high selectivity over other AGC kinases.
  • MKI-3 exhibited nanomolar cellular activity, suppressed ENSA phosphorylation, and activated protein phosphatase 2A.
  • MKI-3 showed robust antiproliferative effects in multiple breast cancer cell lines.
  • In vivo, MKI-3 significantly reduced tumor growth in treatment-refractory 4T1 triple-negative breast cancer without observable toxicity.
  • MKI-3 disrupted the MASTL-ENSA-Aurora A signaling axis, leading to mitotic catastrophe and apoptosis.

Conclusions:

  • MKI-3 is a potent, selective, and metabolically stable MASTL inhibitor with demonstrated in vivo efficacy.
  • MKI-3 effectively inhibits tumor growth in triple-negative breast cancer models.
  • MKI-3 represents a promising therapeutic candidate for MASTL-targeted cancer therapy.