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Pharmaceutics
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Kinase Inhibitor for Cancer Therapy, 2nd Edition
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Kinase Inhibitor for Cancer Therapy, 2nd Edition

A special issue of Pharmaceutics (ISSN 1999-4923). This special issue belongs to the section "Drug Targeting and Design".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 4099

Special Issue Editor

Dr. Francesca Musumeci

E-Mail Website
Guest Editor
Department of Pharmacy, University of Genoa, Viale Benedetto XV, 3, 16132 Genoa, Italy
Interests: pyrazolo[3,4-d]pyrimidines; kinase inhibitors; anticancer agents; small molecules
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer is one of the leading causes of death worldwide, and still, considerable effort is needed to make this pathology curable. Despite the limits of available approaches, kinase inhibitors have marked a turning point in the treatment of different types of tumors. This class of compounds has been the first oral targeted therapy approved for neoplasia, and about 30 compounds have entered the market in the last five years. Kinase inhibitors include small molecules and monoclonal antibodies and are endowed with fewer side effects than classical antitumor agents. The potential for application of this class of drugs is still huge, and this Special Issue focuses on the discovery and development of kinase inhibitors in terms of in silico studies, synthesis and identification of new compounds, drug delivery, formulation studies, and biological and pharmacokinetic evaluation.

In this Special Issue, original research articles and reviews are welcome.

I look forward to receiving your contributions.

Dr. Francesca Musumeci
Guest Editor

Manuscript Submission Information

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Keywords

  • kinase inhibitor
  • cancer
  • targeted therapy
  • small molecule
  • monoclonal antibody
  • drug delivery
  • formulation studies

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Related Special Issue

Published Papers (2 papers)

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Research

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14 pages, 1675 KiB  
Article
Ponatinib Induces a Procoagulant Phenotype in Human Coronary Endothelial Cells via Inducing Apoptosis
by Bálint Krajcsir, Marianna Pócsi, Zsolt Fejes, Béla Nagy, Jr., János Kappelmayer and Ildikó Beke Debreceni
Pharmaceutics 2024, 16(4), 559; https://doi.org/10.3390/pharmaceutics16040559 - 19 Apr 2024
Viewed by 1334
Abstract
BCR-ABL tyrosine kinase inhibitors (TKIs) are effective drugs in the treatment of patients with chronic myeloid leukemia. However, based on clinical studies, ponatinib was associated with the development of thrombotic complications. Since endothelial cells (ECs) regulate blood coagulation, their abnormal phenotype may play [...] Read more.
BCR-ABL tyrosine kinase inhibitors (TKIs) are effective drugs in the treatment of patients with chronic myeloid leukemia. However, based on clinical studies, ponatinib was associated with the development of thrombotic complications. Since endothelial cells (ECs) regulate blood coagulation, their abnormal phenotype may play a role in the development of thrombotic events. We here aimed to investigate the effect of ponatinib on the procoagulant activity of cultured endothelial cells in vitro. Human coronary artery endothelial cells (HCAECs) were incubated with 50, 150, and 1000 nM of ponatinib. Subsequently, phosphatidylserine (PS) exposure and endothelial microvesicles (EMVs) were measured by flow cytometry. In addition, EC- and EMV-dependent thrombin generation was analyzed. To investigate pro-apoptotic effects of ponatinib, the level of Bax and Bcl-xL proteins were studied using Western blot and F3, THBD, and VCAM1 mRNAs were quantified by qPCR. Therapeutic concentrations of ponatinib significantly increased PS expression on ECs and the amount of EMVs which significantly shortened the time parameters of thrombin generation. In addition, these changes were associated with an increased ratio of Bax and Bcl-xL proteins in the presence of the decreased THBD mRNA level. Overall, ponatinib enhances the procoagulant activity of ECs via inducing apoptosis, which may contribute to thrombotic events. Full article
(This article belongs to the Special Issue Kinase Inhibitor for Cancer Therapy, 2nd Edition)
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Review

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24 pages, 3499 KiB  
Review
Mirk/Dyrk1B Kinase Inhibitors in Targeted Cancer Therapy
by Nikolaos Kokkorakis, Marios Zouridakis and Maria Gaitanou
Pharmaceutics 2024, 16(4), 528; https://doi.org/10.3390/pharmaceutics16040528 - 11 Apr 2024
Cited by 1 | Viewed by 1843
Abstract
During the last years, there has been an increased effort in the discovery of selective and potent kinase inhibitors for targeted cancer therapy. Kinase inhibitors exhibit less toxicity compared to conventional chemotherapy, and several have entered the market. Mirk/Dyrk1B kinase is a promising [...] Read more.
During the last years, there has been an increased effort in the discovery of selective and potent kinase inhibitors for targeted cancer therapy. Kinase inhibitors exhibit less toxicity compared to conventional chemotherapy, and several have entered the market. Mirk/Dyrk1B kinase is a promising pharmacological target in cancer since it is overexpressed in many tumors, and its overexpression is correlated with patients’ poor prognosis. Mirk/Dyrk1B acts as a negative cell cycle regulator, maintaining the survival of quiescent cancer cells and conferring their resistance to chemotherapies. Many studies have demonstrated the valuable therapeutic effect of Mirk/Dyrk1B inhibitors in cancer cell lines, mouse xenografts, and patient-derived 3D-organoids, providing a perspective for entering clinical trials. Since the majority of Mirk/Dyrk1B inhibitors target the highly conserved ATP-binding site, they exhibit off-target effects with other kinases, especially with the highly similar Dyrk1A. In this review, apart from summarizing the data establishing Dyrk1B as a therapeutic target in cancer, we highlight the most potent Mirk/Dyrk1B inhibitors recently reported. We also discuss the limitations and perspectives for the structure-based design of Mirk/Dyrk1B potent and highly selective inhibitors based on the accumulated structural data of Dyrk1A and the recent crystal structure of Dyrk1B with AZ191 inhibitor. Full article
(This article belongs to the Special Issue Kinase Inhibitor for Cancer Therapy, 2nd Edition)
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