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Articles de revues sur le sujet « Tyrosine Kinase Inhibitors (TKIs) »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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1

Deininger, Michael. "Targeting Tyrosine Kinase Receptors." Blood 122, no. 21 (2013): SCI—25—SCI—25. http://dx.doi.org/10.1182/blood.v122.21.sci-25.sci-25.

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Abstract Protein tyrosine kinases (PTKs) regulate cell growth and other key functions. Constitutive PTK activation by somatic mutations, overexpression, or abnormal upstream signaling is characteristic of many cancers, including hematologic malignancies, providing a rationale for therapeutically targeting PTKs with small molecules. Imatinib, an ATP-competitive inhibitor of BCR-ABL1, the PTK causal to chronic myeloid leukemia (CML), established a paradigm for tyrosine kinase inhibitors (TKIs) as cancer therapeutics. Although a relatively weak inhibitor, imatinib is effective in most patients wi

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Abruzzese, Elisabetta, Malgorzata Monika Trawinska, Paolo De Fabritiis, and Alessio Pio Perrotti. "TYROSINE KINASE INHIBITORS AND PREGNANCY." Mediterranean Journal of Hematology and Infectious Diseases 6, no. 1 (2014): e2014028. http://dx.doi.org/10.4084/mjhid.2014.028.

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The management of patients with chronic myeloid leukemia (CML) during pregnancy has became recently a matter of continuous debate. The introduction of the Tyrosine Kinase Inhibitors (TKIs) in clinical practice has dramatically changed the prognosis of CML patients. Patients diagnosed in chronic phase can reasonably expect many years of excellent disease control and good quality of life, as well as a normal life expectancy. This fact has come the necessity to address issues relating to fertility and pregnancy. Physicians are not infrequently being asked for advice regarding the need for, and or

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Weatherald, Jason, Louise Bondeelle, Marie-Camille Chaumais, et al. "Pulmonary complications of Bcr-Abl tyrosine kinase inhibitors." European Respiratory Journal 56, no. 4 (2020): 2000279. http://dx.doi.org/10.1183/13993003.00279-2020.

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Tyrosine kinase inhibitors (TKIs) targeting the Bcr-Abl oncoprotein revolutionised the treatment of chronic myelogenous leukaemia. Following the success of imatinib, second- and third-generation molecules were developed. Different profiles of kinase inhibition and off-target effects vary between TKIs, which leads to a broad spectrum of potential toxicities.Pulmonary complications are most frequently observed with dasatinib but all other Bcr-Abl TKIs have been implicated. Pleural effusions are the most frequent pulmonary complication of TKIs, usually associated with dasatinib and bosutinib. Pul

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Rajeswari, Aruna, and Balaprakash Bhavani. "The Role of Tyrosine Kinases in Cancer: Signal Transduction Mechanisms and Therapeutic Targets." International Journal of Health Sciences and Research 14, no. 9 (2024): 320–36. http://dx.doi.org/10.52403/ijhsr.20240942.

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Tyrosine kinases are key mediators in cellular signaling, governing essential processes such as growth, differentiation, metabolism, and apoptosis. In cancer, these kinases often become dysregulated due to mutations, overexpression, or autocrine-paracrine signaling, leading to uncontrolled cell proliferation and tumor development. Receptor tyrosine kinases (RTKs), a prominent subset, are frequently implicated in cancer, with many tumors exhibiting dependency on aberrant RTK signaling. This dependency has made RTKs a major focus for targeted cancer therapies, particularly through the developmen

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Hu, Chunqi, and Xiaowu Dong. "Cysteine-targeted Irreversible Inhibitors of Tyrosine Kinases and Key Interactions." Current Medicinal Chemistry 26, no. 31 (2019): 5811–24. http://dx.doi.org/10.2174/0929867325666180713124223.

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Tyrosine kinases are a subgroup of a large class of protein kinases that transfer phosphate groups from ATP to various amino acid residues. By phosphorylating the tyrosine residues, the tyrosine kinases are responsible for the activation of various proteins through signal transduction cascades, which serves as a ubiquitous mechanism of cell signaling. The frequent success of many tyrosine kinase inhibitors (TKIs) in clinical success and diseasecausing mutations in protein kinases suggests that a large number of kinases may represent therapeutically relevant targets. To date, most of the clinic

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Jacobs, Chaja F., Eric Eldering, and Arnon P. Kater. "Kinase inhibitors developed for treatment of hematologic malignancies: implications for immune modulation in COVID-19." Blood Advances 5, no. 3 (2021): 913–25. http://dx.doi.org/10.1182/bloodadvances.2020003768.

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Abstract Tyrosine kinase inhibitors (TKIs) are used to target dysregulated signaling pathways in virtually all hematologic malignancies. Many of the targeted signaling pathways are also essential in nonmalignant immune cells. The current coronavirus severe acute respiratory syndrome coronavirus 2 pandemic catalyzed clinical exploration of TKIs in the treatment of the various stages of COVID-19, which are characterized by distinct immune-related complications. Most of the reported effects of TKIs on immune regulation have been explored in vitro, with different class-specific drugs having nonove

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Moradpour, Zahra, and Leila Barghi. "Novel Approaches for Efficient Delivery of Tyrosine Kinase Inhibitors." Journal of Pharmacy & Pharmaceutical Sciences 22 (January 13, 2019): 37–48. http://dx.doi.org/10.18433/jpps29891.

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Epidermal growth factor receptors (EGFRs) have potential to be considered as therapeutic target for cancer treatment especially in cancer patients with overexpression of EGFR. Cetuximab as a first monoclonal antibody and Imatinib as the first small molecule tyrosine kinase inhibitor (SMTKI) were approved by FDA in 1998 and 2001. About 28 SMTKIs have been approved until 2015 and a large number of compound with kinase inhibitory activity are at the different phases of clinical trials. Although Kinase inhibitors target specific intracellular pathways, their tissue or cellular distribution are not

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Jabbar, Sarah, and Mohammed Mohammed. "An in silico study of new 1-aminoquinoline-2(1H)-one derivatives as tyrosine kinase inhibitors." Turkish Computational and Theoretical Chemistry 9, no. 1 (2024): 63–74. https://doi.org/10.33435/tcandtc.1500969.

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The field of oncology has been revolutionized by the discovery and development of targeted therapies for cancer. A study focuses on the development of tyrosine kinase inhibitors (TKIs) as effective targeted therapies. Although TKIs have shown promise in targeting cancer cell signaling pathways, the emergence of resistance poses a significant challenge, necessitating the development of novel and potent inhibitors. Virtual docking simulations, which use molecular docking algorithms and scoring functions, predict how these TKIs bind to the enzyme and assess their binding strength. Preliminary res

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Aldaz, Paula, and Imanol Arozarena. "Tyrosine Kinase Inhibitors in Adult Glioblastoma: An (Un)Closed Chapter?" Cancers 13, no. 22 (2021): 5799. http://dx.doi.org/10.3390/cancers13225799.

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Glioblastoma (GBM) is the most common and lethal form of malignant brain tumor. GBM patients normally undergo surgery plus adjuvant radiotherapy followed by chemotherapy. Numerous studies into the molecular events driving GBM highlight the central role played by the Epidermal Growth Factor Receptor (EGFR), as well as the Platelet-derived Growth Factor Receptors PDGFRA and PDGFRB in tumor initiation and progression. Despite strong preclinical evidence for the therapeutic potential of tyrosine kinase inhibitors (TKIs) that target EGFR, PDGFRs, and other tyrosine kinases, clinical trials performe

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Roy, Bhaskar, Avash Das, Kumar Ashish, et al. "Neuropathy with vascular endothelial growth factor receptor tyrosine kinase inhibitors." Neurology 93, no. 2 (2019): e143-e148. http://dx.doi.org/10.1212/wnl.0000000000007743.

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ObjectiveTo explore the association of peripheral neuropathy with vascular endothelial growth factor receptor tyrosine kinase inhibitors (VEGFR-TKIs) use in patients with cancer.MethodsPublished data search up to November 2018 reporting peripheral neuropathy in patients with cancer treated with VEGFR-TKIs was performed. The primary outcome was presence of peripheral neuropathy at the end of the trial. Random-effects meta-analysis was performed to estimate relative risk (RR) of individual treatment.ResultsThirty randomized clinical trials (RCTs) including 12,490 patients with cancer were includ

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Zheng, Tony J., Elizabeth R. Lofurno, Alexander R. Melrose, et al. "Assessment of the effects of Syk and BTK inhibitors on GPVI-mediated platelet signaling and function." American Journal of Physiology-Cell Physiology 320, no. 5 (2021): C902—C915. http://dx.doi.org/10.1152/ajpcell.00296.2020.

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Spleen tyrosine kinase (Syk) and Bruton’s tyrosine kinase (BTK) play critical roles in platelet physiology, facilitating intracellular immunoreceptor tyrosine-based activation motif (ITAM)-mediated signaling downstream of platelet glycoprotein VI (GPVI) and GPIIb/IIIa receptors. Small molecule tyrosine kinase inhibitors (TKIs) targeting Syk and BTK have been developed as antineoplastic and anti-inflammatory therapeutics and have also gained interest as antiplatelet agents. Here, we investigate the effects of 12 different Syk and BTK inhibitors on GPVI-mediated platelet signaling and function.

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Ruzickova, Eliska, Nikola Skoupa, Petr Dolezel, Dennis A. Smith, and Petr Mlejnek. "The Lysosomal Sequestration of Tyrosine Kinase Inhibitors and Drug Resistance." Biomolecules 9, no. 11 (2019): 675. http://dx.doi.org/10.3390/biom9110675.

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The Lysosomal sequestration of weak-base anticancer drugs is one putative mechanism for resistance to chemotherapy but it has never been directly proven. We addressed the question of whether the lysosomal sequestration of tyrosine kinase inhibitors (TKIs) itself contributes to the drug resistance in vitro. Our analysis indicates that lysosomal sequestration of an anticancer drug can significantly reduce the concentration at target sites, only when it simultaneously decreases its extracellular concentration due to equilibrium, since uncharged forms of weak-base drugs freely diffuse across cellu

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Honeywell, Richard, Sarina Hitzerd, Ietje Kathmann, and Godefridus Peters. "Subcellular localization of several structurally different tyrosine kinase inhibitors." ADMET and DMPK 6, no. 3 (2018): 258–66. http://dx.doi.org/10.5599/admet.514.

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Protein tyrosine kinases form an important target for a new class of anticancer drugs, the tyrosine kinase inhibitors (TKIs). Recently we demonstrated that sunitinib, an inhibitor of the membrane-associated vascular endothelial growth factor receptor (VEGFR), is trapped in lysosomes which isolates the drug from its intended target. Therefore we investigated whether this also holds for other TKIs, targeted against different protein kinases. For this purpose we used the ProteoExtractR kit, which enables a subcellular extraction separating cellular proteins into four distinct fractions covering t

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Grigorescu, Alexandru C., and Laura Mihaela Teodorescu. "Tirosyne Kinase Inhibithors (TKIs) in the Treatment of Non –Small Cell Lung Cancer (NSCLC), Practical Pharmacological Aspects." Journal of Drug Delivery and Therapeutics 10, no. 1 (2020): 135–38. http://dx.doi.org/10.22270/jddt.v10i1.3830.

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Tyrosine Kinase Inhibitors are new drugs developed in the last decade. For Non-Small Cell Lung Cancer this drug brought more hope for patients with this disease. Also TKIs are better tolerated then chemotherapy. The efficacy of TKIs is dependent of the presence of Epidermal Grows Factor Receptor gene mutation. This mutation account for about 9% of patients with lung cancer in Europe. This short review try to give the minimal knowledge to clinicians, especially medical oncologists, about mechanism of action, pharmacokinetics of TKIs used in the treatment NSCLC. Keywords: Tyrosine Kinase I

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Mastrangelo, Stefano, Giorgio Attina, and Antonio Ruggiero. "Tyrosine Kinase Inhibitors and Thyroid Toxicity." Biomedical and Pharmacology Journal 16, no. 3 (2023): 1343–51. http://dx.doi.org/10.13005/bpj/2713.

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Some multithyrosine kinase inhibitors have been reported to cause changes in thyroid function. For the management of sunitinib-induced hypothyroidism, an evaluation of thyroid hormone and antibody profile is recommended before starting treatment with tyrosine kinase inhibitors. Patients with pre-existing thyroid dysfunction should undergo dose adjustment of L-thyroxine during treatment with tyrosine kinase inhibitors. Thyroid dysfunction is not a reason to discontinue or reduce the dosage of sunitinib. Their occurrence appears to correlate with increased antitumour efficacy of the inhibitor. T

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Mongre, Raj Kumar, Chandra Bhushan Mishra, Arvind Kumar Shukla, et al. "Emerging Importance of Tyrosine Kinase Inhibitors against Cancer: Quo Vadis to Cure?" International Journal of Molecular Sciences 22, no. 21 (2021): 11659. http://dx.doi.org/10.3390/ijms222111659.

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GLOBOCAN 2020 estimated more than 19.3 million new cases, and about 10 million patients were deceased from cancer in 2020. Clinical manifestations showed that several growth factor receptors consisting of transmembrane and cytoplasmic tyrosine kinase (TK) domains play a vital role in cancer progression. Receptor tyrosine kinases (RTKs) are crucial intermediaries of the several cellular pathways and carcinogenesis that directly affect the prognosis and survival of higher tumor grade patients. Tyrosine kinase inhibitors (TKIs) are efficacious drugs for targeted therapy of various cancers. Theref

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Munker, Reinhold, Cory Cordova, Paula Polk, Charles V. Wendling, Amanda W. Sun, and James A. Cardelli. "Activity of Tyrosine Kinase Inhibitors in Multiple Myeloma." Blood 110, no. 11 (2007): 4804. http://dx.doi.org/10.1182/blood.v110.11.4804.4804.

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Abstract Tyrosine kinase inhibitors (TKIs) have been successfully introduced for the treatment of cancer. Imatinib, dasatinib and nilotinib target bcr/abl and were found to induce molecular remissions in chronic myeloid leukemia. Imatinib has also been found to be active in other malignancies like gastrointestinal stromal tumors. Sunitinib and sorafenib are multi-targeted tyrosine kinase inhibitors and so far, have shown activity against renal cell carcinoma and other cancers. Gefitinib targets the tyrosine kinase of epidermal growth factor receptor and has been found to be active against some

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Qi, Yi-Tian, Yi Hou, and Liang-Chen Qi. "Efficacy of Next-Generation EGFR-TKIs in Patients With Non-Small Cell Lung Cancer: A Meta-Analysis of Randomized Controlled Trials." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382094042. http://dx.doi.org/10.1177/1533033820940426.

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Background: The efficacy of next-generation epidermal growth factor receptor-tyrosine kinase inhibitors in patients with advanced non-small cell lung cancer who have failed first-generation epidermal growth factor receptor-tyrosine kinase inhibitors still remains under investigation. Objective: The aim of this meta-analysis was to systematically assess the efficacy and safety profiles of next-generation epidermal growth factor receptor-tyrosine kinase inhibitors in patients with advanced non-small cell lung cancer who failed first-generation epidermal growth factor receptor-tyrosine kinase inh

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Kaczmarska, Agnieszka, Patrycja Śliwa, Monika Lejman, and Joanna Zawitkowska. "The Use of Inhibitors of Tyrosine Kinase in Paediatric Haemato-Oncology—When and Why?" International Journal of Molecular Sciences 22, no. 21 (2021): 12089. http://dx.doi.org/10.3390/ijms222112089.

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The fundamental pathophysiology of malignancies is dysregulation of the signalling pathways. Protein tyrosine kinases (PTKs) are among the enzymes which, if mutated, play a critical role in carcinogenesis. The best-studied rearrangement, which enhances PTK activity and causes atypical proliferation, is BCR-ABL1. Abnormal expression of PTKs has proven to play a significant role in the development of various malignancies, such as chronic myelogenous leukaemia, brain tumours, neuroblastoma, and gastrointestinal stromal tumours. The use of tyrosine kinase inhibitors (TKIs) is an outstanding exampl

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Asadi, Anoosh, Cathrine Korsholm, and Michael Asger Andersen. "Arrhythmogenic effects of tyrosine kinase inhibitors: a narrative review." Adverse Drug Reaction Bulletin 352, no. 1 (2025): 1367–70. https://doi.org/10.1097/fad.0000000000000082.

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Summary Tyrosine kinase inhibitors (TKIs) are essential in cancer therapy but increasingly linked to arrhythmias, including long QT syndrome (LQT), atrial fibrillation, and ventricular arrhythmias. This review synthesizes current evidence on the arrhythmogenic potential of TKIs across drug classes and targets. Literature was sourced from PubMed, Google Scholar, and regulatory data up to November 2024. TKIs such as endothelial growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), FLT3, breakpoint cluster region-Abelson murine leukemia viral oncogene homolog (BCR-ABL), vascular endoth

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Rassy, Elie, Ronan Flippot, and Laurence Albiges. "Tyrosine kinase inhibitors and immunotherapy combinations in renal cell carcinoma." Therapeutic Advances in Medical Oncology 12 (January 2020): 175883592090750. http://dx.doi.org/10.1177/1758835920907504.

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The treatment landscape of metastatic renal cell carcinoma (mRCC) has been transformed with the advent of antiangiogenics, notably tyrosine kinase inhibitors (TKIs) targeting vascular endothelial growth factor receptor (VEGFR), and immune checkpoint inhibitors (ICIs). Both treatment options have improved outcomes of patients and modified the natural history of mRCC. Clinical investigations have focused on evaluating combination regimens containing ICIs and VEGFR-directed TKIs. Namely, the combinations of axitinib plus pembrolizumab (KEYNOTE-426) and axitinib plus avelumab (JAVELIN RENAL 101) h

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Dimou, Maria, and Panagiotis Panagiotidis. "TYROSINE KINASE INHIBITORS AND INTERFERON." Mediterranean Journal of Hematology and Infectious Diseases 6, no. 1 (2014): e2014006. http://dx.doi.org/10.4084/mjhid.2014.006.

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The use of interferon-a (INF) in chronic myeloid leukemia, when it started in the 80s, was considered as a breakthrough in the therapy of this disease; INF administered alone or in combination with aracytine was the standard choice for treatment for Chronic Myeloid Leukemia (CML) patients unfit for bone marrow transplantation. With the appearance of the first Tyrosine Kinase Inhibitor (TKI) (imatinib) and based on the results of the pivotal IRIS trial, imatinib monotherapy was the new treatment of choice for CML, according to the ELN recommendations. The possibility of combining INF with imati

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Hu, Jiming, Kai Xing, Yan Zhang, Miao Liu, and Zhiwei Wang. "Global Research Trends in Tyrosine Kinase Inhibitors: Coword and Visualization Study." JMIR Medical Informatics 10, no. 4 (2022): e34548. http://dx.doi.org/10.2196/34548.

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Background Tyrosine kinase inhibitors (TKIs) have achieved revolutionary results in the treatment of a wide range of tumors, and many studies on this topic continue to be published every year. Some of the published reviews provide great value for us to understand TKIs. However, there is a lack of studies on the knowledge structure, bibliometric analysis, and visualization results in TKIs research. Objective This paper aims to investigate the knowledge structure, hotspots, and trends of evolution of the TKIs research by co-word analysis and literature visualization and help researchers in this

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Zheng, Tony, Elizabeth R. Lofurno, Sarah Elgamal, et al. "Tyrosine Kinase Inhibitors (TKIs) Targeting Syk and BTK Signaling Differentially Affect PI3K Signalosome Organization and Platelet Function." Blood 134, Supplement_1 (2019): 2074. http://dx.doi.org/10.1182/blood-2019-129066.

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Small molecule tyrosine kinase inhibitors (TKIs) serve increasingly important roles in the treatment of hematologic malignancies and also have shown efficacy in a range of immunological and inflammatory conditions. However, many successful TKI therapies are associated with problematic effects - particularly on platelets - as bleeding complications have been reported for many TKIs, both on and off clinical trials. Bleeding risk is especially apparent for patients treated with ibrutinib and other irreversible inhibitors of Bruton's tyrosine kinase (BTK), several of which now effectively treat mu

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Preda, Mariana, Andrei Seferian, Etienne-Marie Jutant, et al. "Tyrosine Kinase Inhibitor–Induced Pulmonary Arterial Hypertension." Advances in Pulmonary Hypertension 17, no. 2 (2018): 69–74. http://dx.doi.org/10.21693/1933-088x-17.2.69.

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The treatment of the malignant hematological diseases has been revolutionized by the use of tyrosine kinase inhibitors (TKI): for example, imatinib in patients with chronic myeloid leukemia. Dasatinib, a second-generation TKI, has been reported to induce severe pulmonary arterial hypertension (PAH). The mechanism of PAH development is presumed to be endothelial cell toxicity through the production of mitochondrial reactive oxygen species. There are other TKIs that are reported to cause PAH, such as: ponatinib, bosutinib, lapatinib, and lorlatinib. The management of PAH due to TKIs primarily in

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Ergün Barış, Kaya, and Şener Yusuf Ziya. "Hypertensive toxicity of thyrosine kinase inhibitors; Friend or Foe?" Annals of Clinical Hypertension 5, no. 1 (2021): 001–2. http://dx.doi.org/10.29328/journal.ach.1001025.

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Tyrosine kinase inhibitors (TKIs) are widely used in Oncology practice. Hypertension may develop during cancer treatment and TKIs are well known drugs that are associated with drug related hypertensive toxicity. TKI related hypertensive toxicity is not always the indicator of worse clinical outcomes and it may be the sign of treatment efficacy.

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Baselga, José, and Carlos L. Arteaga. "Critical Update and Emerging Trends in Epidermal Growth Factor Receptor Targeting in Cancer." Journal of Clinical Oncology 23, no. 11 (2005): 2445–59. http://dx.doi.org/10.1200/jco.2005.11.890.

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The epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase of the ErbB receptor family that is abnormally activated in many epithelial tumors. The aberrant activation of the EGFR leads to enhanced proliferation and other tumor-promoting activities, which provide a strong rationale to target this receptor family. There are two classes of anti-EGFR agents: monoclonal antibodies (MAbs) directed at the extracellular domain of the receptor and small molecule, adenosine triphosphate–competitive inhibitors of the receptor's tyrosine kinase. Anti-EGFR MAbs have shown antitumor activity

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Krchniakova, Maria, Jan Skoda, Jakub Neradil, Petr Chlapek, and Renata Veselska. "Repurposing Tyrosine Kinase Inhibitors to Overcome Multidrug Resistance in Cancer: A Focus on Transporters and Lysosomal Sequestration." International Journal of Molecular Sciences 21, no. 9 (2020): 3157. http://dx.doi.org/10.3390/ijms21093157.

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Tyrosine kinase inhibitors (TKIs) are being increasingly used to treat various malignancies. Although they were designed to target aberrant tyrosine kinases, they are also intimately linked with the mechanisms of multidrug resistance (MDR) in cancer cells. MDR-related solute carrier (SLC) and ATB-binding cassette (ABC) transporters are responsible for TKI uptake and efflux, respectively. However, the role of TKIs appears to be dual because they can act as substrates and/or inhibitors of these transporters. In addition, several TKIs have been identified to be sequestered into lysosomes either d

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Ciaffaglione, Valeria, Valeria Consoli, Sebastiano Intagliata, et al. "Novel Tyrosine Kinase Inhibitors to Target Chronic Myeloid Leukemia." Molecules 27, no. 10 (2022): 3220. http://dx.doi.org/10.3390/molecules27103220.

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This paper reports on a novel series of tyrosine kinase inhibitors (TKIs) potentially useful for the treatment of chronic myeloid leukemia (CML). The newly designed and synthesized compounds are structurally related to nilotinib (NIL), a second-generation oral TKI, and to a series of imatinib (IM)-based TKIs, previously reported by our research group, these latter characterized by a hybrid structure between TKIs and heme oxygenase-1 (HO-1) inhibitors. The enzyme HO-1 was selected as an additional target since it is overexpressed in many cases of drug resistance, including CML. The new derivati

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Benjamini, Ohad, Hagop M. Kantarjian, Susan O'Brien, et al. "Combination Chemotherapy With Tyrosine Kinase Inhibitors Can Overcome Bcr-Abl Mutations In Acute Lymphoblastic Leukemia Or Blast Crisis CML." Blood 122, no. 21 (2013): 2734. http://dx.doi.org/10.1182/blood.v122.21.2734.2734.

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Background Point mutations in the kinase domain of bcr-abl confer resistance to tyrosine kinase inhibitors (TKIs) in patients with blast phase chronic myeloid leukemia (CML-BC) and Philadelphia positive acute lymphoblastic leukemia (Ph+ ALL). In particular the presence of T315I mutation is highly resistant to most current available TKIs.

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Mokhtari, Dariush, and Nils Welsh. "Potential utility of small tyrosine kinase inhibitors in the treatment of diabetes." Clinical Science 118, no. 4 (2009): 241–47. http://dx.doi.org/10.1042/cs20090348.

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Altered tyrosine kinase signalling has been implicated in several diseases, paving the way for the development of small-molecule TKIs (tyrosine kinase inhibitors). TKIs such as imatinib, sunitinib and dasatinib are clinically used for treating chronic myeloid leukaemia, gastrointestinal stromal tumours and other malignancies. In addition to their use as anti-cancer agents, increasing evidence points towards an anti-diabetic effect of these TKIs. Imatinib and other TKIs counteract diabetes not only in non-obese diabetic mice, but also in streptozotocin diabetic mice, db/db mice, high-fat-treate

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Ravichandran, Pranesh, Cecilia Canizela, Abrahem Sayed, and Rehan M. Hussain. "Tyrosine Kinase Inhibitors: The Next Chapter in Reducing Treatment Burden for Exudative Retinal Diseases?" International Ophthalmology Clinics 65, no. 1 (2024): 9–15. https://doi.org/10.1097/iio.0000000000000551.

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Tyrosine kinase inhibitors (TKIs) serve to inhibit the phosphorylation cascade that usually leads to abnormal processes such as vascular leakage and tumorigenesis. Within retinal diseases specifically, dysregulation of the vascular endothelial growth factor receptor tyrosine kinases can lead to age-related macular degeneration and diabetic macular edema. These diseases have a growing prevalence and are leading causes of vision loss. The current standard of care requires repeated administration of anti–vascular endothelial growth factor injections, which poses a significant burden on patients.

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Frumento, Davide, Giancarlo Grossi, Marta Falesiedi, Francesca Musumeci, Anna Carbone, and Silvia Schenone. "Small Molecule Tyrosine Kinase Inhibitors (TKIs) for Glioblastoma Treatment." International Journal of Molecular Sciences 25, no. 3 (2024): 1398. http://dx.doi.org/10.3390/ijms25031398.

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In the last decade, many small molecules, usually characterized by heterocyclic scaffolds, have been designed and synthesized as tyrosine kinase inhibitors (TKIs). Among them, several compounds have been tested at preclinical and clinical levels to treat glioblastoma multiforme (GBM). GBM is the most common and aggressive type of cancer originating in the brain and has an unfavorable prognosis, with a median survival of 15–16 months and a 5-year survival rate of 5%. Despite recent advances in treating GBM, it represents an incurable disease associated with treatment resistance and high recurre

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Jang, Seong, Bill Strickland, Lynda Finis, et al. "Abstract 4014: Comparative biochemical kinase activity analysis identifies rivoceranib as the most selective VEGFR-2 inhibitor compared with other TKIs with known activity against VEGFR-2." Cancer Research 83, no. 7_Supplement (2023): 4014. http://dx.doi.org/10.1158/1538-7445.am2023-4014.

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Abstract Introduction: Vascular endothelial growth factor receptor 2 (VEGFR-2) is a key regulator of tumor angiogenesis that is highly expressed in several tumor types and is a known target for anti-cancer therapy. Yet the clinical use of VEGFR-2 inhibitors has been challenged by limited efficacy and various side effects, potentially due to the low selectivity of these TKIs for VEGFR-2. Thus, potent VEGFR-2 inhibitors with improved selectivity are needed. Rivoceranib is an oral tyrosine kinase inhibitor (TKI) that potently and selectively inhibits VEGFR-2. A comparison of the potency and selec

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Duggirala, Krishna Babu, and Kwangho Lee. "Abstract B076: Discovery of BBT-176 as fourth generation EGFR tyrosine kinase inhibitor." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): B076. http://dx.doi.org/10.1158/1535-7163.targ-23-b076.

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Abstract Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) improve overall survival rate in patients with EGFR mutated non-small cell lung cancers (NSCLC). However, upon treatment with third-generation EGFR TKIs (Osmertinib) develops C797S resistance[KS1] [u2] in the 20 – 30% of the patients. To date, there is no approved drug for third-generation resistance NSCLC patients. There is an unmet medical need to develop fourth generation EGFR TKIs[KS3] targeting C797S mutation. Extensive structure–activity relationship (SAR) studies led to the discovery of BBT-176 as a rever

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Gvozdeva, Yana. "Nanotechnology-Based Delivery Systems for Enhanced Targeting of Tyrosine Kinase Inhibitors: Exploring Inorganic and Organic Nanoparticles as Targeted Carriers." Kinases and Phosphatases 3, no. 2 (2025): 9. https://doi.org/10.3390/kinasesphosphatases3020009.

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Kinase inhibitors are small molecules that block kinase activity and have significant applications in both therapy and diagnostics. Recent studies suggest that these inhibitors hold great potential as targets for treating a range of diseases, including autoimmune disorders, cardiovascular conditions, cancer, and inflammatory diseases like ulcerative colitis. Ongoing research focuses on developing effective carriers for tyrosine kinase inhibitors (TKIs) to enhance treatment outcomes while reducing side effects. The nano-scale drug carriers have demonstrated the ability to encapsulate a wide ran

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Fatima, Kaynat, Syed Tasleem Raza, Ale Eba, Sanchita Srivastava, and Farzana Mahdi. "A REVIEW ON THE ROLE OF TYROSINE KINASE INHIBITORS AVAILABLE FOR THE MANAGEMENT OF CHRONIC MYELOID LEUKEMIA." Era's Journal of Medical Research 7, no. 2 (2020): 205–11. http://dx.doi.org/10.24041/ejmr2020.34.

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The function of protein kinases is to transfer a γ-phosphate group from ATP to serine, threonine, or tyrosine residues. Many of these kinases are linked to the initiation and development of human cancer. The recent development of small molecule kinase inhibitors for the treatment of different types of cancer in clinical therapy has proven successful. Significantly, after the G-protein-coupled receptors, protein kinases are the second most active category of drug targets. Imatinib mesylate was the first tyrosine kinase inhibitor (TKI), approved for chronic myeloid leukemia (CML) treatment. Imat

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Thompson, Jonathan R., Smitha P. Menon, and Grace K. Dy. "Tyrosine kinase inhibitors for EGFR- and ALK-mutated non-small cell lung cancer." ADMET and DMPK 4, no. 3 (2016): 186. http://dx.doi.org/10.5599/admet.4.3.337.

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<p class="ADMETkeywordsheading">Discovery of the epidermal growth receptor (EGFR) activating mutations and anaplastic lymphoma kinase (ALK) rearrangements has expanded the therapeutic landscape in non-small cell lung cancer (NSCLC). Survival outcomes for patients with these mutations have improved dramatically with EGFR and ALK tyrosine kinase inhibitors (TKIs). Multiple generations of EGFR and ALK TKIs have been rapidly developed, and patients and clinicians now have several options for first- and second-line treatments. While these small molecule TKIs have some similarities in therapeu

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Kong, Jee Hyun, Elliott F. Winton, Leonard T. Heffner, et al. "Outcomes of Chronic Phase Chronic Myeloid Leukemia after Treatment with Multiple Tyrosine Kinase Inhibitors." Journal of Clinical Medicine 9, no. 5 (2020): 1542. http://dx.doi.org/10.3390/jcm9051542.

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We sought to evaluate the outcomes of chronic phase (CP) chronic myeloid leukemia (CML) in an era where five tyrosine kinase inhibitors (TKIs) are commercially available for the treatment of CML. Records of patients diagnosed with CP CML, treated with TKIs and referred to our center were reviewed. Between January 2005 and April 2016, 206 patients were followed for a median of 48.8 (1.4–190.1) months. A total of 76 (37%) patients received one TKI, 73 (35%) received two TKIs and 57 (28%) were exposed to >3 TKIs (3 TKIs, n = 33; 4 TKIs, n = 17; 5 TKIs, n = 7). Nineteen (9.2%) patients progress

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Ata, Fateen, Rola Ghasoub, Maria Benkhadra, et al. "The Applicability of Tyrosine Kinase Inhibitors in Pediatric Chronic Myeloid Leukemia." Blood 142, Supplement 1 (2023): 6372. http://dx.doi.org/10.1182/blood-2023-179341.

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INTRODUCTION The advent of tyrosine kinase inhibitors (TKIs) has shifted the treatment paradigm of adult CML, limiting SCT to a last-resort option for TKI-ineligible or resistant cases. However, determination of the optimal dosing and duration, potential long-term side effects, and the viability of therapy discontinuation remain under-explored aspects of TKIs in pediatric CML. Emerging data supports administering novel TKIs as initial or second-line treatments in pediatric CML amid variable results. This review discusses the RCTs conducted on pediatric patients with CML who received TKIs, aidi

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Peng, Cong, Julia Brain, Yiguo Hu, et al. "Inhibition of heat shock protein 90 prolongs survival of mice with BCR-ABL-T315I–induced leukemia and suppresses leukemic stem cells." Blood 110, no. 2 (2007): 678–85. http://dx.doi.org/10.1182/blood-2006-10-054098.

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Abstract Development of kinase domain mutations is a major drug-resistance mechanism for tyrosine kinase inhibitors (TKIs) in cancer therapy. A particularly challenging example is found in Philadelphia chromosome–positive chronic myelogenous leukemia (CML) where all available kinase inhibitors in clinic are ineffective against the BCR-ABL mutant, T315I. As an alternative approach to kinase inhibition, an orally administered heat shock protein 90 (Hsp90) inhibitor, IPI-504, was evaluated in a murine model of CML. Treatment with IPI-504 resulted in BCR-ABL protein degradation, decreased numbers

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Kondapalli, Lavanya, Sarah Worth, Riem Hawi, et al. "Collaborative cardiovascular management of patients with chronic myeloid leukemia on tyrosine kinase inhibitors." Vascular Medicine 25, no. 3 (2020): 246–54. http://dx.doi.org/10.1177/1358863x20906868.

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Tyrosine kinase inhibitors (TKIs) of the BCR-ABL fusion protein have dramatically changed the mortality of chronic myeloid leukemia (CML) but they carry a risk of serious vascular morbidity. While TKIs do not cure CML, daily oral administration of a TKI can control CML and TKIs are chronic medications. Interestingly, vascular complications can occur at any time a patient is on a TKI. Therefore, it is imperative that all care team members and patients are aware of and watching for possible vascular complications. In the following review, a case of arterial thrombosis secondary to the TKI ponati

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Katopodis, Chudasama, Wander, et al. "Kinase Inhibitors and Ovarian Cancer." Cancers 11, no. 9 (2019): 1357. http://dx.doi.org/10.3390/cancers11091357.

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Ovarian cancer is fifth in the rankings of cancer deaths among women, and accounts for more deaths than any other gynecological malignancy. Despite some improvement in overall-(OS) and progression-free survival (PFS) following surgery and first-line chemotherapy, there is a need for development of novel and more effective therapeutic strategies. In this mini review, we provide a summary of the current landscape of the clinical use of tyrosine kinase inhibitors (TKIs) and mechanistic target of rapamycin (mTOR) inhibitors in ovarian cancer. Emerging data from phase I and II trials reveals that a

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Yamada, Tadaaki, Ryota Nakamura, Hiroyuki Fujii, et al. "Abstract 410: Tumor heterogeneity via AXL activation on primary resistance to EGFR tyrosine kinase inhibitors in EGFR mutated lung cancer." Cancer Research 83, no. 7_Supplement (2023): 410. http://dx.doi.org/10.1158/1538-7445.am2023-410.

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Abstract Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are the standard treatments for patients with advanced non-small cell lung cancer (NSCLC) harboring EGFR mutations. However, some patients show primary resistance to EGFR-TKIs at the first-line treatment setting. AXL, a member of the TAM family of receptor tyrosine kinase, was reported to be involved in primary resistance to EGFR-TKIs for EGFR mutated NSCLC patients. In the present study, we investigated spatial tumor heterogeneity using autopsy specimens from EGFR mutated NSCLC patients, showing primary resista

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Yoshimoto, Mitsuyoshi, Hiroaki Kurihara, and Hirofumi Fujii. "Theragnostic Imaging Using Radiolabeled Antibodies and Tyrosine Kinase Inhibitors." Scientific World Journal 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/842101.

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During the past decade, the efficacy of new molecular targeted drugs such as tyrosine kinase inhibitors (TKIs) and monoclonal antibodies has been proven worldwide, and molecular targeted therapies have become the mainstream in cancer therapy. However, clinical use of these new drugs presents unexpected adverse effects or poor therapeutic effects. Therefore, we require diagnostic tools to estimate the target molecule status in cancer tissues and predict therapeutic efficacy and adverse effects. Although immunohistochemical, polymerase chain reaction (PCR) and fluorescence in situ hybridization

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Puliani, Giulia, and Marialuisa Appetecchia. "Endocrine Toxicities of Antineoplastic Therapy." Cancers 13, no. 2 (2021): 294. http://dx.doi.org/10.3390/cancers13020294.

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Brar, Harpinder K., Jiney Jose, Zimei Wu, and Manisha Sharma. "Tyrosine Kinase Inhibitors for Glioblastoma Multiforme: Challenges and Opportunities for Drug Delivery." Pharmaceutics 15, no. 1 (2022): 59. http://dx.doi.org/10.3390/pharmaceutics15010059.

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Glioblastoma multiforme (GBM) is an aggressive brain tumor with high mortality rates. Due to its invasiveness, heterogeneity, and incomplete resection, the treatment is very challenging. Targeted therapies such as tyrosine kinase inhibitors (TKIs) have great potential for GBM treatment, however, their efficacy is primarily limited by poor brain distribution due to the presence of the blood–brain barrier (BBB). This review focuses on the potential of TKIs in GBM therapy and provides an insight into the reasons behind unsuccessful clinical trials of TKIs in GBM despite the success in treating ot

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Kohno, Takashi, Junya Tabata, and Takashi Nakaoku. "REToma: a cancer subtype with a shared driver oncogene." Carcinogenesis 41, no. 2 (2019): 123–29. http://dx.doi.org/10.1093/carcin/bgz184.

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Abstract RET (REarranged during Transfection), which encodes a receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor, plays a role as driver oncogene in a variety of human cancers. Fusion of RET with several partner genes has been detected in papillary thyroid, lung, colorectal, pancreatic and breast cancers, and tyrosine kinase inhibitors (TKIs) for RET (particularly RET-specific inhibitors) show promising therapeutic effects against such cancers. Oncogenic mutations within the extracellular cysteine-rich and intracellular kinase domains of RET drive medullar

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Nguyen, Elena, and Jason Ear. "Abstract 1665: Investigating Daple-FLT3 gene fusion in leukemia cells and its response to kinase inhibitors." Cancer Research 84, no. 6_Supplement (2024): 1665. http://dx.doi.org/10.1158/1538-7445.am2024-1665.

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Abstract Gene fusions are frequently found in leukemia and other cancers. The signaling scaffold protein, Daple (CCDC88C), has been found to undergo gene fusion to the receptor tyrosine kinase, FLT3. Specifically, a fragment of the coiled-coil domain from Daple and tyrosine kinase domain (TKD) of FLT3 are found fused together. How the gene product from this gene fusion functions in rewiring the signaling network in cells and whether this gene product can be targeted though pharmacological inhibitions remain unclear. Cell surface receptors, such as receptor tyrosine kinases (RTKs), activate cel

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Nagappa, Anantha N., Shvetank Bhatt, and Jovita Kanoujia. "Studies on Structures and Functions of Kinases leading to Prostate Cancer and Their Inhibitors." Current Enzyme Inhibition 16, no. 1 (2020): 90–105. http://dx.doi.org/10.2174/1573408016666200324152018.

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Background: Cancer is the uncontrolled growth of abnormal cells in any part of the body. These abnormalities in the cells make them cancer cells, malignant cells, or tumour cells. These cells can infiltrate normal body tissues. Prostate Cancer begins when cells in the prostate gland start to grow out of control. Introduction: According to the National Cancer Institute, an estimated 20 percent of men experience Prostate Cancer in their lifetimes. Prostate Cancer can be divided into castration sensitive or hormone- sensitive Prostate Cancer (CSPC or HSPC) and castration-resistant Prostate Cancer

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