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Small-Molecule Targeted Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Side effects commonly associated with gefitinib include skin (e.g., acne, dry skin, nail disorders, pruritus, rash, and other skin reactions), GI (e.g., anorexia, dry mouth, and diarrhea), and eye (e.g., blepharitis, conjunctivitis, and dry eye) disorders, epistaxis, hematuria, asthenia, interstitial lung disease, proteinuria, and pyrexia. Less-common side effects include corneal erosion and pancreatitis, and treatment should be discontinued if severe changes to liver function occur.
Novel Anti-Cancer Drugs Based On Hsp90 Inhibitory Mechanisms: A Recent Report
Published in Debarshi Kar Mahapatra, Sanjay Kumar Bharti, Medicinal Chemistry with Pharmaceutical Product Development, 2019
The side effects of targeted therapy are due to the similar binding site morphology of target proteins and normal cellular enzymes. For example, the anticancer drug, gefitinib exhibits its action by inhibiting tyrosine kinases of cancer cells. However, this drug also has an affinity for normal cell epidermal growth factor receptor (EGFR), which is involved in the maturation of keratinocytes in the skin. Hence, folliculitis (acne-like rash) is a major side effect of gefitinib [9, 10]. Additionally, the toxic symptoms were also attributed to the presence of the target proteins in a few of the normal cells. The cancer target proteins are usually under-expressed in healthy cells. Nevertheless, in a few instances, they are able to attract the chemotherapeutic agents towards it even in lower cellular concentration, which is sufficient for normal cell destruction. An example of the aforestated adverse effect is ventricular dysfunction associated with dasatinib therapy. This drug suppresses ABL kinase of cancer cells as well as that of the cardiac myocytes. This leads to cardiac failure in approximately 2% of patients treated with dasatinib in clinical trials [11].
Capitalizing on being “othered”
Published in Shirley Sun, Socio-economics of Personalized Medicine in Asia, 2016
Then, on June 17, 2005, the FDA disallowed the administration of IRESSA to new patients. This was because clinical trials did not show that IRESSA benefited patients, as noted on the U.S. National Cancer Institute (NCI) website (2011): The FDA has carefully reviewed data from two failed clinical studies of gefitinib, one of which was required by the agency as part of the drug’s accelerated approval. This trial enrolled patients with regionally advanced or metastatic NSCLC who had failed one or two prior treatment regimens. In this large study, 1,692 patients were given either gefitinib or [a] placebo. There was no significant survival benefit either in the overall study population or in patients who had high levels of a surface marker called “EGFR.”In the second trial in patients with stage III NSCLC, after completion of induction and consolidation chemotherapy and radiation therapy, patients were given either gefitinib or placebo maintenance therapy. No gefitinib survival benefit could be demonstrated.
The combination of MnO2@Lipo-coated gefitinib and bevacizumab inhibits the development of non-small cell lung cancer
Published in Drug Delivery, 2022
Jisong Zhang, Li Xu, Huihui Hu, Enguo Chen
On the other hand, it is extremely rare that only one anti-cancer drug is used in clinical treatment. Under certain circumstances, combined treatment with multiple anti-cancer drugs can effectively increase the cure rate of cancer, which aims to integrate the efficacy of several drugs and effectively interrupt the growth and spread of cancer (Liao et al., 2014; Zhu et al., 2018). The antiangiogenic drug bevacizumab (Beb) can inhibit angiogenesis, growth and metastasis of tumor by acting on vascular endothelial growth factor (VEGF) signaling pathway. In the treatment of advanced non-small cell lung cancer (NSCLC), Beb in combination with other drugs can effectively improve the survival rate of patients. Therefore, this study combined Beb with gefitinib (Geb), an anti-cancer drug that inhibits epidermal growth factor receptor (EGFR), to exert their anti-cancer advantages and effectively inhibit the growth of NSCLC.
Circ_SETD3 regulates gefitinib sensitivity and tumor progression by miR-873-5p-dependent regulation of APPBP2 in non-small cell lung cancer
Published in Journal of Chemotherapy, 2022
Jun Sheng, Leyi Liu, Ting Dong, Xiang Wu
Lung cancers are the most frequently diagnosed types of aggressive carcinomas [1]. The long-term overall survival of patients with non-small-cell lung cancer (NSCLC), which constitutes more than 80% of all lung cancers, is only 16%, mainly caused by local and distant metastasis [2, 3]. Many lung cancer patients miss the best surgery opportunity owing to the immature diagnostic methods. To date, molecular targeted drugs are still the first-line standard therapy for these advanced-stage lung cancer cases, and gefitinib-based target therapy is deemed to be the common one [4]. Gefitinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (EGFR-TKI), can block EGFR activation by repressing EGFR phosphorylation, and thus inactivates some signaling pathways to mediate cancer cell processes [4]. In despite of the good clinical efficacy of gefitinib, the lung cancer patients who undergo continuous gefitinib treatment acquire resistance to gefitinib [5]. Considering the great therapeutic value of gefitinib, revealing the underlying mechanism behind the resistance of NSCLC to gefitinib is necessary for the treatment of NSCLC.
Host-directed therapies for malaria and tuberculosis: common infection strategies and repurposed drugs
Published in Expert Review of Anti-infective Therapy, 2022
Piyush Baindara, Sonali Agrawal, O. L. Franco
Gefitinib, a drug for metastatic non-small cell lung cancer, inhibits the intracellular phosphorylation of numerous tyrosine kinases associated with transmembrane cell surface receptors, including the tyrosine kinases associated with the epidermal growth factor receptor. Treatment with gefitinib in infected macrophages has shown an increase in lysosomal number and therefore increased Mtb trafficking to lysosomes [200]. In malaria, it has been reported that Gefitinib could disrupt the P. falciparum life cycle by preventing its egress from the red cell [201]. Imatinib is a tyrosine kinase inhibitor that is reported to inhibit intracellular Mtb growth by increasing the autophagic flux by cathepsin D activation and phagolysosomal acidification [202]. Nilotinib is another tyrosine kinase inhibitor that regulates autophagy and restricts Mtb growth in macrophages by inhibiting the phosphorylation of PI3k/Akt/mTOR signaling via blocking of Abelson tyrosine kinase [203]. Ibrutinib inhibits Bruton’s tyrosine kinase (BTK) and increases the autophagic flux by blocking the BTK/Akt/mTOR pathway, which restricts Mtb growth in infected macrophages [204].