Poziotinib‐induced cutaneous adverse reactions in the treatment of non‐small cell lung cancer: A case report

Hui, Hai-Zhen; Wang, Mengxin; Guo, Hongwei; Wang, Yingjun; Shi, Bing-Jun

doi:10.1111/ijd.16205

Cited by 3 publications

(3 citation statements)

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“…Although poziotinib is generally well‐tolerated in clinical trials, its accumulation can induce serious cutaneous reactions. 30 Our results demonstrated that Schisandrins were potent inhibitors of CYP3A4 and CYP2D6 and could increase the exposure of poziotinib. Therefore, the combination of SA/SB and poziotinib should be avoided or carefully monitored in clinic.…”

Section: Discussionmentioning

confidence: 56%

“…CYP450‐mediated DDIs are the common causes of adverse drug reactions, which can significantly affect drug efficacy and lead to serious consequences. Although poziotinib is generally well‐tolerated in clinical trials, its accumulation can induce serious cutaneous reactions 30 . Our results demonstrated that Schisandrins were potent inhibitors of CYP3A4 and CYP2D6 and could increase the exposure of poziotinib.…”

Section: Discussionmentioning

confidence: 65%

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Inhibitory effect of Schisandrin on the pharmacokinetics of poziotinib in vivo and in vitro by UPLC‐MS/MS

et al. 2023

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Background As a pan‐HER tyrosine kinase inhibitor with a promising application prospect, poziotinib is likely to be coadministered with Schisandrins in clinical treatment due to its anticancer activities. Methods Eighteen Sprague–Dawley rats were randomly divided into three groups: Schisandrin A group and Schisandrin B group (20 mg/kg daily for 1 week), and control group (vehicle). On day 8, poziotinib (2 mg/kg) was administered by oral gavage 30 min later. An in vitro study was developed to identify the possible mechanisms of Schisandrins on poziotinib metabolism. All analytes were detected by UPLC/MS–MS, and molecular docking was performed by AutoDock Tools. Results When rats were preadministered with Schisandrin A, AUC (0−∞) and Cmax of poziotinib were obviously increased by 0.79‐ and 1.17‐fold, whereas the Vz/F and CLz/F values were dramatically decreased. The results in Schisandrin B group presented similarly. Both Schisandrin A and Schisandrin B were mixed inhibitors of poziotinib in RLMs, and Schisandrin B showed stronger inhibitory activity with IC 50 values of 2.55 μM for M1 and 6.97 μM for M2. Molecular docking analysis demonstrated that Schisandrin A and Schisandrin B exhibited a strong binding ability towards CYP2D6 as compared to CYP3A4. Conclusion All results provided the direct evidence of the pharmacokinetic drug–drug interactions (DDIs) between Schisandrin and poziotinib. Thus, particular attention should be paid when poziotinib is taken together with Schisandrins in clinical practice.

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Section: Discussionmentioning

confidence: 56%

Section: Discussionmentioning

confidence: 65%

Inhibitory effect of Schisandrin on the pharmacokinetics of poziotinib in vivo and in vitro by UPLC‐MS/MS

et al. 2023

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“…In the treatment of patients with lung cancer, standard platinum-based doublet therapy, which is the traditional chemotherapy regimen, has not made a breakthrough in the improvement of the survival rate ( 6 ). In addition, there can be serious adverse reactions, including cutaneous adverse reactions and diabetic ketoacidosis, to certain drugs, including poziotinib and pembrolizumab ( 7 , 8 ). Therefore, the development of alternative effective treatments is an important topic in lung cancer research.…”

Section: Introductionmentioning

confidence: 99%

Britannin inhibits cell proliferation, migration and glycolysis by downregulating KLF5 in lung cancer

Wang,

Yu,

et al. 2024

Exp Ther Med

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Lung cancer is a harmful type of malignancy and the leading cause of cancer-associated mortality. It is therefore imperative to develop novel drugs effective for treating this cancer. The Traditional Chinese Medicine compound Britannin has been previously reported to inhibit the development of certain cancers, such as pancreatic, breast and liver cancer. Moreover, Kruppel-like factor 5 (KLF5) has been identified an on oncogene in lung cancer. In the present study, the possible regulatory effects and underlying mechanism of Britannin in lung cancer were investigated. A549 and 16HBE cells were treated with different concentrations of Britannin. Subsequently, Cell counting kit-8, EdU staining and colony formation assays were used to detect the proliferative ability of these cells. Cell migration was detected by wound healing and Transwell assays, respectively. XF96 extracellular flux analyzer was used to analyze the extent of extracellular acidification and oxygen consumption rate in cells, whereas assay kits were used to detect glucose and lactic acid levels in the cell supernatant. The targeting effect between Britannin and the KLF5 protein was investigated using molecular docking technology. The protein expression levels of KLF5 in cells challenged with Britannin was detected by western blotting. Finally, overexpression of KLF5 in A549 cells was performed before cell proliferation, migration and the glycolysis rate were measured to explore the regulatory effects of Britannin. Britannin was found to inhibit the proliferation, migration and glycolysis of lung cancer cells, during which the protein expression levels of KLF5 were decreased. This suggests that Britannin regulated the expression of KLF5 in A549 cells. Overexpression of KLF5 reversed the inhibitory effects of Britannin on the proliferation, migration and glycolysis in lung cancer cells. In conclusion, these results suggest that Britannin can inhibit cell proliferation, migration and glycolysis by downregulating KLF5 expression in lung cancer cells.

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Poziotinib

2022

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Poziotinib‐induced cutaneous adverse reactions in the treatment of non‐small cell lung cancer: A case report

Cited by 3 publications

References 4 publications

Inhibitory effect of Schisandrin on the pharmacokinetics of poziotinib in vivo and in vitro by UPLC‐MS/MS

Inhibitory effect of Schisandrin on the pharmacokinetics of poziotinib in vivo and in vitro by UPLC‐MS/MS

Britannin inhibits cell proliferation, migration and glycolysis by downregulating KLF5 in lung cancer

Poziotinib

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