Abstract: A method of treating a subject, in particular a human, suffering from non-small cell lung cancer includes administering a bufadienolide to the subject. A method of inhibiting the proliferation and inducing the cell death of non-small cell lung cancer cells, a method of inhibiting the Epidermal growth factor receptor (EGFR) kinase activity in non-small cell lung cancer cells harboring an abnormality in the EGFR gene, and a method of inhibiting Na+/K+-ATPase in non-small cell lung cancer cells includes contacting those cells with a bufadienolide. Proscillaridin A as bufadienolide, with the structure of Formula (III) has advantageously high cytotoxicity against EGFR-dependent non-small cell lung cancer at nano-molar levels while having low toxicity to normal lung cells.

Abstract: A compound suitable for treating EGFR-dependent non-small cell lung cancer exceptionally inhibits activity of the EGFR kinase, in particular in EGFR-dependent non-small cell lung cancer with intrinsic or acquired resistance against at least one EGFR inhibitor. Methods for inhibiting EGFR kinase activity in non-small cell lung cancer cells which harbor an abnormality in the EGFR gene and for targeting cancer cells harboring an abnormality in EGFR gene by contacting EGFR-dependent non-small cell lung cancer cells with said compound are also provided. The compounds allow for an advantageous inhibition of the EGFR kinase activity and induction of apoptosis of the non-small cell lung cancer cells with abnormality in the EGFR gene. Hence, said compounds represent a highly promising treatment option for patients harboring EGFR-dependent cancer.

Abstract: One embodiment relates to a method of treating lung cancer by administering a compound of formula I to a patient.

Abstract: One example embodiment relates to a method of treating non-small cell lung cancer by administering a compound of formula (I) to a patient.

Abstract: A compound suitable for treating EGFR-dependent non-small cell lung cancer exceptionally inhibits activity of the EGFR kinase, in particular in EGFR-dependent non-small cell lung cancer with intrinsic or acquired resistance against at least one EGFR inhibitor. Methods for inhibiting EGFR kinase activity in non-small cell lung cancer cells which harbor an abnormality in the EGFR gene and for targeting cancer cells harboring an abnormality in EGFR gene by contacting EGFR-dependent non-small cell lung cancer cells with said compound are also provided. The compounds allow for an advantageous inhibition of the EGFR kinase activity and induction of apoptosis of the non-small cell lung cancer cells with abnormality in the EGFR gene. Hence, said compounds represent a highly promising treatment option for patients harboring EGFR-dependent cancer.

Abstract: The present invention relates to a method for treating gefitinib-resistant non-small-cell lung cancer (NSCLC) comprising administering an effective amount of a resveratrol analog, (Z)3,4,5,4?-tetramethoxystilbene (TMS), to a subject in need thereof. The present invention also relates to a method for inducing apoptosis in gefitinib-resistant NSCLC cells comprising contacting the resveratrol analog to the cells at an effective amount. The present methods are mediated by different signaling pathways connected to cell proliferation and differentiation such as mTOR, JNK, and certain EGFR phosphorylated tyrosine kinase.

Abstract: The present invention relates to methods for novel drug discovery, treatment and selective targeting for Gefitinib-resistant non-small-cell lung cancer (NSCLC) harboring an additional mutation, in particular, to the discovery of a drug candidate or agent identified by the presently claimed method for use in treating and selective targeting Gefitinib-resistant NSCLC harboring T790M mutation.

Abstract: The present invention relates to a method for treating gefitinib-resistant non-small-cell lung cancer (NSCLC) comprising administering an effective amount of a resveratrol analogue, (Z)3,4,5,4?-tetramethoxystilbene (TMS), to a subject in need thereof. The present invention also relates to a method for inducing apoptosis in gefitinib-resistant NSCLC cells comprising contacting the resveratrol analogue to the cells at an effective amount. The present methods are mediated by different signaling pathways connected to cell proliferation and differentiation such as mTOR, JNK, and certain EGFR phosphorylated tyrosine kinase.

Abstract: The present invention discloses a method of treating Gefitinib-resistant non-small-cell lung cancer, comprising administering an effective amount of an alkaloid. A pharmaceutical composition comprising an alkaloid admixed with a pharmaceutical carrier for treating Gefitinib-resistant non-small-cell lung cancer is also disclosed therein.

Abstract: The present invention relates to methods for novel drug discovery, treatment and selective targeting for Gefitinib-resistant non-small-cell lung cancer (NSCLC) harboring an additional mutation, in particular, to the discovery of a drug candidate or agent identified by the presently claimed method for use in treating and selective targeting Gefitinib-resistant NSCLC harboring T790M mutation.

Abstract: The present invention discloses a method of preventing and treating Gefitinib-resistant non-small-cell lung cancer, comprising administering an effective amount of an alkaloid. A pharmaceutical composition comprising an alkaloid admixed with a pharmaceutical carrier for treating Gefitinib-resistant non-small-cell lung cancer is also disclosed therein.