Drug class
Antineoplastic - Anaplastic Lymphoma Kinase (ALK) Inhibitors
Antineoplastic anaplastic lymphoma kinase (ALK) inhibitors are a targeted therapeutic class of small-molecule tyrosine kinase inhibitors designed to selectively block oncogenic ALK signaling. Read more about Antineoplastic - Anaplastic Lymphoma Kinase (ALK) Inhibitors
11 drugs in this class 8 manufacturers
Drugs in Antineoplastic - Anaplastic Lymphoma Kinase (ALK) Inhibitors
ZYKADIA (ceritinib)
Antineoplastic anaplastic lymphoma kinase (ALK) inhibitors are a targeted therapeutic class of small-molecule tyrosine kinase inhibitors designed to selectively block oncogenic ALK signaling.
By binding to the ATP-binding pocket of the ALK receptor kinase, these agents disrupt constitutive phosphorylation and shut down downstream oncogenic cascades—such as the STAT3, AKT, and MAPK pathways—that promote malignant cell proliferation and survival.
Therapeutically, this class is primarily indicated for patients with locally advanced or metastatic non-small cell lung cancer harboring an ALK rearrangement.
Select agents within the class also have approved roles or established utility in other ALK-driven malignancies, including relapsed or refractory systemic anaplastic large-cell lymphoma and unresectable inflammatory myofibroblastic tumors.
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pdr.net
Antineoplastic anaplastic lymphoma kinase (ALK) inhibitors are a targeted therapeutic class of small-molecule tyrosine kinase inhibitors designed to selectively block oncogenic ALK signaling Therapeutically, this class is primarily indicated for patients with locally advanced or metastatic non-small cell lung cancer harboring an ALK rearrangement
-
nih.gov
Antineoplastic anaplastic lymphoma kinase (ALK) inhibitors are a targeted therapeutic class of small-molecule tyrosine kinase inhibitors designed to selectively block oncogenic ALK signaling By binding to the ATP-binding pocket of the ALK receptor kinase, these agents disrupt constitutive phosphorylation and shut down downstream oncogenic cascades—such as the STAT3, AKT, and MAPK pathways—that promote malignant cell proliferation and survival
-
nih.gov
By binding to the ATP-binding pocket of the ALK receptor kinase, these agents disrupt constitutive phosphorylation and shut down downstream oncogenic cascades—such as the STAT3, AKT, and MAPK pathways—that promote malignant cell proliferation and survival
-
pdr.net
Therapeutically, this class is primarily indicated for patients with locally advanced or metastatic non-small cell lung cancer harboring an ALK rearrangement Select agents within the class also have approved roles or established utility in other ALK-driven malignancies, including relapsed or refractory systemic anaplastic large-cell lymphoma and unresectable inflammatory myofibroblastic tumors
-
nih.gov
Therapeutically, this class is primarily indicated for patients with locally advanced or metastatic non-small cell lung cancer harboring an ALK rearrangement
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