Dr. Sandler Discusses the Tivantinib Mechanism of Action

Alan Sandler, MD
Published: Monday, Jun 25, 2012

Alan Sandler, MD, division chief of Hematology and Medical Oncology at Oregon Health & Science University, discusses the mechanism of action for tivantinib (formally ARQ 197), an oral, small molecule, c-Met inhibitor currently being investigated in several trials, including MARQUEE, a phase III trial for patients with advanced, non-squamous, non-small cell lung cancer.

Sandler explains that the overexpression of the c-Met protein is associated with malignant tumor growth and has been linked to increased proliferation, invasion, metastasis, tumor angiogenesis and decreased tumor apoptosis. Additionally, the overexpression of c-Met has been implicated in the malignant growth of multiple tumors, making it an important anticancer target.

The agent tivantinib is thought to prevent the downstream effects of c-Met overexpression, by binding to the c-Met receptor, which disrupts the c-Met signal transduction pathways.

Alan Sandler, MD, division chief of Hematology and Medical Oncology at Oregon Health & Science University, discusses the mechanism of action for tivantinib (formally ARQ 197), an oral, small molecule, c-Met inhibitor currently being investigated in several trials, including MARQUEE, a phase III trial for patients with advanced, non-squamous, non-small cell lung cancer.

Sandler explains that the overexpression of the c-Met protein is associated with malignant tumor growth and has been linked to increased proliferation, invasion, metastasis, tumor angiogenesis and decreased tumor apoptosis. Additionally, the overexpression of c-Met has been implicated in the malignant growth of multiple tumors, making it an important anticancer target.

The agent tivantinib is thought to prevent the downstream effects of c-Met overexpression, by binding to the c-Met receptor, which disrupts the c-Met signal transduction pathways.


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