The Thing You Have No Idea About Aurora B inhibitor BI-1356

The primary endpoint, an ACR20 response at week 12, was achieved by the vast majority of patients getting 150 mg or 100 mg twice daily.

Improvement from the rst biologics, Aurora B inhibitor TNF inhibitors, expanded our knowledge of the pathogenesis of inammatory conditions. As TNF inhibitors have been available to rheumatologists for more than a decade, a large body of data has accumulated regarding their safety and ecacy. More recently, biologics with a distinct mechanism of action have been approved. Numerous other targets within the inammatory cascade continue to be identied, and biologic and nonbiologic agents to modulate/inhibit the associated pathways are either in the pipeline or have already been developed. The relative ecacy of these agents remains to be established, and, in time, head to head trials will be required to determine the best treatment options for patients.

Before oering treatment options, the rheumatologist needs to be able to identify patients BI-1356 who are likely to respond to a particular treatment. This ability would allow optimal treatment to be initiated sooner, thereby potentially reducing the costs and the risks to patients and preventing radiological progression. The search continues for biomarkers and molecular networks that can help us better understand the variable response to targeted therapy. Today, the key challenge facing rheumatologists is how best to integrate the advanced therapies into daily practice. c MET has gained considerable interest through its apparent deregulation by overexpression or mutation in various cancers, including non small cell lung cancer. Overexpression of c MET, along with HGF, also appears indicative of an increased aggressiveness of tumors.

Firstly, overexpression of circulating cMET in patients with NSCLC has been significantly associated with early tumor recurrence and patients BI-1356 with adenocarcinoma and MET amplification have also demonstrated a trend for poor prognosis. Cappuzzo and colleagues have provided clear evidence that increased MET gene copy number is a negative prognostic factor, further supporting anti c MET therapeutic strategies in this disease.