4627 Background: Sunitinib was shown to induce cardiac toxicity in patients with metastatic RCC. Thus, frequent and detailed assessment of cardiac function and close clinical observation have been considered essential when treating these patients. However, frequent echocardiograms might not be feasible in every single patient in the routine clinical practise. Similarly, electrocardiograms (ECGs) may show a variety of changes, often requiring a cardiologist to interpret the findings within the clinical context. A suitable marker for cardiac toxicity should be easily assessable and detect both pending cardiac damages and clinically relevant cardiac events. Pro-B-type natriuretic peptide (pro-BNP) is a widely studied neuro-hormonal mediator of cardiac damage. The aim of this prospective analysis was to investigate the role of pro-BNP as an early indicator for sunitinib-induced cardiac toxicity. Methods: All patients with mRCC assigned for first-line treatment with sunitinib were analyzed for history or evidence of cardiac diseases. Monitoring included assessment of clinical symptoms, ECGs, echocardiograms and biochemical markers of cardiac damage, i.e. pro-BNP and cardiac Troponin T (TNT). Echocardiograms and ECGs were obtained at baseline, every 3 months and at increase of biochemical markers. Pro-BNP and TNT were assessed at baseline and then every 4 weeks. A significant clinical finding indicating cardiac damage was defined as a pathological echocardiogram, development of clinical symptoms or increased TNT. Results: Twenty two out of 26 patients (84.6%) presented with increased pro-BNP serum levels after a median treatment period of 6 weeks (range 1-71 weeks). Among these patients, 12 (55%) had significant clinical findings, with a pro-BNP level mostly above 1000 pg/ml. Normal pro-BNP levels were always associated with the complete absence of clinical findings for cardiac toxicity. Conclusions: Our observations indicate that pro-BNP serum levels may serve as an easily assessable marker for cardiac toxicity. The cut off level of 1000 ng/ml may represent the threshold for clinically relevant cardiac damage and should lead to temporary treatment interruption and involvement of a cardiologist. Author Disclosure Employment or Leadership Position Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Novartis, Pfizer, Roche, Wyeth