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Sunitinib

In Advanced, Well Differentiated Pancreatic Neuroendocrine Tumors

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Abstract

Sunitinib inhibits several receptor tyrosine kinases involved in cancer growth, metastasis, and neoangiogenesis, with its active metabolite (SU012662) demonstrating similar potency.

In a randomized, double-blind, multinational, phase III trial, continuous treatment with oral sunitinib 37.5 mg/day significantly prolonged median progression-free survival time (primary end-point) ≈2-fold relative to placebo in adults with locally advanced and/or metastatic, well differentiated pancreatic neuroendocrine tumors (pNETs).

Sunitinib was also associated with a significantly greater objective tumor response rate than placebo, although limited data from an updated analysis demonstrated no significant difference between the treatments groups in terms of median overall survival.

Continuous treatment with sunitinib generally had no detrimental effect on health-related quality of life and was generally well tolerated in patients with pNETs in this trial, with most adverse events being manageable and of grade 1 or 2 severity.

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Acknowledgments and Disclosures

The manuscript was reviewed by: E. Grande, Medical Oncology Department, Ramón y Cajal University Hospital, Madrid, Spain; T.R. Halfdanarson, University of Iowa, Iowa City, IA, USA; A. Teulé,Medical Oncology Department, Institut Català d’Oncologia, Barcelona, Spain.

The preparation of this review was not supported by any external funding. During the peer review process, the manufacturer of the agent under review was offered an opportunity to comment on this article. Changes resulting from comments received were made by the authors on the basis of scientific and editorial merit. Eric Raymond has received honoraria and grants from Pfizer. He has also provided consultancy and expert opinion for Pfizer.

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Correspondence to Emma D. Deeks.

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Deeks, E.D., Raymond, E. Sunitinib. BioDrugs 25, 307–316 (2011). https://doi.org/10.2165/11207360-000000000-00000

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