Dr. Colao had nothing to disclose. The study was supported by Novartis Pharma AG.
Two posters at meeting shed light on pasireotide’s biochemical mechanisms of action. Dr. Rob van der Pas of Erasmus Medical Center in Rotterdam, the Netherlands, suggested that the reason the somatostatin analogue octreotide is not effective in Cushing’s disease is because it prefers the somatostatin receptor subtype 2 (sst2), whereas it is the somatostatin receptor 5 (sst5) that plays a key role in sst targeted therapy for Cushing’s disease (Endocr. Rev. 2011;32:P3-520). Dr. Robert R. Henry of the University of California, San Diego, found that the hyperglycemia associated with pasireotide is related to decreases in insulin secretion, with no change in insulin sensitivity, and this effect is most likely mediated by the sst5 receptor, which may also play an important role in glucose metabolism (Endocr. Rev. 2011;32:P3-274).