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Cellular Ca 2+ signals play a critical role in cell physiology and pathology. In most non-excitable cells, store-operated Ca 2+ entry (SOCE) is an important mechanism by which intracellular Ca 2+ signaling is regulated. However, few drugs can selectively modulate SOCE. 2-Aminoethoxydiphenyl borate (2APB) and its analogs (DPB162 and DPB163) have been reported to inhibit SOCE. Here, we examined the effects of another 2-APB analog, DPB161 on SOCE in acutely-isolated rat submandibular cells. Both patch-clamp recordings and Ca 2+ imaging showed that upon removal of extracellular Ca 2+ ([Ca 2+ ] o =0), rat submandibular cells were unable to maintain ACh-induced Ca 2+ oscillations, but restoration of [Ca 2+ ] o to refill Ca 2+ stores enable recovery of these Ca 2+ oscillations. However, addition of 50 μM DPB161 with [Ca 2+ ] o to extracellular solution prevented the refilling of Ca 2+ store. Fura-2 Ca 2+ imaging showed that DPB161 inhibited SOCE in a concentration-dependent manner. After depleting Ca 2+ stores by thapsigargin treatment, bath perfusion of 1 mM Ca 2+ induced [Ca 2+ ] i elevation in a manner that was prevented by DPB161. Collectively, these results show that the 2-APB analog DPB161 blocks SOCE in rat submandibular cells, suggesting that this compound can be developed as a pharmacological tool for the study of SOCE function and as a new therapeutic agent for treating SOCE-associated disorders.

The 2-aminoethoxydiphenyl borate analog, DPB161 blocks store-operated Ca2+ entry in acutely dissociated rat submandibular cells