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OCT, a non-calcemic analogue of 1,25(OH)2D3 has been found to have a more potent activity than that of 1,25(OH)2D3 regarding cell differentiation and immunopotentiation activity, and to prolong the average life span of MRL/l mice. Recently, we found that OCT effectively suppressed the secretion and synthesis of PTH without inducing hypercalcemia. In primary cultures of bovine parathyroid cells, OCT was capable of suppressing PTH release in a dose-dependent manner. OCT was also active in vivo, and, like 1,25(OH)2D3, decreased the pre-pro(PTH) mRNA levels. In a group of rats with CRF, daily administration of OCT, 8 ng i.p. for 2 weeks returned PTH levels to normal without changes in serum calcium. Preliminary results in dogs with CRF indicated that after the administration of OCT 5 micrograms i.v., N-terminal PTH decreased by 76% without changes in Ca. In conclusion, OCT may provide a unique contribution to the treatment of secondary hyperparathyroidism.