This study evaluates the utility of the rhesus monkey (Macaca mulatta) as a model for calcitonin (iCT) dynamics in humans. Two different anticalcitonin antisera were used, each having different region specificities for the hormone. Basal levels of iCT in both serum and urine were lower than those encountered in humans, whether measured with midportion (Ab‐IIIb) or carboxyl terminal (Ab‐IV) antisera. The totally thyroidectomized monkey continues to have detectable serum iCT while, in contrast to humans, urine iCT is undetectable by direct assay but measurable after concentration. Immunoperoxidase studies revealed a relatively larger concentration of C cells in the thyroid of the monkey, with, as in humans, a distribution in the central region along the median axis of the lateral lobes. Extraction of iCT from the thyroid gland demonstrated a higher concentration in the monkey than in humans. Many extrathyroidal tissues of the monkey contained iCT, which did not differ immunochemically from that in thyroid; this finding is also true of comparable human tissue. The very high concentration of iCT in liver decreased markedly after thyroidectomy, suggesting that hepatic iCT may be receptor‐bound hormone of thyroid origin. Other extrathyroidal sources of iCT persisted after thyroidectomy in the monkey, with the highest concentrations being found in thymus and in lung. The demonstration of the presence of extrathyroidal iCT may have important implications for its function as a tumor marker and for its presumed role in calcium metabolism. These studies demonstrate that the rhesus monkey, regardless of some differences from man, is nonetheless a useful animal model for the investigation of the pathophysiology of calcitonin.