Review of the literature reveals a number of recent insights concerning the metabolic fate of human choriogonadotropin (hCG). In man, only a fraction (21.7%) of the circulating hCG molecules is excreted in urine. Results from animal studies indicate that the retained hCG is taken up by various tissues, principally kidney, liver, and ovary, where degradation occurs. Ovarian uptake is receptor mediated and saturable. Hepatic uptake of hCG is not proceeded by desialylation, and blockade of hepatic receptors for galactose-terminated glycoproteins does not impair hepatic accumulation of hCG. Kidney uptake is quantitatively the most important; parenchymal metabolism, as well as excretion in urine constitute major renal components of hCG disposal. The intracellular products of hCG catabolism in kidney include certain fragments of the hCG molecule that exhibit relative resistance to processing by degradative enzymes. These products are fragments of the hCGβ subunit that lack the hCGβ carboxyterminal antigenic determinant, but retain an hCGβ core antigenic determinant, and, thus, they are designated β-core molecules. Both kidney from hCG-infused rat and urine from pregnant women contain β-core molecules in great abundance, in fact, in greater abundance than hCG, itself. Structural characterizations of the β-core purified from pregnancy urine indicate a mol. wt of about 10,000 and an absence of sialic acid, galactose, and carboxyterminal peptide region, including O-linked oligosaccharides. Human volunteers given purified hCG or hCGβ by infusion excrete β-core in their urines, which establishes the existence of catabolic pathways in humans for the production of β-core. Thus, urinary excretion of β-core may reflect an important fate for the metabolic products of hCG degradation.