Cyanate as an Inhibitor of Red-Cell Sickling

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Abstract
THE finding of the anti-sickling activity of cyanate originated with the hypothesis that cyanate rather than urea was responsible for the reported beneficial use of urea in the treatment of patients with sickle-cell disease.1 The rationale for the urea therapy as proposed by Nalbandian2 was that the urea disrupted hydrophobic bonds that formed when deoxygenated hemoglobin S gelled within the cell. Although urea is known to disrupt hydrophobic bonds, concentrations of 1 to 8 M are usually required.3 Thus, since urea is rapidly cleared by the kidneys, it seemed unlikely that such levels could be attained and maintained in the . . .