Conversion of uridine and cytidine to their 5′-O-tosyl derivatives, followed by cyanation with tetraethylammonium cyanide, reduction and deamination, led to isolation of the hitherto un- known homouridine (1-(5′-deoxy-β-D-allofuranosyl)uracil) and homocytidine (1-(5′-deoxy-β-ᴅ-allofuranosyl)cytosine), analogues of uridine and cytidine in which the exocyclic 5′-CH 2 OH chain is extended by one carbon to CH 2 CH 2 OH. Homocytidine was also phosphorylated to its 6′-phosphate and 6′-pyrophosphate analogues. In addition, it was converted, via its 2,2′-anhydro derivative, to arahomocytidine, an analogue of the chemotherapeutically active araC. The structures of all the foregoing were established by various criteria, including 1 H and 13 C NMR spectroscopy, both of which were also applied to analyses of the solution conformations of the various compounds, particularly as regards the conformations of the exocyclic chains. The behaviour of the homo analogues was examined in several enzymatic systems. Homo- cytidine was a feeble substrate, without inhibitory properties, of E. coli cytidine deaminase. Homocytidine was an excellent substrate for wheat shoot nucleoside phosphotransferase; while homouridine was a good substrate for E. coli uridine phosphorylase. Although homoCMP was neither a substrate, nor an inhibitor, of snake venom 5′-nucleotidase, homoCDP was a potent inhibitor of this enzyme (K i ~6 μм). HomoCDP was not a substrate for M. luteus polynucleotide phosphorylase. None of the compounds exhibited significant activity vs herpes simplex virus type 1, or cytotoxic activity in several mammalian cell lines.