AbstractProcedures for the synthesis of branched Xylβ(1→3)[Galβ(1→2)]‐Glc and Xylβ(1→3)[Galβ(1→2)]‐GlcUA trisaccharides β‐linked to the 3‐Oof cholesterol, cholestanol, and friedelanol, respectively, were developed. To this end, β‐selective glucosylation of cholesterol with glucosyl donors giving selective access to 2‐O, 3‐O, and 6‐Owas studied. This way intermediates10and21having 2‐O‐acyl, 3‐O‐benzyl and 4,6‐O‐benzylidene or also benzyl protection were obtained. Removal of the 2‐O‐acyl group and then galactosylation afforded β(1→2)‐linked disaccharide intermediates14and23. Standard manipulations with theO‐benzylidene and/orO‐benzyl protecting groups gave selective access to the 3‐Oof the glucosyl residue, thus affording with a xylosyl donor the trisaccharide β‐linked to the cholesteryl residue (compound18) as decisive intermediate. Also an alternative procedure to this compound via attachement of a Xylβ(1→3)Glc residue to cholesterol and then galactosylation could be developed. Total deprotection of18or regioselective introduction of a sulfate group and of a dodecylcarbamoyl residue at 6a‐Ofurnished saponins34,36, and38, respectively. Hydrogenation of cholesteryl disaccharide23led directly to a 3a‐O‐unprotected cholestanyl disaccharide39. β‐Selective xylosylation and transformation of the liberated glucose hydroxymethyl group into a carboxylic group afforded target molecule1bhaving the desired Xyl(1→3)[Gal(1→2)]‐GlcUA β‐linked to cholestanol. Similarly, a saponin analog was obtained having an α‐linkedL‐rhamnosyl residue instead of the β‐linkedD‐xylosyl residue. Application of the glycosylation sequence, as worked out for cholesterol, to friedelanol led to attachment of the Xylβ(1→3)[Galβ(1→2)]‐Glc residue to the 3‐O(compound54). CompleteO‐deacylation led to saponin55; oxidation of the hydroxymethyl group of the glucose residue to the carboxylic group and then deprotection afforded target molecule2containing the same trisaccharide residue as1b. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)