Nosyl group

DBU, DMF, HSCH2CH2OH, >48% yield. These conditions were used to remove the nosyl group from A -methylated peptides." ... 

A similar scaffold for the preparation of peptidomimetics was prepared by Mitsunobu cyclization of the molecule coming from the coupling of 4-benzylprolinol and iV-nosyl(o-nitrobenzensulfonyl) tryptophan 316 (Scheme 41). A Mitsunobu cyclization occurred easily due to the acidity of the NH of the nosyl group that could be further selectively deprotected under very mild conditions. The so-formed bicyclic amine 317 can be further coupled with different amino acids to give compounds 318, employed in the search of a new somatostatin pharmacophore <2005BML4033>. 

This enzyme [EC 4.2.2.3], also referred to as poly(j8-D-mannuronate) lyase and poly(mana) alginate lyase, catalyzes the eliminative cleavage of polysaccharides containing /3-D-mannuronate residues to give oligosaccharides with 4-deoxy-o -L-eryt/iro-hex-4-enopyranuro-nosyl groups at their ends. 

Methylmalonyl-CoA mutase (EC 5.4.99.2). Failure to convert (/ )-methylmalonyl-CoA into succinyl-CoA. Large quantities of methylmalonic acid appear in plasma and urine. Affected children fail to thrive and show pronounced ketoacidosis. Often fatal in early life. Hyperammonemia and intermittent hyperglycinemia are also typical. Restricted protein intake and synthetic diets are helpful, in particular low intakes of leucine, isoleucine, valine, threonine and methionine. A similar condition may arise from a congenital deficiency of methylmalonyl-CoA epimerase (EC 5.1.99.1). Both conditions unresponsive to vitamin Bj2. Another type of methylmalonyl aciduria is thought to result from an hereditary deficiency of deoxyadenosyl transferase (transfers the 5 -deoxyade-nosyl group in cobalamin synthesis), which provides the coenzyme of methylmalonyl-CoA mutase. This condition responds to injection of B,2. Dietary B12 deficiency also results in methylmalonic aciduria. 

During an exploration of practical syntheses of a GnRH antagonist, Farr et al. examined two key substrates for the Mitsunobu reaction.Both reactions were carried out at kilo-scale. Typically, four equivalents of the pyridyl ethanol 181 were required to drive the reaction to completion. Since the dinitrosulfonamide product 182 proved to be labile during the hydrolysis of the methyl ester, further exploratory work was carried out with the p-nitrosulfonamide 183. The nosyl group of the crude reaction product 184 was removed with thioglycolic acid. After an aqueous workup, the desired product 185 was obtained in 58% yield over three steps after recrystallisation from ethyl acetate. Eventually, this route was abandoned due to supply issues with the pyridyl ethanol and byproduct removal issues arising firom the Mitsunobu reaction and the nosyl deprotection. 

The main chain is structured of 1,4-P-linked AGU (principally, a - cellulose backbone). The side chains are trisaccharide units, bound in 0-3 positions. They are constructed of the groups p-D-mannopyranosyl-, P-D-glucopyianosyl-, a-D-mannopyranosyl-, and pyruvic acid as an a-4,6-di-0-acetale, linked with half of the P-D-mannopyra-nosylic groups. 

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