Triggering N(2) Uptake via Redox Induced Expulsion of Coordinated NH(3) and N(2) Silylation at Trigonal Bipyramidal Iron

The biological reduction of nitrogen to ammonia may occur via one of two predominant pathways in which nitrogenous N(x)H(y) intermediates including hydrazine (N(2)H(4)), diazene (N(2)H(2)), nitride (N(3-)) and imide (NH(2-)) may be involved. To test the validity of hypotheses concerning iron’s direct role in the stepwise reduction of N(2), iron model systems are needed. Such systems can test the chemical compatibility of iron with various proposed N(x)H(y) intermediates, and the reactivity patterns of such species. Here we describe a TBP (SiP(R)(3))Fe-L scaffold (SiP(R)(3) represents [Si(o-C(6)H(4)PR(2))(3)](−); R = Ph and iPr) where the apical site is occupied by nitrogenous ligands such as N(2), N(2)H(4), NH(3) and N(2)R. The system accommodates terminally bound N(2) in the three formal oxidation states (iron(0), +1, and +2). N(2) uptake is demonstrated via displacement of its reduction partners NH(3) and N(2)H(4), and N(2) functionalizaton is illustrated via electrophilic silylation.