With the goal of understanding how the nature of the tridentate macrocyclic supporting ligand influences the relative stability of isomeric mu-eta 2:eta 2-peroxo- and bis(mu-oxo)dicopper complexes, a comparative study was undertaken of the O2 reactivity of Cu(I) compounds supported by the 10- and 12-membered macrocycles, 1,4,7-R3-1,4,7-triazacyclodecane (R3TACD; R = Me, Bn, iPr) and 1,5,9-triisopropyl-1,5,9-triazacyclododecane (iPr3TACDD). While the 3-coordinate complex [(iPr3TACDD)Cu]SbF6 was unreactive with O2, oxygenation of [(R3TACD)Cu(CH3CN)]X (R = Me or Bn; X = ClO4- or SbF6-) at -80 degrees C yielded bis(mu-oxo) species [(R3TACD)2Cu2(mu O)2]X2 as revealed by UV-vis and resonance Raman spectroscopy. Interestingly, unlike the previously reported system supported by 1,4,7-triisopropyl-1,4,7-triazacyclononane (iPr3TACN), which yielded interconverting mixtures of peroxo and bis(mu-oxo) compounds (Cahoy, J.; Holland, P. L.; Tolman, W. B. Inorg. Chem. 1999, 38, 2161), low-temperature oxygenation of [(iPr3TACD)Cu(CH3CN)]SbF6 in a variety of solvents cleanly yielded a mu-eta 2:eta 2-peroxo product, with no trace of the bis(mu-oxo) isomer. The peroxo complex was characterized by UV-vis and resonance Raman spectroscopy, as well as an X-ray crystal structure (albeit of marginal quality due to disorder problems). Intramolecular attack at the alpha C-H bonds of the substituents was indicated as the primary decomposition pathway of the oxygenated compounds through examination of the decay kinetics and the reaction products, which included bis(mu-hydroxo)- and mu-carbonato-dicopper complexes that were characterized by X-ray diffraction. A rationale for the varying results of the oxygenation reactions was provided by analysis of (a) the X-ray crystal structures and electrochemical behavior of the Cu(I) precursors and (b) the results of theoretical calculations of the complete oxygenated complexes, including all ligand atoms, using combined quantum chemical/molecular mechanics (integrated molecular orbital molecular mechanics, IMOMM) methods. The size of the ligand substituents was shown to be a key factor in controlling the relative stabilities of the peroxo and bis(mu-oxo) forms, and the nature of this influence was shown by both theory and experiment to depend on the ligand macrocycle ring size.

Linear viscoelastic response and melt microstructure of ultra-high molecular weight poly(α-olefins) (UHMW PO) with bottlebrush architectures, from poly(1-hexene) to poly(1-octadecene) synthesized by metal coordinative insertion polymerization, were measured as a function of side-chain length, N sc . All these bottlebrush POs are highly entangled, with an average number of entanglements per chain, Z, greater than 50, which allows accurate determination of their rubbery plateau moduli, G N 0 , and their entanglement molecular weights, M e . Their plateau moduli scale with their side-chain lengths as G N 0 ∼ N sc −1.47 , in agreement with the scaling theory for the dense bottlebrush limit that predicts. Melt structures of these bottlebrush poly(1-olefin)s and their melt structural changes with temperature were determined by wide-angle X-ray scattering. Concomitant with thermal expansion of these bottlebrush PO melts is a nonmonotonic change in backbone-to-backbone distance (d 1 ) and a monotonic increase in side-chain spacing (d 2 ). Both the melt-flow interchain friction coefficient and the viscosity of these UHMW PO bottlebrushes show a very strong dependence on d 2 , characterized by two exponential decay regimes, with decay constants having an exponential dependence on N sc .

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A crystal structure establishes doxoform as a dimeric formaldehyde conjugate of the oxazolidine of doxorubicin. Doxoform is a prodrug of doxazolidine, a monomeric doxorubicin formaldehyde-oxazolidine. Both doxoform and doxazolidine inhibit the growth of cancer cells at 1-4 orders of magnitude lower concentration than doxorubicin. They also inhibit the growth of cancer cells better than doxsaliform, a prodrug for an acyclic doxorubicin-formaldehyde conjugate. Doxoform rapidly hydrolyzes to doxazolidine, which then hydrolyzes to doxorubicin with a half-life of 3 min in human serum at 37 degrees C. Both doxoform and doxazolidine are taken up by multidrug-resistant MCF-7/Adr cells 3- to 4-fold better than doxorubicin. A molecular model suggests that doxazolidine can cross-link DNA by direct reaction with a G-base in a tautomeric form with synchronous ring opening of the oxazolidine. These results point to doxoform being a prodrug for doxazolidine that is the reactive species that directly cross-links DNA.