Β-elimination Process Research Articles

Monoamine oxidase B activatable red fluorescence probe for bioimaging in cells and zebrafish

A real-time and specific for the detection of Monoamine Oxidase B (MAO-B) to investigate the MAO-B-relevant disease development and treatment process is urgently desirable. Here, we utilized MAO-B to catalyze the conversion of propylamino groups to aldehyde groups, which was then quickly followed by a β-elimination process to produce fluorescent probes (FNJP) that may be used to detect MAO-B in vitro and in vivo. The FNJP probe possesses unique properties, including favorable reactivity (Km = 10.8 μM), high cell permeability, and NIR characteristics (λem = 610 nm). Moreover, the FNJP probe showed high selectivity for MAO-B and was able to detect endogenous MAO-B levels from a mixed population of NIH-3 T3 and HepG2 cells. MAO-B expression was found to be increased in cells under lipopolysaccharide-stimulated cellular oxidative stress in neuronal-like SH-SY5Y cells. In addition, the visualization of FNJP for MAO-B activity in zebrafish can be an effective tool for exploring the biofunctions of MAO-B. Considering these excellent properties, the FNJP probe may be a powerful tool for detecting MAO-B levels in living organisms and can be used for accurate clinical diagnoses of related diseases.

Cloning, expression and improvement of catalytic activity of alginate lyase by site-directed mutation

Alginate lyase mainly produces active alginate oligosaccharides (AOS) by degrading alginate via β-elimination process. In this study, the Pseudoalteromonas sp. Alg6B alginate lyase-encoding gene alg6B-7 from polysaccharide lyase (PL)-7 family was successfully cloned, sequenced, expressed in Escherichia coli. Based on rational design and amino acid sequence alignment of the alginate lyase from various sources, four positive mutants were obtained. The specific enzyme activities of four mutants I62A, A99K, V132S, and L157T were 38.84%, 42.85%, 75.8% and 51.83% higher than that of the wild enzyme, respectively. The Kcat/Km values of the four mutants were both increased, and the catalytic efficiency of V132S was 1.92-fold higher than that of the wild enzyme, especially. The rational design that was employed in this study achieved the dramatic improvement of catalytic activity, which may provide the application potential in industrial production.

Deuterium-Labeling Studies on the C–H/Olefin Coupling of Aromatic Ketones Catalyzed by Fe(PMe3)4

AbstractDeuterium-labeling experiments were performed for the Fe(PMe3)4-catalyzed C–H/olefin coupling using a deuterium-labeled aromatic ketone with various alkenes. While the reactions with a variety of alkenes provided the linear alkylation products formed via 1,2-insertion of alkene into an Fe–H bond, the reversible 2,1-insertion proceeded during the reaction highly depends on the choice of the alkene. No H/D scrambling resulting from 2,1-insertion/β-elimination was detected for the reactions with a vinylsilane and N-vinylcarbazole, but the reactions­ with styrenes are considered to involve rapid 2,1-insertion/ β-elimination processes to cause significant levels of H/D scrambling.

Reaction mechanisms and kinetics of the β-elimination processes of compounds CHF2CH2SiFnMe3–n (n = 0–3): DFT and CBS-QB3 methods using Rice-Ramsperger-Kassel-Marcus and transition state theories

The gas-phase β-elimination kinetics of 2,2-difluoroethyltrifluorosilane (1), 2,2-difluoroethylmethyldifluorosilane (2), 2,2-difluoroethyldimethylfluorosilane (3), and 2,2-difluoroethyltrimethylsilane (4) have been investigated computationally using M06-2x exchange-correlation functional as well as the benchmark CBS-QB3 quantum chemical approach. The obtained energy profile has been enhanced with kinetic calculations using statistical Rice-Ramsperger-Kassel-Marcus (RRKM) theory and transition state theory (TST). The calculated results are in good agreement with the available experimental data which obtained by the CBS-QB3 approach. The comparison between all our calculations and experiments indicates that a thermodynamically-controlled reaction that gives more stable products derived from the compound 2 species will be the vinyl fluoride and methyltrifluorosilane species, whereas the elimination of compound 1 into the vinyl fluoride and silicon tetrafluoride species is favorable process from kinetic point of view.In proportion to rather larger barrier heights, pressures where P > 10―4 bar are insufficient to ensure a saturation of the calculated rate constant compared with the RRKM unimolecular rate kinetics (in high-pressure limit).Natural bond orbital analysis revealed that in accordance with an increase of barrier height from compounds 1 to 4, the HOMO-LUMO energy-gaps decreases. Furthermore, the obtained order of barrier heights could be explained by the number of electron-withdrawing fluorine atoms attached to the silicon atom. The occupancies of σC1―F3 bonding orbital for the studied compounds are as follows: 1>2>3>4 and those of σ*C1―F3 antibonding orbital increase in the opposite order (4>3>2>1) by NBO analysis. This fact explains a comparatively easier elimination of the σC1―F3 bond in compound 1 compared to the other compounds. The calculated data reveal that the polarization of the C1―F3 bond in the sense C1δ+–F3δ− is the determining factor in the elimination reaction of the studied compounds.

Oligosaccharides from depolymerized fucosylated glycosaminoglycan: Structures and minimum size for intrinsic factor Xase complex inhibition

Fucosylated glycosaminoglycan (FG), a structurally complex glycosaminoglycan found up to now exclusively in sea cucumbers, has distinct anticoagulant properties, notably a strong inhibitory activity of intrinsic factor Xase complex (FXase). Knowledge of the FG structures could facilitate the development of a clinically effective intrinsic FXase inhibitor for anticoagulant drugs. Here, a new fucosylated glycosaminoglycan was obtained from the widely traded sea cucumber Bohadschia argus The precise structure was deduced as {→4)-[l-Fuc3S4S-α-(1→3)-]-d-GlcA-β-(1→3)-d-GalNAc4S6S-β-(1} through analysis of its chemical properties and homogeneous oligosaccharides purified from its β-eliminative depolymerized products. The B. argus FG with mostly 3,4-di-O-sulfated fucoses expands our knowledge on FG structural types. This β-elimination process, producing oligosaccharides with well-defined structures, is a powerful tool for analyzing the structure of complex FGs. Among these oligosaccharides, an octasaccharide displayed potent FXase inhibitory activity. Compared with oligosaccharides with various degrees of polymerization (3n and 3n - 1), our analyses reveal that the purified octasaccharide is the minimum structural unit responsible for the potent selective FXase inhibition, because the d-talitol in the nonsaccharide is unnecessary. The octasaccharide with 2,4-di-O-sulfated fucoses is more potent than that of one with 3,4-di-O-sulfated fucoses. Thus, sulfation patterns can play an important role in the inhibition of intrinsic factor Xase complex.

β-Hydrogen Elimination and Reductive Elimination from a κ3-PPC Nickel Complex

The incorporation of a PPC donor ligand set onto nickel is described. While C–H activation routes using Ni(II) precursors and benzyl- and phenethyl-substituted diphosphines But2PCH2CH2P(But)R failed, success was achieved via oxidative addition of the 2-bromo-benzyl-ligand precursor But2PCH2CH2P(But)(CH2-o-C6H4Br) with Ni(COD)2 to generate [κ3-BnPPC]NiBr. Subsequent reaction with KBEt3H resulted in decomposition unless PPh3 was present, which allowed isolation of the tricoordinate Ni(0) complex [κ2-BnPP]Ni(PPh3). Reaction of [κ3-BnPPC]NiBr with EtMgCl also resulted in the formation of the Ni(0) ethylene complex, [κ2-BnPP]Ni(η2-C2H4), via β-elimination followed by reductive elimination. Deuterium-labeling studies are consistent with a reversible β-elimination process prior to reductive elimination, which scrambles the deuterium isotopes. Reaction of [κ3-BnPPC]NiBr with CH3Li results in the formation of the Ni(II) methyl complex, [κ3-BnPPC]Ni(CH3). Heating this species in the presence of PPh3 results in the ...

Synthesis of carbohydrate-derived (Z)-vinyl halides and silanes: Samarium-promoted stereoselective 1,2-elimination on sugar-derived α-halomethylcarbinol acetates

A general and highly selective method for the synthesis of carbohydrate-derived (Z)-vinyl halides and silanes is described. This reaction takes place through a β-elimination process of sugar-derived α-halomethylcarbinol acetates promoted by samarium diiodide. Starting materials have been easily prepared in two steps consisting in an initial addition of halomethyllithium compounds to the corresponding galactose-derived aldehyde, followed by acetylation. A mechanism that explains both the formation of (Z)-vinyl derivatives and its selectivity is proposed. Finally, the synthetic usefulness of these compounds has been applied in cross-coupling reactions with ethynyl benzene towards the formation of selected enyne derivatives.

TEMPO-mediated oxidation on galactomannan: Gal/Man ratio and chain flexibility dependence

Guar (GG) and locust bean (LBG) galactomannans (GMs) oxidation at C-6 was performed with catalyst TEMPO, in which the reaction progress was monitored by consume of NaOH solution. The products were characterized by spectroscopic analysis, infrared, and 1H-nuclear magnetic resonance, confirming the presence of aldehydes groups as intermediate of reaction to carboxylic acid. From high performance anion exchange chromatography with pulsed amperometric detection Man/Gal molar ratio was determined and demonstrated a preference to oxidize Man during the reaction on both GMs, following a first order kinetics of oxidation. The comparative macromolecular behavior of native and oxidized GMs was obtained through the analysis by high performance size exclusion chromatography, and the persistence length (Lp) was 6nm and 4nm to native LBG and GG, respectively. A more accessible OH-6 at mannose residue in LBG could be related with a two times faster reaction than GG. The selective oxidation with catalyst TEMPO proved to be efficient to increase the flexibility of the GMs during oxidation. Short reaction time and β-elimination process were mainly observed to LBG, probably due to a more favorable oxidation access to the polysaccharide main chain.

Abstract 3418: Mechanism of cell death induced by the DNA strand-breaking nucleoside analogue CNDAC.

Abstract The nucleoside analog CNDAC [2’-C-cyano-2’-deoxy-1-β-D-arabino-pentofuranosylcytosine] has a unique action mechanism of inducing single strand breaks following its incorporation into DNA through a β-elimination process. Transcription-coupled nucleotide excision repair (NER) is partially responsible for repair of such nicks [Cancer Res. 2008, 68:3881-89]. However, DNA replication across the unrepaired nicks generates double strand breaks (DSBs) which are mainly repaired by the ATM-dependent homologous recombination (HR) mechanism [Blood, 2010, 116:1737-46]. Both CNDAC (as DFP-10917) and its orally bioavailable prodrug, sapacitabine are in clinical trials in AML/MDS. Our goal was to define the mechanism by which CNDAC-induced DSBs lead to cell death. First, cytogenetic analysis revealed that chromosomal aberrations (breaks and gaps) in cells lacking XPF, the key 5’-NER endonuclease, increased >2 fold and 16 fold after one (15 hr) and two (30 hr) cell cycles of treatment with 1 μM (non-arresting concentration) CNDAC, respectively (N≥60, P<0.01). However, the wild type AA8 cells showed no change after one cell cycle exposure, and only a 5-fold increase in wild types after two cycles (N≥55, P<0.05). Second, diverse cytogenetic changes were detected in AA8-derived cells lacking Rad51D, a paralog of the key recombinase Rad51 in the HR pathway, with only 13% of metaphases (N=106) free of aberration and >70% bearing chromosomal damage too complex to be scored. By contrast, 78% of Rad51D-complemented cells (N=100) had no aberration, with only 1% unscorable. Third, post-mitosis nuclear alterations were further studied in Giemsa-stained AA8 cells after wash out of CNDAC (24 hr). The percentage of multinucleated cells increased 10 fold (1 μM) and 27 fold (10 μM) relative to control 24 hr after wash. Finally, to test the hypothesis that cells may die from mitotic catastrophe, video microscopy was used to track the fate of AA8 cells stably expressing H2B-GFP after CNDAC (0.5, 1 and 10 μM, 6-hr exposure) washout. Cells entering the 1st mitosis within 5 hr after wash presumably had CNDAC incorporation into DNA and therefore were eligible for analysis. There was no difference in the duration of 1st mitosis among all three treatments and control (N≥24, P>0.05). However, 2nd mitosis was significantly prolonged in a concentration-dependent manner in all treatments (N≥37, P<0.05-0.001). The interval between 1st and 2nd mitoses was also prolonged markedly (1 and 10 μM, P<0.01-0.001). A similar trend was seen in H2B-GFP transfected lung cancer line H460. Notably, large numbers of treated AA8 cells became multinucleated upon completion of an aberrant 2nd mitosis. Frequently this was coupled with or followed by onset of apoptosis. These results indicate that CNDAC-induced DSBs, if not repaired, trigger cells to delay progression after 1st mitosis, and to undergo prolonged 2nd mitosis resulting in multinucleation and subsequent apoptosis. Citation Format: Xiaojun Liu, Billie Nowak, Yingjun Jiang, Walter Hittelman, William Plunkett. Mechanism of cell death induced by the DNA strand-breaking nucleoside analogue CNDAC. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3418. doi:10.1158/1538-7445.AM2013-3418

P(CH)P Pincer Rhodium(I) Complexes: The Key Role of Electron-Poor Imidazoliophosphine Extremities

The coordination chemistry of a potentially pincer-type dicationic meta-phenylene-bis(imidazoliophosphine) ligand 3 to neutral and cationic carbonylrhodium(I) centers has been investigated. Similarly to what was observed previously for its ortho-phenylene counterpart, 3 was found to bind to the RhCl(CO) fragment in a trans-chelating manner that makes possible a weak Rh-C(H) interaction, inferred from the nonbonding but relatively short Rh-C and Rh-H contacts observed in the solid state structure of the dicationic adduct (3)RhCl(CO) (5). Formation of the target PCP-type pincer complex could not be triggered despite multiple attempts to deprotonate the central C-H moiety in the initial dicationic adduct 5, or in the tricationic species [(3)Rh(CO)](+) (8) generated by abstraction of the chloride ion from 5. Complex 8 was identified on the basis of NMR and IR analyses as a Rh(I)-stabilized P(CH)P-intermediate en route to the anticipated classical PCP-type pincer complex. Analysis of the electronic structure of this intermediate computed at the density functional level of theory (DFT level) revealed a bonding overlap between a Rh d-orbital and π-orbitals of the m-phenylene ring. NBO analyses and calculated Wiberg indices confirm that this interaction comprises an η(1)-C-Rh bonding mode, with only secondary contributions from the geminal C and H atoms. Although the target PCP-type pincer complex could not be generated, treatment of the tricationic intermediate with methanol induced a P-CN(2) bond cleavage at both imidazoliophosphine moieties, resulting in the formation of a dicationic "open pincer" species, that is, a nonchelated bis((MeO)PPh(2))-stabilized aryl-Rhodium complex that is the κC-only analogue of the putative κP,κC,κP-PCP complex sought initially. Theoretical studies at the DFT level of experimental or putative species relevant to the final C-H activation process ruled out the oxidative addition pathway. Two alternative pathways are proposed to explain the formation of the "open pincer" complex, one based on an organometallic α-elimination step, the other based on an organic aromatization-driven β-elimination process.

Is cellulose degradation due to β-elimination processes a threat in mass deacidification of library books?

As papers become acidic and brittle over time, libraries apply mass deacidification processes to their collections in order to neutralize acids and deposit an alkaline reserve in the paper. Books commonly treated by mass deacidification have undergone natural aging of up to 150 years. The risk of alkali-induced degradation of cellulosic material upon mass deacidification remains uncertain. In the present study, the extent of β-elimination-type degradation reactions was investigated by comparing deacidified and non-deacidified counterparts, using deacidified library materials and identical issues of non-deacidified books from second-hand book shops. The study dealt with only naturally-aged papers focusing on investigation of immediate effects of mass deacidification rather than a long-term impact. Gel permeation chromatography coupled with carbonyl group labeling gave insight into cellulose chain cleavage as well as into the behavior of oxidized functionalities. Processes occurring under natural aging conditions were compared to those upon artificial oxidation of model pulps. Library books did not show a significant reduction in molecular weight after mass deacidification compared to the non-deacidified controls, which stands in contrast to oxidized model pulps. The models showed a more pronounced loss of molecular weight upon deacidification treatments. A decrease in carbonyl groups other than reducing ends was found to occur. Thus, oxidized functionalities were found to be reactive in mass-deacidification reactions; the different behavior was traced down to particular regions of oxidative damage along the cellulose chains. In general, β-elimination processes did not pose a large risk factor upon mass deacidification treatments of the naturally-aged library material tested.

Abstract 5667: Mechanism-based combinations of agents impacting the homologous recombination and nucleotide excision repair pathways

Abstract Sapacitabine, a prodrug of the nucleoside analog CNDAC [2′-C-cyano-2′-deoxy-1-β-D-arabino-pentofuranosylcytosine], has the advantage of oral bioavailability. CNDAC has a unique action mechanism of inducing single strand breaks following its incorporation into DNA through a β-elimination process. Such nicks caused by sapacitabine/CNDAC are partially repaired through the transcription-coupled nucleotide excision repair (NER) pathway [Cancer Res. 2008, 68:3881-89]. However, DNA replication across the unrepaired nicks generates double strand breaks which are mainly repaired by the ATM-dependent homologous recombination (HR) mechanism [Blood, 2010, 116:1737-46]. Sapacitabine is undergoing clinical trials with encouraging outcomes in AML or MDS patients [J. Clin.Oncol., 2010, 28:285-91]. A trial of sapacitabine in combination with cyclophosphamide and rituximab (SCR regimen) in chronic lymphocytic leukemia (CLL) relapsed from first line therapies has been initiated in populations lacking ATM function. Other candidates for clinical combinations with sapacitabine include bendamustine, an alkylating agent, and oxaliplatin, which are currently used for treatment of CLL. Primary adducts caused by each of these compounds are repaired by NER. To explore mechanistic interactions between sapacitabine/CNDAC and agents impacting the NER pathway, we used median effect analysis to compare cellular clonogenic survival of drug combinations with survival after single agents alone. First, cells deficient in HR components (Rad51D, Xrcc3 and Brca2) were all sensitized to 4-hydroperoxycyclophosphamide (4-HC, readily converted to the active metabolite of cyclophosphamide, 4-hydroxycyclophosphamide), bendamustine, ciplatin and oxaliplatin by 10- to 50-fold, whereas cells lacking the key NER endonuclease XPF were more sensitive to these agents. This indicates that HR is responsible for residual lesions not repaired by NER. Second, CNDAC in combination with 4-HC presented additive to mildly synergistic effect (combination index CI ≤ 1) in cells defective in Xrcc3, Rad51D, Brca2 or XPF. Third, combination of bendamustine with CNDAC showed additive loss of clonogenicity (CI ∼ 1) in cells lacking Rad51D or Xrcc3. Fourth, combination of cisplatin or oxaliplatin with CNDAC also exerted additive effects (CI ∼ 1) in HR- as well as NER-deficient cells. Finally, cisplatin/oxaliplatin combined with CNDAC, both at relatively high concentration ranges lethal to HR-defective cells, had no synergy in wild type cells either. Together these results suggest that agents causing DNA adducts, which are mainly repaired by NER process, are additive in their interaction with sapacitabine/CNDAC. Thus, this study provides rationales for sapacitabine-based combinational and targeted therapeutic strategies for translation into the design of clinical trials. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5667. doi:1538-7445.AM2012-5667

Abstract 962: Mechanism-based drug combinations with the DNA-strand-breaking nucleoside analog CNDAC

Abstract Sapacitabine, an orally bioavailable prodrug of CNDAC (2’-C-cyano-2’-deoxy-1-β-D-arabino-pentofuranosylcytosine), is undergoing clinical trials with encouraging outcomes [J. Clin.Oncol., 2010, 28(2): 285-91]. CNDAC has a unique action mechanism; following its incorporation into DNA, it induces single strand breaks through a β-elimination process, which also generates the chain-terminating analog CNddC. Subsequent processing or DNA replication across the unrepaired nicks generates double strand breaks which are primarily repaired through the ATM-dependent homologous recombination (HR) pathway [Blood, 2010, 116(10): 1737-46]. We hypothesized that agents directly affecting or interacting with the HR pathway may be synergistic with CNDAC, which will provide a rationale for clinical combinations. This study used clonogenic survival assays to explore mechanistic interactions between CNDAC and other chemotherapeutic agents. First, inhibition of ATM kinase by a specific inhibitor, KU55933, greatly sensitized the human myeloid cell line OCI-AML3, as well as primary cells from acute myeloid leukemia patients, to CNDAC. Second, colon carcinoma HCT116 cells pre-treated with the c-Abl kinase inhibitor, imatinib, were sensitized 4-5 fold to CNDAC compared to those exposed to CNDAC alone. This is likely due to inhibition of Rad51 recombinase, the key component of HR, as a consequence to suppression of c-Abl. In contrast, no sensitization resulted from inhibition of DNA-PK (NU7441) or Chk1 (UCN-01). Third, co-incubation of the poly(ADP-ribose) polymerase 1 inhibitor, AZD2281, and CNDAC exhibited greater than additive cell killing selectively in hamster cells deficient in Brca2, a breast cancer susceptibility protein associated with Rad51 function. The mild synergy may result from a synthetic lethal interaction between base excision repair and HR pathways. Fourth, temozolomide, an alkylating agent which causes base methylation that is repaired partially by base excision repair, had greater than additive effect with CNDAC specifically in hamster cells lacking the Rad51 paralogs Rad51D or Xrcc3, based on a median effect analysis (CI < 1). This again suggests a mechanistic interaction selectively targeting HR-defective cells. Finally, combination of the alkylating agent bendamustine with CNDAC showed no synergy (CI > = 1) in cells lacking Rad51D or Xrcc3, although HR-deficient cells were more sensitive to bendamustine alone compared to HR-proficient cells. This suggests that nucleotide excision process by which bendamustine-caused DNA adducts are repaired does not generate a synthetic lethal interaction with HR. Together these results indicate rationales for CNDAC-based combinational and targeted therapeutic strategies for translation into the design of clinical trials. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 962. doi:10.1158/1538-7445.AM2011-962

Water as dual functional cocatalyst: A theoretical study on the mechanism of direct aldol reaction on water catalyzed by a leucine derivative

The role of water and stereoselectivity in the direct syn-aldol reaction involving 3-pentanone and 4-nitrobenzaldehyde catalyzed by amino acid derivatives on water has been investigated by density functional theory. Calculations indicate that the formation of intermediate enamine is the rate determining step via a three-step process with activation enthalpies of 50 kcal/mol in the gas phase and 21 kcal/mol in the presence of water. The subsequent nucleophilic addition of enamine to aldehyde is relatively easier with activation enthalpies below 10 kcal/mol both in the gas phase and in the presence of water. The diastereoselective formation of syn- and anti-aldol products results from the preferential formation of Z-enamine to E-enamine, kinetically and thermodynamically. The enantioselectivity of both syn- and anti-products is controlled by the steric repulsive interactions between the amino alcohol moiety of catalyst and the phenyl ring of aldehyde. Calculations show that water molecule can act as a proton shuttle in the proton-transport catalytic processes. The water-assisted proton-transfer is very efficient to reduce the activation barriers via protonation and deprotonation in the formation of C-N and C-C bonds, dehydration, and β-elimination processes by inhibiting the generation of zwitterionic transition states. The theoretical discoveries indicate that in the present proton-transport assistance, the amino alcohol moiety of the catalyst plays a critical role as hydrogen bond donor to anchor substrates with carbonyl group close to the amine or enamine moiety so that the water molecule can bridge the NH of amine and the oxygen of carbonyl by hydrogen bonding interaction around the reactive site to activate the reactants and promote the reaction effectively.

One-Pot Synthesis of 1,3-Disubstituted Allenes from 1-Alkynes, Aldehydes, and Morpholine

ZnI(2) has been identified as the catalyst for the one-step synthesis of allenes from terminal alkynes and aldehydes with morpholine as the base in toluene. The reaction is believed to proceed via the intermediacy of propargylic amines, which was converted to allenes by a sequential hydride transfer and beta-elimination process. The reaction is applicable for both aromatic and aliphatic aldehydes. Functionalities such as halide, hydroxyl, or amine may be tolerated.

Surface reactions of 2-iodopropane on GaAs(1 0 0)

The surface reactions of 2-iodopropane ((CH 3) 2CHI) on gallium-rich GaAs(1 0 0)-(4 × 1), was studied by temperature programmed desorption (TPD) and X-ray photoelectron spectroscopy (XPS). CH 3CHICH 3 adsorbs molecularly at 120 K but dissociates below room temperature to form chemisorbed 2-propyl ((CH 3) 2CH ) and iodide (I ) species. Thermal activation causes desorption of the molecular species at 240 K, and this occurs in competition with the further reactions of the (CH 3) 2CH and I chemisorbed species. Self-coupling of the (CH 3) 2CH results in the formation of 2,3-dimethylbutane ((CH 3) 2CH–CH(CH 3) 2) at 290 K. β-Hydride elimination in (CH 3) 2CH yields gaseous propene (CH 3CH CH 2) at 550 K while reductive elimination reactions of (CH 3) 2CH with surface hydrogen yields propane (CH 3CH 2CH 3) at 560 K. Recombinative desorption of the adsorbed hydrogen as H 2 also occurs at 560 K. We observe that the activation barrier to carbon–carbon bond formation with 2-propyls on GaAs(1 0 0) is much lower than that in our previous investigations involving ethyl and 1,1,1-trifluoroethyl species where the β-elimination process was more facile. The difference in the surface chemistry in the case of 2-propyl species is attributable to its rigid structure resulting from the bonding to the surface via the second carbon atom, which causes the methyl groups to be further away from the surface than in the case of linear ethyl and 1,1,1-trifluoroethyl species. The β-hydride and reductive elimination processes in the adsorbed 2-propyl species thus occurs at higher temperatures, and a consequence of this is that GaI desorption, which is expected to occur in the temperature range 550–560 K becomes suppressed, and the chemisorbed iodine leaves the surface as atomic iodine.

Phase Transfer Alkylation of Arylacetonitriles Revisited.

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Phase transfer alkylation of arylacetonitriles revisited

Phase transfer alkylations of phenylacetonitrile derivatives carried out in the presence of 60–75% aqueous KOH, instead of the typical 50% NaOH, provide substantial improvements in the overall yields and purity of products. Reactions with simple secondary alkyl halides, as well as cycloalkylations with 1,2- and 1,3-dihaloalkanes proceed with good yields. Increasing the concentration of base diminishes the formation of by-products from competitive β-elimination processes.

Mechanisms of Thermal Decompositions of Polysulfones: A DFT and CBS-QB3 Study

The thermal stabilities of polysulfones with different lengths of the carbon-linker between sulfone groups have been explored. B3LYP and CBS-QB3 calculations on possible thermal decomposition mechanisms of model compounds show that even carbon-linked polysulfonescopolymers of alkenes and SO2decompose by a radical chain mechanism involving facile depolymerization after initial homolysis. Sulfinate impurities [−S(O)−O−CH2−], formed as a minor component in polysulfone synthesis, can serve as good initiators for the radical mechanism. Polysulfones with odd-carbon linkers do not readily depolymerize in this fashion owing to high barriers of depropagation; these polymers undergo thermal degradation by the slower cyclic β-elimination processes.

On the enzymatic hydrolysis of methyl 2-fluoro-2-arylpropionates by lipases

The enzymatic hydrolysis of methyl 2-fluoro-2-arylpropionates was performed using lipases from Candida rugosa and Candida cylindracea (OF-360). A careful analysis of the reaction products revealed that racemic 2-hydroxy-2-arylpropionic acid and traces of 2-arylacrylic acid are formed, in addition to the expected 2-aryl-2-fluoropropionic acid. The presence of powerful electron-releasing groups in the aromatic ring of the substrate increase the amount of 2-hydroxypropionic acid. A mechanistic hypothesis has been formulated according to which the enzyme facilitates the elimination of fluoride ion from the hydrolysed acid with the formation of an α-carboxy-stabilized carbocation which provides 2-hydroxypropionic acids by nucleophilic attack of H 2O and 2-arylacrylic acids by a β-elimination process.