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The conversion of heterosubstituted methanes, such as methyl alcohol, dimethyl ether, methyl mercaptan, dimethyl sulfide, methylamines, and methyl halides, to ethylene and hydrocarbons derived thereof takes place over bifunctional acidic-basic-supported transition-metal oxide or oxyhalide catalysts, such as tungsten oxide supported on alumina, between 300 and 350 °C. The conversion of methyl alcohol starts with bimolecular dehydration to dimethyl ether followed by acid-catalyzed transmethylation giving trimethyloxonium ion (or related catalyst-bound methyloxonium ion). The trimethyloxonium ion then undergoes base-induced deprotonation forming a catalyst surface-bound methylenedimethyloxonium ylide. Intermolecular methylation of the ylide, indicated by experiments using singly 13C-labeled dimethyl ether, gives methylethyloxonium ion thus providing the crucial first C-C bond. No intramolecular Steven's-type rearrangement takes place, and methyl ethyl ether is not a significant intermediate as also shown in experiments comparing the products formed from reacting CD3OCH2CH3 under similar conditions. The ethyloxonium ion readily undergoes ß-elimination forming ethylene. Initialy formed ethylene subsequently can undergo further reaction with the ylide giving via cyclopropane propylene or it can undergo more complex alkylation/oligomerization/cracking reactions giving a mixture of alkenes, alkanes and via cyclization-dehydrogenation aromatics. The complexity of these processes was shown by reacting ethylene itself, as well as 13CH3OH and ethylene, under conditions of the condensation reaction. It is also necessary to differentiate initially formed ethylene via direct C¡ -* C2 conversion from that formed in secondary processes together with higher condensation products. The conversion of methyl mercaptan (dimethyl sulfide), methyl halides, and methylamines to ethylene follows similar onium ylide pathways.

Abstract.The in vitro cytotoxicities of a number of gold(I), silver(I) and copper(I) complexes containing chiral tertiary phosphine ligands have been examined against the mouse tumour cell lines P815 mastocytoma, B16 melanoma [gold(I) and silver(I) compounds] and P388 leukaemia [gold(I) complexes only] with many of the complexes having IC50 values comparable to that of the reference compounds cis-diamminedichloroplatinum(ll), cisplatin, and bis[1,2-bis(diphenylphosphino)ethane]gold(I) iodide. The chiral tertiary phosphine ligands used in this study include (R)-(2-aminophenyl)methylphenylphosphine; (R,R)-, (S,S)-and (R*,R*)-l,2-phenylenebis(methylphenylphosphine); and (R,R )-, (S,S)-and (R*, R')-bis{(2-diphenylphosphinoethyl)phenylphosphino}ethane. The in vitro cytotoxicities of gold(I) and silver(I) complexes containing the optically active forms of the tetra(tertiary phosphine) have also been examined against the human ovarian carcinoma cell lines 41M and CH1, and the cisplatin resistant 41McisR, CHlcisR and SKOV-3 tumour models. IC5o values in the range 0.01 0.04 #M were determined for the most active compounds, silver(I) complexes of the tetra(tertiary phosphine). Furthermore, the chirality of the ligand appeared to have little effect on the overall activity of the complexes: similar IC50 data were obtained for complexes of a particular metal ion with each of the stereoisomeric forms of a specific ligand.Introduction.

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lithium jV-phthaloyl-L-phenylalaninate, 79069-04-8; l,2:5,6-di-0-isopropylidene-3-C-methylene-a-D-ribohexofuranose, 21665-16-7; l,2:5,6-di-0-isopropylidene-3-deoxy-3-oxo-a-D-ribohexofuranose, 2847-00-9; 2',3'-0-isopropylideneuridine, 362-43-6. Notes Synthetic Methods and Reactions. 104.1

The resolution and improved synthesis of the naturally occurring, adamantane-type, tetraarsenical (±)-Arsenicin A is reported. The five-step synthesis of (±)-Arsenicin A from methylenebis(phenylarsinic acid) affords (±)-Arsenicin A as air-stable, colorless crystals having an mp of 182–184 °C after column chromatography and recrystallization from benzene (overall yield: 36%). The resolution of (±)-Arsenicin A was achieved by preparative HPLC on a Chiralpak IA column with the use of dichloromethane as eluent to give both enantiomers in >99% enantiomeric purity (HPLC); the isolated enantiomers had [α]589 20 = −60.2 and +62.3 (0.01% NEt3/CH2Cl2). (S)-(−)-Arsenicin A, having an mp of 241–242 °C from dichloromethane, crystallizes in the space group P212121 with one molecule having the (S As,S As,S As,S As) or overall S configuration in the asymmetric unit. The adamantane-type structure of (±)-Arsenicin A is reminiscent of arsenic(III) oxide (As4O6), but where three of the oxygen atoms in the inorganic oxide have been replaced by methylene groups in a chiral C 2 arrangement. ((±)-Arsenicin A, mp 182–184 °C, crystallizes from benzene in the centrosymmetrical space group P1̅: the unit cell of the crystal contains two independent pairs of molecules, the molecules in each pair being related by an inversion center.) The individual enantiomers of (±)-Arsenicin A racemize in the presence of traces of acid, and high-level ab initio calculations have been performed to examine the mechanism of the process. (±)-Arsenicin A exhibits a 21-fold greater inhibition of the induction of proliferation arrest and induces cell death at a 27-fold lower concentration in the acute promyelocytic leukemia cell line than the current “arsenical gold standard”, arsenic(III) oxide (Trisenox). (±)-Arsenicin A is also more potent than arsenic(III) oxide for the induction of proliferation arrest in two other cancers with particularly bad prognoses: pancreatic adenocarcinoma and glioblastoma.

The synthesis of the natural polyarsenical Arsenicin A and its crystal structure are described. The molecule has the adamantane-type structure of arsenic trioxide in which three of the oxygen atoms have been replaced by methylene groups to generate four arsenic stereocenters of the same configuration in each enantiomer of the racemate.

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