The asymmetric unit of the title cyclic thio-urea derivative, C10H12N2S, comprises two mol-ecules, each of which has a twist about the CH2-CH2 bond within the five-membered ring. The major difference between the independent mol-ecules is manifested in the relative orientations of the five- and six-membered rings [dihedral angles between the least-squares planes = 28.03 (11) and 41.54 (11)°]. A network of C-H⋯π inter-actions consolidates the three-dimensional crystal packing.
In the title compound, C14H8N4O6, the benzoxazin-4-one fused-ring system (r.m.s. deviation = 0.018 Å) is coplanar with the attached benzene ring [dihedral angle = 0.81 (4)°], there being an intra-molecular N-H⋯N hydrogen bond between them. Each nitro group is twisted out of the plane of the attached benzene ring [O-N-C-C torsion angles = 167.94 (11) and 170.38 (11)°]. In the crystal, amine-nitro N-H⋯O hydrogen bonds lead to centrosymmetric dimeric aggregates that are connected into a three-dimensional architecture by oxazin-yl-nitro C-H⋯O and π-π inter-actions [inter-centroid distance between the oxazinyl and terminal benzene rings = 3.5069 (7) Å].
The 21 non-H atoms of the title compound, C15H10Cl2N4, are almost planar (r.m.s. deviation = 0.032 Å); the conformation about the N=C bond [1.277 (6) Å] is E. In the crystal, zigzag supra-molecular chains along the c axis (glide symmetry) are formed via N-H⋯N hydrogen bonds. These associate along the b axis by π-π inter-actions between the fused and terminal benzene rings [inter-centroid distance = 3.602 (3) Å] so that layers form in the bc plane.
The compound with R=CH2CH3 in Bi(S2CNR2)3 (1) is highly cytotoxic against a range of human carcinoma, whereas that with R=CH2CH2OH (2) is considerably less so. Both 1 and 2 induce apoptosis in HepG2 cells with some evidence for necrosis induced by 2. Based on DNA fragmentation, caspase activities and human apoptosis PCR-array analysis, both the extrinsic and intrinsic pathways of apoptosis have been shown to occur. While both compounds activate mitochondrial and FAS apoptotic pathways, compound 1 was also found to induce another death receptor-dependent pathway by induction of CD40, CD40L and TNF-R1 (p55). Further, 1 highly expressed DAPK1, a tumour suppressor, with concomitant down-regulation of XIAP and NF-κB. Cell cycle arrest at the S and G2/M phases correlates with the inhibition of the growth of HepG2 cells. The cell invasion rate of 2 is 10-fold higher than that of 1, a finding correlated with the down-regulation of survivin and XIAP expression by 1. Compounds 1 and 2 interact with DNA through different binding motifs with 1 interacting with AT- or TA-specific sites followed by inhibition of restriction enzyme digestion; 2 did not interfere with any of the studied restriction enzymes.
The title compound, C34H38ClN5O2, has spiro links connecting the pyrrolidine ring and indole residue, as well as the piperidine and pyrrolidine rings. A half-chair conformation is found for the piperidine ring with the C atom connected to the spiro-C atom lying 0.738 (4) Å out of the plane of the remaining five atoms (r.m.s. deviation = 0.0407 Å). The methyl-ene C atom is the flap in the envelope conformation for the pyrrolidine ring. In the crystal, supra-molecular chains are sustained by alternating eight-membered {⋯HNCO}2 and 14-membered {⋯HC5O}2 synthons. Chains are connected into a three-dimensional network by (pyrrolidine-bound phenyl-meth-yl)C-H⋯π(pyrrolidine-bound phen-yl) edge-to-face inter-actions.
Two spiro links are found in the title compound, C31H28Cl3N3O2, one connecting the piperidine and pyrrolidine rings, and the other connecting the pyrrolidine ring and indole residue. The piperidine ring adopts a half-chair conformation, in which the C atom connected to the spiro-C atom lies 0.741 (3) Å out of the plane of the remaining five atoms (r.m.s. deviation = 0.053 Å). The pyrrolidine ring has an envelope conformation with the flap atom being the methyl-ene C atom. Centrosymmetric eight-membered {⋯HNCO}2 amide dimers are the most significant feature of the crystal packing. These are connected into layers parallel to (-120) by C-H⋯O and π-π inter-actions between pyrrolidine-bound benzene rings [inter-centroid distance = 3.8348 (15) Å]. Slipped face-to-face inter-actions between the edges of pyrrolidine-bound benzene [shortest C⋯C separation = 3.484 (4) Å] connect the layers into a three-dimensional architecture.
The title compound, C30H28ClN3O2, features two spiro links, one connecting the piperidine and pyrrolidine rings, and the other connecting the pyrrolidine ring and indole residue. The configuration about the ethene bond is E. The piperidine ring adopts a half-chair conformation where the C atom connected to the spiro-C atom lies 0.713 (3) Å out of the plane of the remaining five atoms (r.m.s. deviation = 0.086 Å). The pyrrolidine ring has an envelope conformation with the flap atom being the methyl-ene C atom. Centrosymmetric eight-membered {⋯HNCO}2 amide synthons feature in the crystal packing. These are consolidated into a three-dimensional architecture by phen-yl-pyrrolidine C-H⋯N and chloro-benzene-pyrrolidine-bound phenyl C-H⋯π inter-actions.
Two independent molecules that differ in terms of rotation about the central S-N bond comprise the asymmetric unit of the title compound 1. The molecules have a V-shape with the dihedral angles between the fused ring system and benzene ring being 79.08(6)° and 72.83(5)°, respectively. The packing is mostly driven by p···p interactions occurring between the tolyl ring of one molecule and the C6 ring of the indole fused ring system of the other. DFT and IRC calculations for these and related 1-(arylsulfonyl)indole molecules showed that the rotational barrier about the S-N bond between conformers is within the 2.5-5.5 kcal/mol range. Crystal data for C16H13NO3S (1): Mr = 299.33, space group Pna21, a = 19.6152(4) Å, b = 11.2736(4) Å, c = 12.6334(3) Å, V = 2793.67(13) Å3, Z = 8, Z' = 2, R = 0.034.
The title dimethyl sulfoxide solvate, [Hg2(C12H9ClN2)I2]·C2H6OS, features tetra-hedrally and linearly coordinated Hg(II) atoms. The distorted tetrahedral coordination sphere is defined by chelating N atoms that define an acute angle [69.6 (3)°] and two I atoms that form a wide angle [142.80 (4)°]. The linearly coordinated Hg(II) atom [177.0 (4)°] exists with a donor set defined by C and Cl atoms. Secondary inter-actions are apparent in the crystal packing with the tetra-hedrally and linearly coordinated Hg(II) atoms expanding their coordination environments by forming weak Hg⋯I [3.772 (7) Å] and Hg⋯O [2.921 (12) Å] inter-actions, respectively. Mercury-containing mol-ecules stack along the a axis, are connected by π-π inter-actions [inter-centroid distance between pyridine and benzene rings = 3.772 (7) Å] and define channels in which the dimethyl sulfoxide mol-ecules reside. The latter are connected by the aforementioned Hg⋯O inter-actions as well as C-H⋯I and C-H⋯O inter-actions, resulting in a three-dimensional architecture.
The complete binuclear molecule of the title compound, [Cd2I4(C14H12N2O2)2], is generated by the application of a centre of inversion. The Cd-I bond lengths of the central core are close and uniformly longer than the exocyclic Cd-I bond. The coordination sphere of the Cd(II) atom is completed by two N atoms of a chelating methyl 4-[(pyridin-2-yl-methyl-idene)amino]-benzoate ligand, and is based on a square pyramid with the terminal I atom in the apical position. The three-dimensional crystal packing is stabilized by C-H⋯O and C-H⋯π inter-actions, each involving the pyridine ring.
The asymmetric unit of the title co-crystal, C12H12N2·2C7H7NO2, comprises a centrosymmetric 4-[2-(pyridin-4-yl)eth-yl]pyridine mol-ecule and a 2-amino-benzoic acid mol-ecule in a general position. The acid has a small twist between the carb-oxy-lic acid residue and the ring [dihedral angle = 7.13 (6)°] despite the presence of an intra-molecular N-H⋯O(carbon-yl) hydrogen bond. Three-mol-ecule aggregates are formed via O-H⋯N(pyrid-yl) hydrogen bonds, and these are connected into supra-molecular layers in the bc plane by N-H⋯O(carbon-yl) hydrogen bonds and π-π inter-actions between pyridine and benzene rings [inter-centroid distance = 3.6332 (9) Å]. Layers are connected along the a axis by weak π-π inter-actions between benzene rings [3.9577 (10) Å].
The asymmetric unit of the title co-crystal, C12H14N4O2S·0.5C6H12N2, comprises the sulfonamide mol-ecule and half a mol-ecule of 1,4-di-aza-bicyclo-[2.2.2]octane (DABCO), the latter being disposed about a crystallographic twofold rotation axis. In the sulfonamide mol-ecule, the aromatic rings are almost perpendicular to one another [dihedral angle = 75.01 (8)°]. In the crystal, mol-ecules are connected into a three-mol-ecule aggregate via amide-DABCO N-H⋯N hydrogen bonds, and these are connected into a three-dimensional architecture via amino-DABCO N-H⋯O and amino-pyrimidine N-H⋯N hydrogen bonds.
The asymmetric unit of the title salt, C12H14N2 (2+)·2C7H3N2O6 (-), comprises half a 4-[2-(pyridin-1-ium-4-yl)eth-yl]pyridin-1-ium dication, being disposed about a centre of inversion, and a 2,6-di-nitro-benzoate anion, in a general position. In the anion, the carboxyl-ate group is inclined to the benzene ring [dihedral angle = 85.45 (9)°], whereas near-coplanar and twisted arrangements are found for the nitro groups [O-N-C-C torsion angles = 179.80 (14) and 20.2 (2)°]. In the crystal, three-component aggregates sustained by charge-assisted N(+)-H⋯O(-) hydrogen bonds are found and these are consolidated into a three-dimensional architecture by C-H⋯O and π-π [inter-centroid distances = 3.6796 (14) and 3.7064 (14) Å] inter-actions.
The Ph3PAu[SC(OR)=NPh], R=Me (1), Et (2) and iPr (3), compounds are significantly cytotoxic to the HT-29 cancer cell line with 1 being the most active. Based on human apoptosis PCR-array analysis, caspase activities, DNA fragmentation, cell apoptotic assays, intracellular reactive oxygen species (ROS) measurements and human topoisomerase I inhibition, induction of apoptosis is demonstrated and both the extrinsic and intrinsic pathways of apoptosis have been shown to occur. Compound 1 activates the p73 gene, whereas each of 2 and 3 activates the p53 gene. An additional apoptotic mechanism is exhibited by 2, that is, via the JNK/MAP pathway.
The synthesis and characterisation of R3PAu[S2CN((i)Pr)CH2CH2OH], for R = Ph (1), Cy (2) and Et (3)4, is reported. Compounds 1-3 are cytotoxic against the doxorubicin-resistant breast cancer cell line, MCF-7R, with 1 exhibiting greater potency and cytotoxicity than either of doxorubicin and cisplatin. Based on human apoptosis PCR-array analysis, caspase activities, DNA fragmentation, cell apoptotic assays, intracellular reactive oxygen species (ROS) measurements and human topoisomerase I inhibition, induction of apoptosis by 1, and necrosis by 2 and 3, are demonstrated, by both extrinsic and intrinsic pathways. Compound 1 activates the p53 gene, 2 activates only the p73 gene, whereas 3 activates both the p53 and p73 genes. Compounds 1 and 3 activate NF-κB, and each inhibits topoisomerase I.
Perovskite-structured lead titanate thin films have been grown on FTO-coated glass substrates from a single-source heterometallic molecular complex, [PbTi(μ2-O2CCF3)4(THF)3(μ3-O)]2 (1), which was isolated in quantitative yield from the reaction of tetraacetatolead(IV), tetrabutoxytitanium(IV), and trifluoroacetic acid from a tetrahydrofuran solution. Complex 1 has been characterized by physicochemical methods such as melting point, microanalysis, FTIR, (1)H and (19)F NMR, thermal analysis, and single-crystal X-ray diffraction (XRD) analysis. Thin films of lead titanate having spherical particles of various sizes have been grown from 1 by aerosol-assisted chemical vapor deposition at 550 °C. The thin films have been characterized by powder XRD, scanning electron microscopy, and energy-dispersive X-ray analysis. An optical band gap of 3.69 eV has been estimated by UV-visible spectrophotometry.
In the title salt, C14H17N2(+)·Cl(-), the central N atom is pyramidal (sum of bond angles = 330.9°) and there is a near orthogonal relationship between the benzene rings [dihedral angle = 89.95 (10)°]. The crystal packing features N-H⋯Cl hydrogen bonds, which lead to a supra-molecular undulating ribbon along the a axis comprising edge-shared eight-membered {⋯HNH⋯Cl}2 synthons. The chains are connected into layers in the ab plane by C-H⋯π inter-actions.
In the title compound, C(16)H(15)N(3)S(2), the central C(2)N(2)S(2) residue is planar (r.m.s. deviation = 0.045 Å) and the pyridyl and benzene rings are inclined and approximately coplanar to this plane, respectively [dihedral angles = 72.85 (9) and 10.73 (9)°], so that, overall, the mol-ecule adopts an L-shape. The conformation about each of the N=C [1.290 (3) Å] and C=C [1.340 (3) Å] bonds is E. Supra-molecular chains along [1-10] are stabilized by N-H⋯N(pyridine) hydrogen bonding and these are connected into a double layer that stacks along the c-axis direction by C-H⋯π(pyridine) inter-actions.
In the title di-hydro-dioxin, C31H28O5, the dioxane ring has a chair conformation, whereas each of the pyran and dioxine rings has an envelope conformation with methyl-ene and quaternary C atoms, respectively, being the flap atoms. The phenyl rings are cis and form a dihedral angle of 82.11 (10)°. The molecular structure is stabilized by C-H⋯O contacts. In the crystal packing, supra-molecular layers parallel to (101) are sustained by C-H⋯π inter-actions.
The asymmetric unit of title co-crystal, C10H8N2·2C7H7NO2, comprises a centrosymmetric 4,4'-bi-pyridine mol-ecule, and a 2-amino-benzoic acid mol-ecule in a general position. The latter is effectively planar [C-C-C-O torsion angle = 5.0 (3)°] owing to an intra-molecular N-H⋯O(carbon-yl) hydrogen bond. Three-mol-ecule aggregates are formed via O-H⋯N(pyrid-yl) hydrogen bonds and these are connected into supra-molecular layers in the bc plane by N-H⋯O(carbon-yl) hydrogen bonds and π-π inter-actions between pyridyl and benzene rings [inter-centroid distance = 3.634 (2) Å]. Layers are connected along the a axis by weak π-π inter-actions between benzene rings [3.964 (2) Å].