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At least 343 records · Page 19Linked to original sources

PubMed1998

Incorporation of phencyclidine and its hydroxylated metabolites into hair.

The incorporation of phencyclidine(PCP) and its three major hydroxylated metabolites, 1-(1-phenylcyclohexyl)-4-hydroxypiperidine(PCHP), trans-4-phenyl-4-piperidinocyclohexanol(t-PPC) and trans-1-phenyl-1-(4'-hydroxypiperidino)-4-cyclohexanol(t-PCPdiol) into rat hair was studied. Three Dark Agouti male rats were intraperitoneally administered with PCP x HCl at a dose of 0.5 or 1.0 mg/kg once a day for 10 successive days. The plasma samples were collected from 5 min to 360 min after injection of each drug. The hair samples were collected 28 days after the first administration. The hair samples were extracted with methanol-5N hydrochloric acid(20:1) for 1 h under sonication. The plasma and hair extracts were extracted or purified with Bond Elut Certify and the extracts were silylated for the determination of PCP and its metabolites by GC/MS. The plasma AUCs were as follows; PCP(2.03 microg x min/ml) > t-PCPdiol(0.60 microg x min/ml) > PCHP(0.11 microg x min/ml) > t-PPC (0.065 microg x min/ml), while the hair concentrations were as follows; PCP(7.51 ng/mg) > PCHP (1.22 ng/mg) > t-PPC(0.10 ng/mg) > t-PCPdiol (0.05 ng/mg). In view of their AUCs, the hair concentration of t-PCPdiol was quite low, whereas that of PCP was so high. PCHP, t-PPC or t-PCPdiol was separately administered as the parent drug to the rats, and then the plasma and hair samples were analyzed in the same manner as PCP experiments. The incorporation rates ([hair concentration]/[AUC]) of PCP and its hydroxylated metabolites were as follows; PCP(2.29) > PCHP(0.79) > t-PPC(0.36) > t-PCPdiol(0.32). These data suggest that the decrease in lipophilicity caused by the hydroxylation of PCP suppresses the incorporation of the metabolites from blood into hair and the hydroxylation on cyclohexane ring(t-PPC) induces the decrease of the drug incorporation into hair more than that on piperidine ring(PCHP).

Animals↗

PubMed2000

A critical histidine in the vesicular acetylcholine transporter.

The role of proton binding sites in the vesicular acetylcholine transporter was investigated by characterization of the pH dependence for the binding of [3H]vesamicol [(-)-trans-2-(4-phenylpiperidino)cyclohexanol] to Torpedo synaptic vesicles. A single proton binds to a site with pKa 7.1 +/- 0.1, which is characteristic of histidine, to competitively inhibit vesamicol binding. The histidine-selective reagent diethylpyrocarbonate causes time-dependent inhibition of [3H]vesamicol binding with a rate constant only about 20-fold lower than for reaction with free histidine. Because its pH titration has a simple, ideal shape, this residue probably controls all pH effects in the transporter between pH 6-8. Inhibition of [3H]vesamicol binding by diethylpyrocarbonate was slowed by vesamicol but not acetylcholine, which binds to a separate site. The data suggest that a critical histidine with a pKa of 7.1 is unhindered when reacting with diethylpyrocarbonate. A conformational model for the histidine is proposed to explain why acetylcholine competes with protons but not with diethylpyrocarbonate. A conserved histidine in transmembrane helix VIII possibly is the histidine detected here.

Animals↗

PubMed2002

Dechlorination of chlorinated phenols by catalyzed and uncatalyzed Fe(0) and Mg(0) particles.

Uncatalyzed, and palladium-catalyzed Fe(0) and Mg(0) systems were examined for their efficiencies of dechlorination of 2.86 mM 4-chlorophenol (4-CP), 2.52 mM 2,6-dichlorophenol (2,6-DCP), 3.03 mM 2,4,6-trichlorophenol (2,4,6-TCP), and 2.48 mM pentachlorophenol (PCP) in 50/50 (v/v) 2-propanol/water under room temperature and pressure conditions. Previous investigators have found that PCP is extremely recalcitrant under these conditions. In this investigation, complete dechlorination of 5.0 ml of 2.48 mM PCP was observed for 1.0 g of 2659 ppm Pd/Mg (20 mesh) after 48 h. The only detectable products were cyclohexanol and cyclohexanone at 25% yield. No other chlorinated or otherwise products were observed by mass spectral analysis. It is hypothesized that volatile low molecular weight species were formed from the Pd/Mg dechlorination of PCP. Under conditions of equal surface area (0.0786 m2), the approximate order of PCP dechlorination power of these systems followed as 2659 ppm Pd/Mg>319 ppm Pd/Mg>Mg approximately 4856 ppm Pd/Fe>Fe. Degradation of the other chlorinated phenols by all metallic systems was more facile than PCP.

Catalysis↗

PubMed1998

Role of protein kinase C in the release of [3H]acetylcholine from myenteric plexus treated with vesamicol.

The present experiments investigated the release of [3H]acetylcholine ([3H]ACh) from the guinea pig myenteric plexus treated with 2-(4-phenylpiperidino)cyclohexanol (vesamicol), a drug that impairs ACh accumulation by synaptic vesicles. Ouabain, an Na+-K+ ATPase inhibitor, released [3H]ACh synthesised in the presence of (-)-vesamicol, while electrical field stimulation or KCl depolarisation were not effective to release the transmitter in this condition. The effect of ouabain was Ca2+-dependent and in the presence of (-)-vesamicol it was blocked by calphostin C, an inhibitor of protein kinase C (PKC). In addition, stimulation of kinase C activity by a phorbol ester, but not by its inactive isomer, prevented (-)-vesamicol from interfering with the release of [3H]ACh in electrically-stimulated myenteric plexus, similar to the effect of ouabain. We conclude that release of [3H]ACh induced by ouabain in the presence of (-)-vesamicol depends on PKC activation.

Acetylcholine↗

PubMed2000

Cannabinoids inhibit excitatory neurotransmission in the substantia nigra pars reticulata.

The substantia nigra pars reticulata belongs to the brain regions with the highest density of CB(1) cannabinoid receptors. Since the level of CB(1) receptor messenger RNA is very low in the pars reticulata, most of the receptors are probably localized on terminals of afferent axons. The hypothesis was tested that terminals of glutamatergic afferents of substantia nigra pars reticulata neurons possess CB(1) cannnabinoid receptors, the activation of which presynaptically modulates neurotransmission. Rat midbrain slices were superfused and the electrophysiological properties of substantia nigra pars reticulata neurons were studied with the patch-clamp technique. Focal electrical stimulation in the presence of bicuculline evoked excitatory postsynaptic currents mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA)/kainate glutamate receptors. The excitatory postsynaptic currents were reduced by the metabotropic glutamate receptor agonist (+/-)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (trans-ACPD; 10(-4)M). The mixed CB(1)/CB(2) cannabinoid receptor agonists R(+)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2, 3-de]-1,4-benzoxazin-yl]-(1-naphthalenyl)methanone (WIN55212-2; 10(-8)-10(-5)M) and (-)-cis-3-[2-hydroxy-4-(1, 1-dimethylheptyl)phenyl]-trans-4-(3-hydroxypropyl)cyclohexanol (CP55940; 10(-6)M) also produced inhibition. The maximal inhibition by WIN55212-2 was 54+/-6%. The CB(1) cannabinoid antagonist N-piperidino-5-(4-chlorophenyl)-1-(2, 4-dichlorophenyl)-4-methyl-3-pyrazole-carboxamide (SR141716A; 10(-6)M) prevented the effect of WIN55212-2, but had no effect when superfused alone. WIN55212-2 (10(-6)M) increased the amplitude ratio of two excitatory postsynaptic currents evoked with an interstimulus interval of 100ms. Currents evoked by short ejection of glutamate on to the surface of the slices were not changed by WIN55212-2. The results show that activation of CB(1) cannabinoid receptors inhibits glutamatergic synaptic transmission between afferent axons and neurons in the substantia nigra pars reticulata. The lack of effect of the cannabinoids on glutamate-evoked currents and the increase of the paired-pulse ratio indicate that the mechanism of action is presynaptic inhibition of transmitter release.

Animals↗

PubMed2002

Cannabinoids inhibit striatonigral GABAergic neurotransmission in the mouse.

The substantia nigra pars reticulata (SNR) belongs to the brain regions with the highest density of CB(1) cannabinoid receptors. Anatomical studies indicate that the great majority of CB(1) receptors in the SNR are localized on terminals of GABAergic axons arriving from the caudate-putamen (striatonigral axons). The aim of the present experiments was to clarify the role of CB(1) receptors on terminals of striatonigral axons. Oblique sagittal slices, including the caudate-putamen and the substantia nigra, were prepared from brains of young mice. Electrical stimulation in the caudate-putamen elicited GABAergic inhibitory postsynaptic currents (IPSCs) in the SNR, which were studied by patch-clamp techniques. The long latency of IPSCs (14+/-1 ms) suggests that striatonigral axons were indeed activated within the caudate-putamen. The synthetic CB(1)/CB(2) cannabinoid receptor agonist WIN55212-2 (R(+)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazin-yl]-(1-naphthalenyl)methanone mesylate; 10(-5) M) decreased the amplitude of IPSCs by 93+/-1%. CP55940 ((-)-cis-3-[2-hydroxy-4-(1,1-dimethylheptyl)phenyl]-trans-4-(3-hydroxypropyl)cyclohexanol; 10(-5) M), another CB(1)/CB(2) receptor agonist, also reduced IPSC amplitude, by 76+/-4%. The CB(1) cannabinoid receptor antagonist SR141716A (N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazole-carboxamide; 10(-6) M) prevented the inhibition produced by WIN55212-2 (10(-5) M). Depolarization of SNR neurons led to suppression of IPSCs; this suppression was prevented by SR141716A (10(-6) M). Three observations indicate that the agonists inhibited neurotransmission presynaptically. (1) CP55940 (10(-5) M) enhanced the ratio of amplitudes of two IPSCs which were elicited by two electrical stimuli 100 ms apart (paired pulses). (2) WIN55212-2 (10(-5) M) did not change the amplitude of miniature IPSCs recorded in the presence of tetrodotoxin. (3) WIN55212-2 (10(-5) M) also had no effect on currents elicited in SNR neurons by ejection of the GABA(A) receptor agonist muscimol from a pipet. In summary, we have established a method which allows selective examination of GABAergic neurotransmission between striatonigral axons and SNR neurons. Using this method, the function of CB(1) cannabinoid receptors on terminals of striatonigral axons was unequivocally clarified. Activation of these receptors causes strong presynaptic inhibition of GABAergic neurotransmission between striatonigral axons and SNR neurons. This effect may be one explanation of the catalepsy observed in animals after cannabinoid administration. Endocannabinoids released from SNR neurons can modulate striatonigral neurotransmission by inhibiting GABA release from terminals of striatonigral axons.

Animals↗

PubMed1998

Inhibition of GABAergic inhibitory postsynaptic currents by cannabinoids in rat corpus striatum.

Electrophysiological consequences of activation of cannabinoid receptors have been mostly investigated on neuronal cell lines and on cells transfected with cannabinoid receptors. The aim of the present experiments was to study cannabinoid effects on identified neurons in situ. Electrically-evoked postsynaptic currents and voltage-dependent calcium currents were investigated in the principal neurons of the corpus striatum, the medium spiny neurons, with the patch-clamp method for brain slices. These neurons were chosen because they produce messenger RNA for cannabinoid receptors and because the density of cannabinoid binding sites in the striatum is high. Activation of muscarinic receptors by carbachol (10(-5) M) reduced inhibitory postsynaptic current amplitude by 67%. The synthetic cannabinoid receptor agonist R(+)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4- benzoxazin-yl]-(1-naphtalenyl)methanone (WIN55212-2; 10(-8) to 10(-5) M) dose-dependently reduced striatal inhibitory postsynaptic currents; the maximum effect, inhibition by 52%, was observed at 10(-6) M. Another cannabinoid agonist, (-)-cis-3-[2-hydroxy-4-(1,1-dimethylheptyl)phenyl]-trans-4-(3-hydr oxypropyl)cyclohexanol (CP55940; 10(-6) M), also reduced inhibitory postsynaptic currents, by 50%. The CB1 cannnabinoid receptor antagonist N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)4-methyl-3-pyra zolecarboxamide (SR141716A; 10(-6) M) had no effect when given alone but abolished the effect of WIN55212-2 (10(-6) M). WIN55212-2 (10(-6) M) did not change the current evoked by the GABA(A)-receptor agonist muscimol (10(-6) M). Activation of muscarinic receptors by carbachol (10(-5) M) inhibited voltage-dependent calcium currents by 21%, but the cannabinoid receptor agonist WIN55212-2 (10(-6) M) was without effect. The results show that activation of CB1 cannabinoid receptors reduces GABAergic inhibitory postsynaptic currents in medium spiny neurons of the corpus striatum: the likely mechanism is presynaptic inhibition of GABA release from terminals of recurrent axons of the medium spiny neurons themselves.

Animals↗

PubMed1997

Determination of tramadol in human plasma by capillary gas chromatography-mass spectrometry using solid-phase extraction.

An analytical method using solid-phase extraction, capillary gas chromatography and mass selective detection in the electron-impact ionization (EI) mode was developed for the determination of tramadol (2-[(dimethylamino)methyl]-1-(3-methoxyphenyl)cyclohexanol) in human plasma. The advantages of this method are the high sensitivity and selectivity and the linearity over the concentration range 2-500 ng/ml. Quantification was made using nefopam as an internal standard, and the detection limit was found to be 1 ng/ml. The standard deviations of the intra-day precision test ranged from 4.5 to 6.0% with respect to the concentration. Accuracy ranged from 1.0 to 4.0% (inter-day). The method was used for the determination of tramadol in a bioequivalence study.

Analgesics, Opioid↗

PubMed2001

Validation of an HPLC method for the quantification of ambroxol hydrochloride and benzoic acid in a syrup as pharmaceutical form stress test for stability evaluation.

A method is described for ambroxol, trans-4-(2-amino-3,5-dibromobenzylamino) cyclohexanol hydrochloride, and benzoic acid separation by HPLC with UV detection at 247 nm in a syrup as pharmaceutical presentation. Optimal conditions were: Column Symmetry Shield RPC8, 5 microm 250 x 4.6 mm, and methanol/(H(3)PO(4) 8.5 mM/triethylamine pH=2.8) 40:60 v/v. Validation was performed using standards and the pharmaceutical preparation which contains the compounds described above. Results from both standards and samples show suitable validation parameters. The pharmaceutical grade substances were tested by factors that could influence the chemical stability. These reaction mixtures were analysed to evaluate the capability of the method to separate degradation products. Degradation products did not interfere with the determination of the substances tested by the assay.

Ambroxol↗

PubMed1998

Determination of tramadol in various dosage forms by capillary isotachophoresis.

Cationic capillary isotachophoresis (ITP) with conductometric detection has been used for separating and determining milligram amounts of tramadol [2-dimethylaminomethyl-1-(3-methoxyphenyl)-cyclohexanol hydrochloride] (I) in seven commercial mass-produced pharmaceutical preparations. The optimised ITP electrolyte system consisted of 5 mM potassium picolinate + 5 mM picolinic acid (pH 5.25) as the leading electrolyte and 10 mM formic acid as the terminating electrolyte. The driving and detection currents were 50 microA (for 320 s) and 10 microA, respectively (a single analysis took 12-15 min). Under such conditions the effective mobility of I was determined as 24.26 x 10(-9) m2 V(-1) s(-1) (with tetraethylammonium ion as standard); thermodynamic pKa value of I was 9.44 +/- 0.03 (n = 8) as determined by UV spectrophotometry at 25 degrees C and I = 0.01 (NaCl). The calibration graph relating the ITP zone length to the concentration of I was rectilinear (r = 0.99997) in the range 15-180 mg l(-1) of I. The relative standard deviation (RSD) was 0.21% (n = 6) when determining 60 mg l(-1) of I in pure test solution. Sample pre-treatment of the dosage forms involved dilution or extraction of I with water (for suppositories the extraction was carried out in an ultrasonic bath at 40 degrees C for 10 min). The method was suitable for determining 50 or 100 mg ml(-1) of I in injections and drops, 50 mg of I in capsules, and 100 mg of I in suppositories with RSD values 0.4 to 1% (n = 6). According to the validation procedure based on the standard addition technique the recoveries were 97.2-100.1% of I.

Analgesics, Opioid↗

PubMed2002

Cardiotoxic interaction of metabolites from a prodrug segment cilexetil (cyclohexyloxy-carbonyloxy-ethyl) with digoxin in the canine failing heart.

Potential risks of cyclohexanol (CH) and cyclohexanediol (CHD) isomers, which are the metabolites derived from cilexetil ester side-chain of several prodrugs such as antibiotics (e.g. cefotiam hexetil) and an antihypertensive agent (candesartan cilexetil), were examined in beagles that were made congestive heart failure (CHF) by rapid ventricular pacing. The following three experiments tested the cardiac effects of i.v. doses of: (1) the metabolites alone, (2) the metabolites under the digoxin-induced bradycardia, and (3) the metabolites given concomitantly with digoxin (0.02 mg kg(-1)). Experiment 1: t-1,2- or 1,4-CHD alone (0.1-12 mg kg(-1)) exerted transient yet reproducible supraventricular or ventricular arrhythmia dose-dependently, whereas CH and 1,3-CHD at 12 mg kg(-1) showed no cardiac effect at all. Experiment 2: t-1,2-CHD (0.1-4 mg kg(-1)), but not CH or 1,3-CHD, induced the additive arrhythmia dose-dependently; t-1,2-CHD (12 mg kg(-1)) caused frequent premature supraventricular contractions and/or irreversible paroxysmal supraventricular tachycardia. Experiment 3: t-1,2-CHD, not CH or 1,3-CHD, caused fatal arrhythmia: one dog showed torsade de pointes followed by ventricular fibrillation, while another showed 3rd degree atrioventricular block and eventually cardiac arrest. In both Experiments 2 and 3, saline vehicle added onto digoxin never caused the irreversible, fatal arrhythmia. In a separate study using healthy dogs without CHF, none of these metabolites did produce cardiac effect. Given the potential risk of generating cardiotoxic metabolites from cilexetil-bearing prodrugs, the use of such prodrugs should be avoided from the patients with CHF, particularly from those who are receiving cardiac glycosides.

Animals↗

PubMed1998

Tramadol and its enantiomers differentially suppress c-fos-like immunoreactivity in rat brain and spinal cord following acute noxious stimulus.

Tramadol hydrochloride, (1RS,2RS)-2-[(dimethylamino)methyl]-1-(3-methoxyphenyl)-cyclohexanol hydrochloride, is an orally-active, centrally-acting analgesic with a putative dual mechanism of action, including an opioid and non-opioid component. The analgesic properties of tramadol and the possible co-existence of dual mechanisms has been postulated to be due to complementary and interactive pharmacologies of its enantiomers. We examined the ability of tramadol, its enantiomers, and morphine as reference to suppress c-fos-like immunoreactivity (c-fos-ir) in rat spinal cord and brain regions following a noxious stimulus (i.p. administration of 3.5% acetic acid). c-fos-ir was measured by immunocytochemistry and the stained cells in each region were counted 2 h after the acetic-acid injection (2:25 h after tramadol or morphine). Equi-analgesic doses of s.c. morphine (10 mg/kg) or tramadol (30 mg/kg) significantly suppressed c-fos-ir in all areas examined, except dorsal central gray of the spinal cord. The enantiomers of tramadol had distinctive patterns of suppression, neither one suppressed c-fos-ir in all of the regions, and hence neither one alone accounted for the suppression produced by the racemate. These findings support differential and complementary effects of tramadol enantiomers in sub-populations of spinal and supraspinal nociceptive neurons, consistent with the proposed antinociceptive interaction between the enantiomers.

Journal Article↗

PubMed2003

Preparation of porous cobalt and nickel oxides from corresponding alkoxides using a sonochemical technique and its application as a catalyst in the oxidation of hydrocarbons.

Porous nickel and cobalt oxides were prepared using their alkoxides as inorganic precursors. The stabilization of the mesostructure is especially critical for divalent elements such as Ni and Co, which do not form any network structure, like silicates. The lack of a network-forming multivalent bond is the probable reason why no stable mesoporous oxides have been synthesized for divalent elements yet. Here we have reported our attempt to synthesize porous oxides of Ni and Co. Octadecylamine has been used as the organic structure-directing agent. The product obtained was put under solvent extraction and calcination at various temperatures to remove the surfactant, followed by characterization using XRD, TEM and BET measurements. The FT/IR and thermal analyses (TGA and DSC) were also carried out for supporting information, such as extent of removal of surfactant from the pores of the metal oxide. A relatively better surface area has been obtained for the Co oxide, but in Ni the surface area found is not as good. A possible reason for that has been discussed. The porous (solvent extracted) cobalt oxide has been used as a catalyst in the oxidation reaction of cyclohexane in mild conditions. The catalyst has shown relatively better conversion of cyclohexane into cyclohexanone and cyclohexanol than the nanostructured cobalt oxide catalyst of regular structure.

Journal Article↗

PubMed2000

Sonochemical hydrosilylation of 2-substituted cyclohexanones in the presence of Wilkinson complex.

The sonochemical hydrosilylation of alkyl substituted cyclohexanones catalyzed by Rh (PPh3)3Cl is described. The application of ultrasonic irradiation during the reaction highly enhances the reaction rates and produces higher yields than those obtained in silent reactions. The stereoselectivity of the reaction has not been changed, the isomeric distribution, i.e. the cis/trans ratio of the 2-substituted cyclohexanols formed, is very close to those obtained in conventional stirred reactions.

Journal Article↗

PubMed2002

Designing membrane electrochemical reactors for oxidoreductase-catalysed synthesis.

The purpose of this work was to design an electrochemical reactor to enhance the high selectivity of enzyme-catalysed processes. In order to develop economically efficient syntheses, the enzymes must be confined in the strict vicinity of the electrode surface. Here the confinement was achieved with a dialysis membrane in a so-called Dialysis-Membrane Electrochemical Reactor (D-MER). Oxidation of glucose into gluconic acid catalysed by glucose oxidase was a first example. The ADH-catalysed reduction of cyclohexanone into cyclohexanol was also tested in a new type of MER. NADH was electrochemically regenerated thanks to mediator (methyl viologen or rhodium complex). The key point in developing electro-enzymatic process is to ensure the perfect fitting of the reactor design to the reactions that are to be processed.

Alcohol Dehydrogenase↗

PubMed2000

Chiral monolithic columns for enantioselective capillary electrochromatography prepared by copolymerization of a monomer with quinidine functionality. 1. Optimization of polymerization conditions, porous properties, and chemistry of the stationary phase.

Monolithic columns for chiral capillary electrochromatography have been prepared within the confines of untreated fused-silica capillaries in a single step by a simple copolymerization of mixtures of O-[2-(methacryloyloxy)ethylcarbamoyl]-10,11-dihydroquinidine , ethylene dimethacrylate, and glycidyl methacrylate or 2-hydroxyethyl methacrylate in the presence of mixture of cyclohexanol and 1-dodecanol as a porogenic solvent. The porous properties of the monolithic columns can easily be controlled through changes in the composition of the binary porogenic solvent. Although both thermal- and UV light-initiated polymerizations afford useful capillary columns, monoliths prepared using the former approach exhibit better chromatographic properties. The ability to control pore size independently of the polymerization mixture composition enables the preparation of monoliths with varying percentages of the chiral monomer and cross-linker, as well as the optimization of their separation properties. Very good separations of model racemate (R,S)-N-3,5-dinitrobenzoylleucine were achieved using an optimized monolithic CEC column, with high efficiencies of up to 74000 plates/m for the retained peaks.

Chromatography, Liquid↗

PubMed1994

Capillary electrophoresis with chiral selectors: optimization of separation and determination of thermodynamic parameters for binding of tioconazole enantiomers to cyclodextrins.

A systematic approach is outlined for optimization of enantiomeric separations in free solution capillary electrophoresis using chiral mobile-phase additives. Maximum electrophoretic mobility difference between the enantiomers occurs when the concentration of free selector is equal to the reciprocal of the average binding constant. General equations and data analysis methods are presented to relate mobilities to equilibrium constants in simple and competitive binding equilibria and used to determine thermodynamic parameters for host-guest complexation of tioconazole enantiomers with a range of cyclodextrin selectors. Selectivities are found to be in the reverse order of binding constants in the series dimethyl-beta-cyclodextrin (K1 = 6.9 x 10(3) M-1, alpha = 1.10) to hydroxypropyl-beta-cyclodextrin (K1 = 0.72 x 10(3) M-1, alpha = 1.29). For beta-cyclodextrin (K1 = 1.32 x 10(3)M-1, alpha = 1.20), delta H zero provides the dominant contribution to binding but delta delta H zero and T delta delta S zero terms give comparable contributions to the selectivity. Addition of alcohol does not affect the selectivity, but allows displacement of the optimum separation conditions to higher cyclodextrin concentration through either competitive binding (with cyclohexanol) or preferential solvation of reactants (with methanol).

Antifungal Agents↗

PubMed2001

Molecular sieve catalysts for the regioselective and shape- selective oxyfunctionalization of alkanes in air.

Framework-substituted, molecular-sieve, aluminophosphate, microporous solids are the centerpieces of a new approach to the aerobic oxyfunctionalization of saturated hydrocarbons. The sieves, and the few percent of the Al(III) sites within them that are replaced by catalytically active, transition-metal ions in high oxidation states (Co(III), Mn(III), Fe(III)), are designed so as to allow free access of oxygen in to and out of the interior of these high-area solids. Certain metal-substituted, molecular sieves permit only end-on approach of linear alkanes to the active centers, thereby favoring enhanced reactivity of the terminal methyl groups. By optimizing cage dimension, with respect to that of the hydrocarbon reactant, as well as adjusting the average separation of active centers within a cage, and by choosing the sieve with the appropriate pore aperture, highly selective conversions such as n-hexane to hexanoic acid or adipic acid, and cyclohexane to cyclohexanol, cyclohexanone, or adipic acid, may be effected at low temperature, heterogeneously in air.

Aerobiosis↗