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PubMed1994

Effects of diabetes on spontaneous locomotor activity in mice.

Spontaneous locomotor activity in diabetic mice was significantly greater than that in non-diabetic mice. Haloperidol and SCH23390, a selective dopamine D1-receptor antagonist, significantly reduced spontaneous locomotor activity in diabetic mice, but not in non-diabetic mice. Spontaneous locomotor activity in diabetic mice was also reduced by pretreatment with naltrindole, a selective delta-opioid receptor antagonist, and 7-benzylidenenaltrexone, a selective delta1-opioid receptor antagonist. The rate of dopamine turnover in the limbic forebrain in diabetic mice was significantly higher than that in non-diabetic mice. These findings suggest that the enhanced spontaneous locomotor activity in diabetic mice may result from increased dopamine neurotransmission, which might be due to an increase in dopamine release in mesolimbic dopamine systems. The increased dopamine neurotransmission in diabetic mice may also be due to the up-regulation of delta-opioid receptor-mediated functions.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

A novel nicotinic agonist facilitates induction of long-term potentiation in the rat hippocampus.

Long-term potentiation (LTP) can be modulated by a number of neurotransmitter receptors including muscarinic and GABAergic receptor types. We have found that a novel nicotinic agonist, 2,4-dimethoxybenzylidene anabaseine (DMXB), facilitated the induction of LTP in the hippocampus in a dose-dependent and mecamylamine-sensitive manner. DMXB displaced high affinity nicotinic [125I]alpha-bungarotoxin and [3H]acetylcholine binding in rat brain. Xenopus oocyte studies demonstrated that DMXB has agonist activity at alpha 7 but not alpha 4/beta 2 nicotinic receptor subtypes. These results indicated that DMXB is a novel nicotinic agonist with apparent specificity for the alpha 7/alpha-bungarotoxin nicotinic receptor subtype and indicate that nicotinic receptor activation is capable of modulating the induction of long-term potentiation.

Acetylcholine↗
PubMed1994

Thin-layer chromatography and mass spectrometry of pentafluorobenzylidene derivatives of members of the phthiocerol family from Mycobacterium tuberculosis and Mycobacterium marinum.

The difference in relative stereochemistry of the 1.3-diol unit of mycobacterial phthiocerols can be determined by simple thin-layer chromatographic analysis of pentafluorobenzylidene acetal derivatives. The threo phthiocerol acetals from Mycobacterium tuberculosis are composed of equal amounts of two axial-equatorial stereoisomers but the erythro phthiocerols from Mycobacterium marinum form only one acetal with diequatorial substituents. The two acetals formed from a threo phthiocerol can be separated by thin-layer chromatography and mass spectra of the two stereoisomers allowed assignment of their structures.

Acetals↗
PubMed1986

Iodine-131-labeled diphosphonates for the palliative treatment of bone metastases--III. Considerations of interaction, binding and absorbed dose.

General considerations about the possible mechanisms of action of rather low dose ionizing radiation with bone metastases and stimulated nerve fibers reveal that only minute amounts of chemicals are produced by direct interaction of energetic electrons. Thus changes of the chemical milieu due to direct interaction must be ruled out in favour of a radiation-induced trigger reaction which may then initiate a cascade of cellular responses. Organ distribution studies of a series of radioiodinated benzylidenediphosphonates with H-, HO- and H2N- in the alpha- and p-position revealed best results for pHO-NH2 (BDP3). The microscopic distribution of 131I-DBP3 in bone tissue was monitored by autoradiography. Elevated uptake in normal (tibia) and neoplastic bone (experimental osteosarcoma) corresponded with the degree of vascularization and formation of new hydroxylapatite. Unlike the uptake in human osteoblastic bone metastases the experimental osteosarcoma of SD-rats accumulated 131I-BDP3 less than normal bone. This was due to the short volume doubling time, the delay of hydroxyl-apatite deposition and the formation of necroses. Theoretical replacement of 131I in iodinated BDP3 with radioisotopes emitting higher energy electrons yielded best bone metastasis/organ ratios for 32P labeled BDP3. The bone metastasis/bone marrow dose ratio by comparison with 131I labeled BDP3 is, however, almost equal. The isotopes 130I and 133I are not suited to the achievement of higher tumor/background doses although they are higher energy beta- -emitters than 131I. Because of their short physical half life and absence of different kinetics in normal and neoplastic bone no dose enhancement in bone metastases can be attained.

Animals↗
PubMed1987

131I labeled diphosphonates for the palliative treatment of bone metastases--IV. Syntheses of benzylidenediphosphonates and their organ distribution in rats.

Palliative treatment of bone pain induced by disseminated bone metastases can be performed with osteotropic, beta(-)-emitting radionuclides. Newly developed 131I labeled benzylidenediphosphonic acid (BDP) derivatives show osteotropic characteristics which suggest that they might possibly be useful radiopharmaceuticals for that purpose. Six BDP derivatives were synthesized with H, OH or NH2 in the 4- and alpha-position. Syntheses were performed by the formal addition of 2 mol of phosphorous acid in the presence of PBr3 to 1 mol of the respective benzonitrile. Transformation of the 4-methoxy and 4-nitro substituents, which were stable during the diphosphonate formation, to 4-HO and 4-NH2 was achieved by hydrolytic ether cleavage in boiling HBr and catalytic hydrogenation with Pd/C, respectively. Transformation of the alpha-amino to alpha-hydroxy group was achieved by the action of NaNO2 in HCl. 4-Hydroxybenzylidenediphosphonic acid (9) was formed unexpectedly during the reaction of 4-hydroxybenzoic acid with H3PO3/PBr3. The addition of 2 mol of phosphorous acid to the benzoic acid was accompanied by an additional reduction at the alpha-carbon. The new BDP derivatives were analyzed by HPLC, NMR and elemental analysis. After labeling with 131I the BDP derivatives were tested in female Sprague-Dawley rats to obtain organ uptake and kinetic data. The various substituents showed an influence on the bone affinity and the uptake in other organs. Among the BDP derivatives tested alpha-amino-(3-[131I]iodo-4-hydroxybenzylidene)diphosphonate (4a) showed the best biological characteristics.

Animals↗
PubMed2003

Alpha 7 nicotinic acetylcholine receptor-mediated protection against ethanol-induced neurotoxicity.

The alpha(7)-selective nicotinic partial agonist 3-[2,4-dimethoxybenzylidene]anabaseine (DMXB) was examined for its ability to modulate ethanol-induced neurotoxicity in primary cultures of rat neurons. Primary cultures of hippocampal neurons were established from Long-Evans, embryonic day (E)-18 rat fetuses and maintained for 7 days. Ethanol (0-150 mM), DMXB (0-56 microM), or both were subsequently co-applied to cultures. Ethanol was added two additional times to the cultures to compensate for evaporation. After 5 days, neuronal viability was assessed with the MTT cell proliferation assay. Results demonstrated that ethanol reduces neuronal viability in a concentration-dependent fashion and that DMXB protects against this ethanol-induced neurotoxicity, also in a concentration-dependent fashion. These results support the suggestion that nicotinic partial agonists may be useful in treating binge drinking-induced neurotoxicity and may provide clues as to why heavy drinkers are usually smokers.

Animals↗
PubMed2004

Design of hypoxia-targeting protein tyrosine kinase inhibitor using an innovative pharmacophore 2-methylene-4-cyclopentene-1,3-dione.

We review in this report our strategy and tactics for the design of 2-hydroxyarylidene-4-cyclopentene-1,3-diones as protein tyrosine kinase (PTK) inhibitors having low mitochondrial toxicities and/or hypoxia-targeting function. We based our synthetic design on an innovative pharmacophore, 2-methylene-4-cyclopentene-1,3-dione. We first showed the effectiveness of this pharmacophore in the development of 2-methylene-4-cyclopentene-1,3-dione as PTK inhibitor that have lower mitochondrial toxicity than the potent PTK inhibitor tyrphostin AG17. Our results show that the cyclopentenedione-derived TX-1123 is a more potent antitumor tyrphostin and also shows lower mitochondrial toxicity than the malononitrile-derived AG17. The O-methylation product of TX-1123 (TX-1925) retained its tyrphostin-like properties, including mitochondrial toxicity and antitumor activities. However, the methylation product of AG17 (TX-1927) retained its tyrphostin-like antitumor activities, but lost its mitochondrial toxicity. Our comprehensive evaluation of these agents with respect to PTK inhibition, mitochondrial inhibition, antitumor activity, and hepatotoxicity demonstrates that PTK inhibitors TX-1123 and TX-1925 are more promising candidates for antitumor agents than tyrphostin AG17. Secondly, as a further investigation of the promising power of this 4-cyclopentene-1,3-dione as an innovative pharmacophore, we discuss our strategy of development of hypoxia-targeting PTK inhibitor TX-1123 analogues, 2-nitroimidazole-aminomethylenecyclopentenediones, such as TX-2036, for cancer treatment, especially for pancreatic cancers, which have a high level of hypoxia.

Animals↗
PubMed2005

Theoretical studies of Alzheimer's disease drug candidate 3-[(2,4-dimethoxy)benzylidene]-anabaseine (GTS-21) and its derivatives.

Theoretical and molecular modeling studies have been conducted for understanding the details of how 3-[(2,4-dimethoxy)benzylidene]-anabaseine dihydrochloride (GTS-21) and its metabolism derivatives bind with the receptor of alpha7 nicotinic acetylcholine dimer. Good accordance with experimental results has been achieved. It was found that the van der Waals repulsion makes the dominant contribution to the binding energy. GTS-21 and its metabolites are apparently too large for the binding sites of the alpha7 dimer. To improve the effectiveness of the drug, a possible approach is to reduce its volume while maintaining the presence of the active groups. Our studies, in combination with experimental studies, will lead to a promising basis for practical drug design against Alzheimer's disease.

Alzheimer Disease↗
PubMed2004

Remote preconditioning by infrarenal aortic occlusion is operative via delta1-opioid receptors and free radicals in vivo in the rat heart.

BACKGROUND: Ischemic preconditioning (PC) is a powerful mechanism in reducing infarct size of the heart. Protection can be performed either by an ischemic stimulus of the heart itself or by ischemia of an organ distant to the heart (remote PC). We have previously shown that remote PC by infrarenal occlusion of the aorta [IOA] in the rat is as powerful as classical ischemic PC. This protection may be transmitted by humoral factors, and protein kinase C is a mediator in the signal transduction mechanism. Focus of the present study was to address the question whether remote preconditioning is dependent on the activation of the delta1-opioid receptor and/or free radicals, the infarct size was determined after either inhibition of the delta1-opioid receptor or scavenging free radicals. METHODS AND RESULTS: IOA was performed in rats by occlusion of the infrarenal aorta for 15 min followed by a 10-min reperfusion period. Infarction of the heart was induced by 30 min regional ischemia followed by 30 min of reperfusion. The area of infarct was determined by propidium iodide and the risk zone was demarcated by zinc cadmium sulfide fluorescent particles. Control hearts (30 min regional ischemia of the heart followed by 30 min of reperfusion; no IOA) had an infarct size of 54 +/- 3%, whereas classical preconditioning by three ischemia/reperfusion [I/R] cycles, 5 min each, reduced it to 12 +/- 1% of the risk zone (p<0.05). Fifteen minutes IOA with 10 min of reperfusion was highly protective and reduced the infarct size to 20 +/- 5% (p<0.05 vs. control). Inhibition of the delta1-opioid receptors by 7-benzylidenenaltrexone [BNTX] blocked the protection obtained by PC and IOA (41 +/- 4% and 44 +/- 2%, respectively; p<0.05 vs. the group without BNTX). BNTX in control hearts had no influence on infarct size (52 +/- 2%). Inhibition of endogenously released radicals by N-2-mercaptopropionyl glycine [MPG] blocked the infarct size reduction of IOA (46 +/- 3%; p<0.05 vs. IOA), but had no influence on the protection in classically preconditioned hearts protected by three cycles I/R (13 +/- 4%). Only if the number of the preconditioning stimuli was reduced to one was MPG able to overcome the protection (43 +/- 4%, p<0.05 vs. PC with one I/R cycle (21 +/- 4%)). CONCLUSION: Remote preconditioning using IOA protects the rat heart from infarction. Classical and remote PC share both the delta1-opioid-receptor and free radicals as common elements in their signal transduction pathways. MPG can block protection from IOA and from one, but not from three, classical preconditioning cycles. This indicates that the protection by remote preconditioning is comparable to classical PC with one I/R cycle.

Animals↗
PubMed2006

On the regioselectivity of the Hanessian-Hullar reaction in 4,6-O-benzylidene protected galactopyranosides.

The N-bromosuccinimide mediated fragmentation of methyl 4,6-O-benzylidene-beta-D-galactopyranoside results in the formation of methyl 4-O-benzoyl-6-bromo-6-deoxy-beta-D-galactopyranoside and methyl 4-O-benzoyl-3-bromo-3-deoxy-beta-D-gulopyranoside, as opposed to the methyl 6-O-benzoyl-3-bromo-3-deoxy-beta-D-gulopyranoside originally reported. The kinetic methyl 4-O-benzoyl-6-bromo-6-deoxy-beta-D-galactopyranoside rearranges to the thermodynamic methyl 4-O-benzoyl-3-bromo-3-deoxy-beta-D-gulopyranoside under the reaction conditions, likely via a 3,6-anhydro galactopyranoside. The NBS-mediated cleavage of 4,6-O-benzylidene acetals in the galactopyranoside series is therefore shown to conform to the regiochemistry observed in the corresponding gluco- and mannopyranoside series with preferential cleavage of the C6-O6 bond by an ionic mechanism.

Benzylidene Compounds↗
PubMed2004

Deltorphin II enhances extracellular levels of dopamine in the nucleus accumbens via opioid receptor-independent mechanisms.

The effects of the delta2-opioid receptor agonist, deltorphin II, on extracellular levels of dopamine in the rat nucleus accumbens were investigated in awake animals by in vivo brain microdialysis. In agreement with previous studies, perfusion of deltorphin II (50.0 nmol) into the nucleus accumbens significantly increased the extracellular amount of accumbal dopamine. The effect of deltorphin II (50.0 nmol) was not altered by the selective delta2-opioid receptor antagonist, naltriben (1.5 nmol), which alone did not significantly affect the basal levels of dopamine. Selective antagonists of neither the mu-opioid receptors, D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Phe-Thr-NH2 (0.15 nmol), nor the delta1-opioid receptors, (E)-7-benzylidenenaltrexone tartrate (0.15 nmol), failed to significantly alter the effects of deltorphin II. The nonselective opioid receptor antagonist, naloxone (0.75 and 1.5 nmol), which alone did not significantly affect the basal levels of dopamine, also failed to affect the effects of deltorphin II. Moreover, under the condition that the sodium channel blocker, tetrodotoxin (0.1 nmol), was perfused continuously into the nucleus accumbens, the deltorphin II-induced increase in extracellular levels of dopamine was reduced by 72%. These results suggest that deltorphin II enhances extracellular dopamine in the nucleus accumbens via opioid receptor-independent, tetrodotoxin-sensitive mechanisms.

Analysis of Variance↗
PubMed2005

Septal innervation regulates the function of alpha7 nicotinic receptors in CA1 hippocampal interneurons.

The hippocampus receives substantial input from the medial septum/diagonal band of broca (MS/DB) via the fibria-fornix (FF). Projections from the MS/DB innervate hippocampal interneurons that express alpha7 nicotinic receptors and regulate excitation in principal cell populations. In the present report we used stereotaxic surgery, whole-cell patch clamping, and immunohistochemical techniques to evaluate the effects of FF and MS/DB lesions on alpha7 nicotinic receptors in stratum radiatum interneurons. Focal somatic application of ACh (1 mM) evoked methyllycaconitine (MLA)-sensitive currents that were markedly reduced following aspirative lesions of the FF. Reductions in current amplitudes were prevented or restored to levels not significantly different from controls following in vivo treatment with the alpha7-selective agonist GTS-21, and GTS-21 treatment did not change current amplitudes measured in tissue from unlesioned animals. MS/DB injections of the selective cholinergic neurotoxin 192 IgG-saporin did not affect alpha7 receptor currents, although MS/DB ChAT and hippocampal AChE immunolabeling were significantly reduced. In contrast, kainic acid lesions of the MS/DB, potentially more selective for GABAergic projection neurons, produced significant reductions in current amplitudes. These findings are the first to show functional changes in alpha7 receptors following hippocampal denervation and suggest that MS/DB hippocampal innervation regulates functional aspects of hippocampal alpha7 receptors. The results confirm hippocampal alpha7 nicotinic receptors as viable therapeutic targets in diseases that involve degradation of the septohippocampal pathway and may indicate that GABAergic MS/DB hippocampal input plays a more substantial role in the regulation of alpha7 nicotinic receptor function than MS/DB hippocampal cholinergic input.

Acetyl-CoA C-Acetyltransferase↗
PubMed2006

Synthesis, characterization, and sorption properties of silica gel-immobilized pyrimidine derivative.

5-Benzylidene-2-thiobarbituric acid (BzTBA), a pyrimidine derivative, was used to modify the surface of silica gel-chloropropyltrimethoxysilane (Si-Cl) via chemical immobilization to produce a new pyrimidine silica phase (Si-BzTBA). Identification of the surface modification was characterized and performed on the basis of infrared as well as elemental analysis. Thermal desorption method was found to give 0.129-0.143 mmol g(-1) as surface coverage values. Metal sorption properties of Si-BzTBA were also studied and the evaluated results refer to the high metal sorption of Si-BzTBA for copper(II), mercury(II), cadmium(II), and lead(II) with the same order. These four Si-BzTBA-metal complexes were also synthesized and the stoichiometric ratios were identified as 1:1 except lead complex was found to give a 1:2 ratio. Electron impact-mass spectrometric analysis (EI-MS) with 70 eV ionization energy was used as a potential thermal method for the confirmation of surface modification of Si-BzTBA and its metal complexes based on fragmentation elucidation of thermally desorbed ion peaks. The EI-MS of Si-BzTBA was found to show several characteristic fragment ion peaks that are directly related to the chemical binding of BzTBA to SiCl phase. Differential scanning calorimetry study (DSC) was also performed to evaluate the various kinetic and thermodynamic parameters of thermal degradation processes and have been enumerated. The results of EI-MS and DSC are very similar in many respects.

Adsorption↗
PubMed2005

delta-Opioid receptor agonist SNC80 elicits peripheral antinociception via delta(1) and delta(2) receptors and activation of the l-arginine/nitric oxide/cyclic GMP pathway.

In this study, we characterized the role of delta(1) and delta(2) opioids receptors, as well the involvement of the l-arginine/NO/cGMP pathway in the peripheral antinociception induced by delta-opioid receptor agonist (+)-4-[(alphaR)-alpha-((2S,5R)-4-Allyl-2,5-dimethyl-1-piperazinyl)-3-methoxybenzyl]-N,N-diethylbenzamide (SNC80). The paw pressure test was utilized, in which pain sensitivity is increased by intraplantar injection of prostaglandin E(2) (2 microg). Administration of SNC80 (20, 40 and 80 microg/paw) decreased the hyperalgesia induced by prostaglandin E(2) in a dose-dependent manner. The possibility that the higher dose of SNC80 (80 microg) has a central or systemic effect was excluded, since administration of the drug into the contralateral paw did not elicit antinociception in the right paw. 7-Benzylidenenaltrexone (BNTX), 5, 10 and 20 microg/paw, and 17-(Cyclopropylmethyl)-6,7-didehydro-3,14beta-dihydroxy-4,5alpha-epoxy-6,7-2',3'-benzo[b]furanomorphinan (naltriben), 2.5, 5 and 10 microg/paw, delta(1) and delta(2) opioid receptor antagonist respectively, elicited partial antagonism of the peripheral antinociceptive effect of the SNC80 (80 microg). The BNTX (10 microg/paw)-naltriben (5 microg/paw) combination completely antagonized the peripheral antinociception induced by SNC80 (80 microg). Further, blockers of the l-arginine/NO/cGMP pathway, N(G)-nitro-l-arginine (12, 18 and 24 microg/paw) and methylene blue (125, 250 and 500 microg/paw) were observed reverting the peripheral antinociceptive effect of SNC80. This study provides evidence that the peripheral antinociception induced by SNC80 occurs via delta(1) and delta(2) receptors and may result from l-arginine/NO/cGMP pathway activation.

Analgesics↗
PubMed2026

Long-term safety and efficacy of ponesimod, an oral S1P1 receptor modulator, in relapsing-remitting multiple sclerosis (RRMS): Results from randomized phase 2b core and extension studies spanning up to 13 years.

BACKGROUND: Ponesimod demonstrated efficacy and safety in relapsing-remitting multiple sclerosis (RRMS) in 24-week phase-2 core study, further confirmed by an interim combined analysis of the core and open-label long-term extension (LTE) studies (NCT01093326; up to 8 years). Current study evaluated safety and efficacy of ponesimod using combined core and LTE studies data for up to 13 years. METHODS: Of 393 participants completing the core study, 353 (90%) entered LTE, having 3 treatment periods (TP). In TP1 (&#x223c;1.85 years), participants continued core treatment (ponesimod: 10, 20, or 40&#x202f;mg QD) whereas placebo-treated participants were re-randomized (1:1:1) to respective ponesimod doses. In TP2 (TP2 and TP3 combined duration: &#x223c;10.4 years), participants on 40&#x202f;mg were re-randomized (1:1) to 10/20&#x202f;mg, while others continued same dose; in TP3 all participants received 20&#x202f;mg. Study outcomes included safety and efficacy (ARR, time-to 24-week confirmed-disability-accumulation [24-week CDA], total T1-weighted Gadolinium-enhanced (T1 Gd+) lesions, new/enlarging T2 lesions and Combined Unique Active Lesions [CUALs]). RESULTS: For 20&#x202f;mg dose, total 92.4% participants experienced &#x2265;1 TEAEs (73.1% mild/moderate severity) and 19 (13%) participants discontinued study. Mean (95% CI) ARR=0.14 (0.10-0.20); Kaplan-Meier estimate (95% CI) of confirmed relapse and 24-week CDA=52.5% (42.3-63.5) and 31.3% (22.6-42.3). Mean [SD] T1 Gd+ lesions decreased from ponesimod baseline (2.62 [7.06]) to 12.4 years (0.26 [1.48]), mean (95% CI) CUALs per participant/year=3.97 (2.75-5.73). CONCLUSION: Ponesimod treatment for up to 13 years was not associated with new safety concerns. Participants continued to experience low levels of disease activity consistently across clinical and MRI outcomes.

Humans↗
PubMed2005

alpha7 Nicotinic acetylcholine receptor as a target to rescue deficit in hippocampal LTP induction in beta-amyloid infused rats.

Continuous intracerebroventricular infusion of beta-amyloid peptide 1-40 (Abeta(1-40)) in animal models induces learning and memory impairment associated with dysfunction of the cholinergic neuronal system, which has been considered to be a pathological model of Alzheimer's disease [Nitta, A., Itoh, A., Hasegawa, T., Nabeshima, T., 1994. Beta-amyloid protein-induced Alzheimer's disease animal model. Neurosci. Lett. 170, 63-66.]. Here, using a real-time optical recording technique, we demonstrate that basal synaptic transmission and several forms of synaptic plasticity, including long-term potentiation (LTP), post-tetanic potentiation (PTP) and paired-pulse facilitation (PPF) are deficient at the Schaffer collateral-CA1 synapse in hippocampal slices from Abeta-infused brain. Throughout this study, an effort was made to address whether the alpha7 nicotinic acetylcholine receptor (alpha7nAChR), which is believed to be a primary target of Abeta [Wang, H.Y., Lee, D.H., Davis, C.B., Shank, R.P., 2000a. Amyloid peptide Abeta (1-42) binds selectively and with picomolar affinity to alpha 7 nicotinic acetylcholine receptors. J. Neurochem. 75, 1155-1161.], is responsible for the deficits in synaptic plasticity observed in the Abeta-infused rats. First, we found that Abeta-infusion markedly depressed the response of alpha7nAChR to a selective alpha7nAChR agonist [3-(2,4-dimethoxybenzylidene)-anabaseine] (DMXB). Second, blockade of alpha7nAChR with either methyllycaconitine (MLA) or alpha-bungarotoxin (alpha-BTX) in control rats inhibited LTP induction, suggesting that the activation of alpha7nAChR is required for LTP induction. Finally, pre-treatment of the slices from Abeta-infused rats with 10 microM DMXB rescued CA1 synapses from the deficit in LTP and PPF. These results suggest that Abeta-impaired LTP and PPF arise as a consequence of dysfunctional alpha7nAChR, and that alpha7nAChR may be an important target to help ameliorate AD patient cognitive deficits.

Amyloid beta-Peptides↗