Academic literature on the topic 'Nicotinic partial agonist'
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Journal articles on the topic "Nicotinic partial agonist"
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Gonzalez-Gutierrez, Juan Pablo, Martin Hodar, Franco Viscarra, Pablo Paillali, Nicolás Guerra-Díaz, Hernán Pessoa-Mahana, Juan José Hernández-Morantes, et al. "Minimal Structural Changes Determine Full and Partial Nicotinic Receptor Agonist Activity for Nicotine Analogues." Molecules 24, no. 15 (July 24, 2019): 2684. http://dx.doi.org/10.3390/molecules24152684.
Full textAbstract:
Neuronal α4β2 nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels (LGIC) that have been implicated in nicotine addiction, reward, cognition, pain disorders, anxiety, and depression. Nicotine has been widely used as a template for the synthesis of ligands that prefer α4β2 nAChRs subtypes. The most important therapeutic use for α4β2 nAChRs is as replacement therapy for smoking cessation and withdrawal and the most successful therapeutic ligands are partial agonists. In this case, we use the N-methylpyrrolidine moiety of nicotine to design and synthesize new α4β2 nicotinic derivatives, coupling the pyrrolidine moiety to an aromatic group by introducing an ether-bonded functionality. Meta-substituted phenolic derivatives were used for these goals. Radioligand binding assays were performed on clonal cell lines of hα4β2 nAChR and two electrode voltage-clamp experiments were used for functional assays. Molecular docking was performed in the open state of the nAChR in order to rationalize the agonist activity shown by our compounds.
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Hussy, N., M. Ballivet, and D. Bertrand. "Agonist and antagonist effects of nicotine on chick neuronal nicotinic receptors are defined by alpha and beta subunits." Journal of Neurophysiology 72, no. 3 (September 1, 1994): 1317–26. http://dx.doi.org/10.1152/jn.1994.72.3.1317.
Full textAbstract:
1. Functional neuronal nicotinic receptors were reconstituted in Xenopus oocytes by the nuclear injection of different combinations of chick and rat cDNAs encoding alpha and beta subunits. The pharmacology of these nicotinic receptors was investigated using two-electrode voltage clamp. 2. The sensitivity of the chick alpha 3/beta 2, alpha 3/beta 4, and alpha 4/beta 2 receptors to acetylcholine (ACh) and neuronal bungarotoxin differed markedly, indicating that both subunits contribute to the pharmacological properties of the receptors. 3. Nicotine acted as an agonist on the chick alpha 3/beta 4 and alpha 4/beta 2 receptors and rat alpha 3/beta 2 receptor. In contrast, nicotine (at concentrations > 3 microM) was only a weak partial agonist of the chick alpha 3/beta 2 receptor. Moreover, nicotine coapplied with 3 microM ACh on the chick alpha 3/beta 2 receptor acted as a potent competitive antagonist, with an IC50 of 0.43 microM. No antagonist effect of nicotine could be revealed on the other nicotinic receptors. 4. The effect of nicotine was tested on hybrid receptors obtained by coinjection of chick and rat cDNAs encoding the alpha 3 and beta 2 subunits (yielding the rat alpha 3/chick beta 2 and chick alpha 3/rat beta 2 receptors). Nicotine (10 microM) strongly inhibited both hybrid receptors. 5. Chimeric subunits were constructed by exchanging a segment located in the extracellular N-termini of chick alpha 3 and alpha 4 subunits and chick alpha 3 and rat alpha 3 subunits. These subunits were coexpressed in oocytes with chick or rat beta 2 subunits. The effect of nicotine on these receptors pointed to the importance of a 15 amino acid stretch located 3' of the first transmembrane segment in the determination of the agonist and antagonist action of nicotine. 6. Within this 15 amino acid segment, a single residue differs in chick and rat alpha 3 subunits, at position 198, within the ligand binding site of alpha subunits. Gln198 of the rat alpha 3 subunit was replaced by Thr as found in the chick alpha 3 subunit, using site-directed mutagenesis. The mutant subunit was coexpressed with the rat beta 2 subunit, yielding receptors which were inhibited by nicotine. 7. It is concluded that both alpha and beta subunits not only alter considerably the sensitivity of the nicotinic receptor to agonists and antagonists, but also can turn an agonist into a potent antagonist of one receptor subtype.(ABSTRACT TRUNCATED AT 400 WORDS)
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Jamali, Qutub. "Galantamine as a Treatment Option for Nicotine Addiction." Journal of Smoking Cessation 2021 (July 17, 2021): 1–3. http://dx.doi.org/10.1155/2021/9975811.
Full textAbstract:
The pharmacological therapy for smoking cessation recommended by National Institute for Health and care Excellence (NICE) guidelines is nicotine replacement therapy such as gum, inhalator, lozenge, nasal spray, oral spray, sublingual tablet, and transdermal patch. Medications such as bupropion and varenicline are also used. Varenicline is the only established drug used to alleviate symptoms of craving as it acts as a partial nicotine agonist. Galantamine has a similar mechanism of action where it is an acetylcholinesterase inhibitor and nicotinic receptor agonist. However, varenicline is the only recommended drug. There are not many studies to illustrate the effectiveness of galantamine for smoking cessation. This article explores the possibility of potential use of galantamine in alleviating the symptoms of nicotine withdrawal.
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Jancin, Bruce. "Selective Nicotinic Receptor Partial Agonist May Be Cessation Advance." Family Practice News 35, no. 13 (July 2005): 34. http://dx.doi.org/10.1016/s0300-7073(05)70953-1.
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Potasiewicz, Agnieszka, Joanna Golebiowska, Piotr Popik, and Agnieszka Nikiforuk. "Procognitive effects of varenicline in the animal model of schizophrenia depend on α4β2- and α7-nicotinic acetylcholine receptors." Journal of Psychopharmacology 33, no. 1 (December 3, 2018): 62–73. http://dx.doi.org/10.1177/0269881118812097.
Full textAbstract:
Background: Varenicline, a partial agonist of the α4β2 nicotinic acetylcholine receptor (α4β2-nAChR), is currently used to facilitate smoking cessation. Preclinical and clinical studies have suggested that this compound may also be effective in treating cognitive impairments in schizophrenia. However, it is unclear which nicotinic acetylcholine receptor subtypes may be involved because varenicline is not only a partial agonist for α4β2-nAChRs but also a full agonist for α7 nicotinic acetylcholine receptors (α7-nAChRs). Aim: We investigated the effects of varenicline, compared to the α4β2-nAChR partial agonist TC-2403 and the α7-nAChR full agonist PNU-282987, in a ketamine-based model of schizophrenia-like cognitive deficits on the attentional set-shifting task in rats. The second goal was to elucidate whether the procognitive efficacy of varenicline was due to the compound’s action on α4β2-nAChRs or α7-nAChRs. Methods: Ketamine was administered to rats for 10 consecutive days and the test was performed 14 days following the last injection. The tested compounds were administered 30 min prior to the attentional set-shifting task. Results: Varenicline, TC-2403 and PNU-282987 ameliorated ketamine-evoked set-shifting deficits. While the α4β2-nAChR antagonist dihydro-β-erythroidine and the α7-nAChR antagonist methyllycaconitine completely prevented the procognitive actions of TC-2403 and PNU-282987, respectively, varenicline’s effect was only partially blocked by any given antagonist. Moreover, the combined treatment with TC-2403 and PNU-282987 more effectively facilitated rats’ set-shifting ability than activation of either type of nicotinic acetylcholine receptor alone. Conclusion: The present findings demonstrated that varenicline’s actions on both α7-nAChRs and α4β2-nAChRs may be necessary to produce its full procognitive effect in the present experimental setting.
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McCaul, Mary E., Gary S. Wand, Hiroto Kuwabara, Robert F. Dannals, Dean Wong, and Xiaoqiang Xu. "The Relationship of Varenicline Agonism of α4β2 Nicotinic Acetylcholine Receptors and Nicotine-Induced Dopamine Release in Nicotine-Dependent Humans." Nicotine & Tobacco Research 22, no. 6 (May 16, 2019): 892–99. http://dx.doi.org/10.1093/ntr/ntz080.
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Abstract Introduction Cigarette smoking continues to be one of the most important behavioral causes of morbidity and mortality in the world. Varenicline, an α4β2 nicotinic acetylcholine receptor (nAChR) partial agonist, has been shown to increase smoking quit rates compared with nicotine-based products. This human laboratory, double-blind, placebo-controlled study examined varenicline and placebo effects on α4β2-nAChRs occupancy, nicotine-induced change in [11C]raclopride non-displaceable binding potential (BPND), and behavioral measures of cigarette smoking, nicotine craving, and withdrawal. Methods Current nicotine dependent daily smokers (N = 17) were randomized to varenicline 1 mg twice daily or placebo for 13 days. Using positron emission tomography), we characterized α4β2-nAChRs occupancy using [18F]AZAN and dopamine receptor binding using [11C]raclopride as well as behavioral measures of cigarettes smoked, craving, and nicotine withdrawal. Results Varenicline compared with placebo resulted in significant reductions in [18F]AZAN BPND in multiple brain regions including thalamus, midbrain, putamen, and ventral striatum. Following administration of a controlled-dose nicotine cigarette, dopamine release was significantly suppressed in the ventral striatum in the varenicline-treated compared with the placebo group. There was a significant relationship between α4β2-nAChRs BPND measured in thalamus during the [18F]AZAN scan and nicotine-induced change in raclopride BPND in the ventral striatum. Conclusion This is the first human study to demonstrate a direct relationship between the extent of varenicline occupancy of α4β2-nAChRs and the magnitude of dopamine release following nicotine use. Implications It has remained unclear how nicotinic receptor blockade through partial agonist medications such as varenicline promotes smoking cessation. One hypothesized mechanism is downstream dampening of the mesolimbic reward dopamine system. For the first time in human smokers, we observed a direct relationship between the extent of varenicline blockade of α4β2-nACh nicotinic receptors and the magnitude of dopamine release following smoking. This has mechanistic and therapeutic implications for improving smoking cessation interventions.
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Akinola, Lois S., Deniz Bagdas, Yasmin Alkhlaif, Asti Jackson, Cenk O. Gurdap, Elnaz Rahimpour, F. Ivy Carroll, Roger L. Papke, and M. Imad Damaj. "Pharmacological characterization of 5-iodo-A-85380, a β2-selective nicotinic receptor agonist, in mice." Journal of Psychopharmacology 36, no. 11 (November 2022): 1280–93. http://dx.doi.org/10.1177/02698811221132214.
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Background: Because of their implications in several pathological conditions, α4β2* nicotinic acetylcholine receptors (nAChRs) are potential targets for the treatment of nicotine dependence, pain, and many psychiatric and neurodegenerative diseases. However, they exist in various subtypes, and finding selective tools to investigate them has proved challenging. The nicotinic receptor agonist, 5-iodo-A-85380 (5IA), has helped in delineating the function of β2-containing subtypes in vitro; however, much is still unknown about its behavioral effects. Furthermore, its effectiveness on α6-containing subtypes is limited. Aims: To investigate the effects of 5IA on nociception (formalin, hot-plate, and tail-flick tests), locomotion, hypothermia, and conditioned reward after acute and repeated administration, and to examine the potential role of β2 and α6 nAChR subunits in these effects. Lastly, its selectivity for expressed low sensitivity (LS) and high sensitivity (HS) α4β2 receptors is investigated. Results: 5IA dose-dependently induced hypothermia, locomotion suppression, conditioned place preference, and antinociception (only in the formalin test but not in the hot-plate or tail-flick tests). Furthermore, these effects were mediated by β2 but not α6 nicotinic subunits. Finally, we show that 5-iodo-A-85380 potently activates both stoichiometries of α4β2 nAChRs with differential efficacies, being a full agonist on HS α4(2)β2(3) nAChRs, and a partial agonist on LS α4(3)β2(2) nAChRs and α6-containing subtypes as well.
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Kerr, Jessica L., Erin M. Timpe, and Julie P. Karpinski. "Varenicline: A Novel Nicotinic Receptor Partial Agonist for Smoking Cessation." Journal of Pharmacy Technology 23, no. 1 (January 2007): 23–29. http://dx.doi.org/10.1177/875512250702300105.
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Dunbar, Geoffrey C., and Ramana Kuchibhatla. "Cognitive Enhancement in Man With Ispronicline, A Nicotinic Partial Agonist." Journal of Molecular Neuroscience 30, no. 1-2 (2006): 169–72. http://dx.doi.org/10.1385/jmn:30:1:169.
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Coe, Jotham W., Paige R. Brooks, Michael G. Vetelino, Michael C. Wirtz, Eric P. Arnold, Jianhua Huang, Steven B. Sands, et al. "Varenicline: An α4β2 Nicotinic Receptor Partial Agonist for Smoking Cessation." Journal of Medicinal Chemistry 48, no. 10 (April 23, 2005): 3474–77. http://dx.doi.org/10.1021/jm050069n.
Full textDissertations / Theses on the topic "Nicotinic partial agonist"
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BAVO, FRANCESCO. "SUBTYPE-SELECTIVE NEURONAL NICOTINIC ACETYLCHOLINE RECEPTOR AGONISTS AND ANTAGONISTS." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/607332.
Full textAbstract:
This PhD thesis focuses on two specific targets, belonging to the same receptor class of Nicotinic Acetylcholine Receptors (nAChRs): the α4β2 subtype and the α7 subtype. This elaborate is divided in two parts. The aim of the first part is the design and synthesis of α4β2 selective partial agonists as potential smoking-cessation agents. The aim of the second part is the design and synthesis of α7 antagonists with mitocan properties as antitumoral agents.
Part 1.
In the first project, a series of 3-nitrophenyl ethers and 3-hydroxyphenyl ethers of (S)-N-methylprolinol bearing bulky and lipophilic substituents at the C5 were designed, synthesized and assayed as putative selective α4β2 ligands. Two of them, 5-substituted with a 6-hydroxy-1-hexynyl, had high α4β2 affinity and increased α4β2/α3β4 selectivity when compared with the correspondent unsubstituted parent compounds.
In the second project, each -CH= of the unselective antagonist (S,R)-N-methyl-2-pyrrolidinyl-1,4-benzodioxane and of its epimer at the benzodioxane stereocenter, was replaced by a nitrogen. The resulting four diastereomeric pairs of pyrrolidinyl-pyridodioxanes, also designed as the product of rigidification of the flexible scaffolds of pyridyl ethers of N-methyl prolinol, were studied for their nicotinic affinity at the α4β2 and α3β4. The isosteric -CH= to N substitution was detrimental for all the compounds, with the only exception of N-Methyl-pyrrolidinyl 5-pyridodioxane, with the nitrogen at position 5. Indeed, this ligand had similar affinity to its benzodioxane parent compound, but it had high α4β2/α3β4 selectivity and it was shown to be a selective partial agonist.
In the third project, the unselective antagonist (S,R)-N-methyl-2-pyrrolidinyl-1,4-benzodioxane and of its epimer at the benzodioxane stereocenter were substituted at position 5 of the benzodioxane moiety, to explore the possibility of introducing selectivity and/or partial agonist as previously done with -CH= to N replacement. Among the synthesized compounds, (S,S)-N-Methyl-pyrrolidinyl-5-amino-benzodioxane had slightly improved affinity at the α4β2 affinity and highly enhanced α4β2/α3β4 selectivity than the unsubstituted parent compound, and it was shown to be a very potent partial agonist.
In the fourth project, we applied computational techniques to support the interpretation of the biological results regarding N-Methyl-pyrrolidinyl 5-substituted benzodioxanes and pyridodioxanes. From these findings, we suggested that partial agonism and α4β2/α3β4 selectivity could be achieved when the benzodioxane scaffold is appropriately substituted with an HBA/HBD system, that can displace a water molecule from a small and hydrophilic subpocket of the binding site.
Part 2.
Adenocarcinoma and glioblastoma cell lines express α7 and α9-α10 nAChRs, whose activation promotes tumor cells growth. On these cells, the triethylammoniumethyl ether of 4-stilbenol MG624, a known selective antagonist of α7 and α9-α10 nAChRs, has antiproliferative activity. The structural analogy of MG624 with the mitocan RDM-
4’BTPI, triphenylphosphoniumbutyl ether of pterostilbene, suggested us that molecular hybridization among their three substructures might result in novel antitumour agents with higher potency and selectivity. We found that replacement of ethylene with butylene in the triethylammonium derivatives results in more potent and selective toxicity towards adenocarcinoma and glioblastoma cells, which was paralleled by increased α7 and α9-α10 nAChR antagonism and improved ability of reducing mitochondrial ATP production. Further elongation to octylene (26) provided a compound with 40-fold and 10-fold increased antiglioblastoma and antiadenocarcinoma activity respectively, when compared to MG624. Elongation of the alkylene linker was greatly advantageous also for the triphenylphosphonium derivatives. RDM-
4’BTPI did not acquire, as expectable, antinicotinic activity by hybridization with MG624 stilbene scaffold, but it was surpassed in glioblastoma cell viability reduction by its stilbene analogues with > 4C alkylene linker. In particular, the analogue with decylene between stilbenoxyl and triphenylphosphonium head (24) was ten-
fold and two-fold more potent than RDM-4’BTPI in reducing glioblastoma cell viability and in increasing ROS production respectively. Overall, the ammonium compound
26 reached antiproliferative activities at glioblastoma and adenocarcinoma cells in the same range of the phosphonium 24, but showed good selectivity against neuroblastoma and healthy mouse astrocytes.
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Woodcock, Thomas Matt. "MODULATION OF THE ALPHA-7 NICOTINIC ACETYLCHOLINE RECEPTOR FOLLOWING EXPERIMENTAL RAT BRAIN INJURY IMPROVES CELLULAR AND BEHAVIORAL OUTCOMES." UKnowledge, 2010. http://uknowledge.uky.edu/gradschool_diss/770.
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Traumatic brain injury (TBI) is a leading cause of death and long-term disability worldwide, and survivors are often left with cognitive deficits and significant problems with day to day tasks. To date, therapeutic pharmacological treatments of TBI remain elusive despite numerous clinical trials. An improved understanding of the molecular and cellular response to injury may help guide future treatment strategies. One promising marker for brain injury is the translocator protein (TSPO), which is normally expressed at a low level, but is highly expressed following brain damage and is associated with neuroinflammation. The isoquinoline carboxamide PK11195 binds selectively to the TSPO in many species, and has therefore become the most-studied TSPO ligand. To characterize the time-course of TSPO expression in the controlled cortical injury (CCI) model of TBI we subjected Sprague-Dawley rats to CCI and euthanatized them after 30 minutes, 12 hours, 1, 2, 4, or 6 days. Autoradiography with radiolabelled PK11195 was used to assess the time-course of TSPO binding following CCI. Autoradiographs were compared to adjacent tissue slices stained with the microglia/macrophage marker ED-1, with which a moderate positive correlation was discovered. PK11195 autoradiography was used as a tool with which to assess neuroinflammation following CCI and the administration of an α7 nAChR antagonist, methyllycaconitine (MLA). We hypothesized that blocking the calcium permeable α7 nAChR after brain injury would have a neuroprotective effect by attenuating excitotoxicity in the shortterm. Our study revealed clear dose-dependent tissue sparing in rats administered MLA after trauma and a modest improvement in functional outcome. The relatively modest recovery of function with MLA, which could be due to prolonged α7 nAChR blockade or downregulation lead us to explore the potential of α7 nAChR partial agonists in treating TBI. The α7 nAChR partial agonists tropisetron, ondansetron, and DMXB-A produced a moderate attenuation of cognitive deficits, but did not have a neuroprotective effect on tissue sparing. These studies show that following TBI, α7 nAChR modulation can have neuroprotective effects and attenuate cognitive deficits. Whether this modulation is best achieved through partial agonist treatment alone or a combination antagonist/agonist treatment remains to be determined.
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APPIANI, REBECCA. "ALPHA4BETA2 NEURONAL NICOTINIC ACETYLCHOLINE RECEPTOR LIGANDS: FROM SUBTYPE SELECTIVE TO STOICHIOMETRIC ISOPHORM SELECTIVE PARTIAL AGONISM." Doctoral thesis, Università degli Studi di Milano, 2023. https://hdl.handle.net/2434/950273.
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This PhD thesis focuses on the study of the α4β2 nicotinic acetylcholine receptors (nAChRs). This dissertation is divided into two parts. The first part is centred on the design, synthesis, and biological evaluation of compounds selective for the orthosteric and unorthodox binding sites of the α4β2 nAChRs. In the second part, attention is paid to the study of a photoactivatable α4β2 nAChRs full agonist.
Part 1
The first goal of Part 1 was the mutational studies of Ser108 residue of the hydrophilic pocket of the β2(-) side of the α4β2 orthosteric binding site with the purpose of studying the importance of the hydroxyl group of serine residue and the steric encumbrance in the pocket. For this reason, binding experiments were performed on the heterologously expressed human α4β2 receptor and its three Ser108àLeu, Ser108àPhe and Ser108àAla mutants using the most promising partial agonists synthesized previously.
The second goal was the synthesis and pharmacological evaluation of the naked and hydroxy/methoxy decorated benzofuran-based compound in order to study the implications of the flexibility reduction, abolishment of cycle stereogenic and of the one of the two oxygen in comparison with previously tested benzodioxane derivatives. Subsequently, the most promising benzodioxane compounds and the obtained benzofuran derivatives were evaluated for their affinity and activity on the two distinct α4β2 nAChR isoforms: (α4)2(β2)3 and (α4)3(β2)2.
The third goal was the study of the in vivo effects of prolinol aryl ethers and pyrrolidinyl benzodioxanes full and partial agonists. These compounds were tested for their effects on zebrafish behaviour. In particular, full agonists were tested for their ability to improve spatial memory and attention, and partial agonist for its ability to block the rewarding effects of nicotine and therefore its potential use for smoking cessation.
The fourth goal was the design, synthesis and pharmacological evaluation of selective agonists for the α4α4 unorthodox binding site of the α4β2 nAChR based on the structure of NS9283, an α4α4selective compound, described in the literature. The main aim was to identify new hit
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compounds potentially selective at the (α4)3(β2)2 receptor isoform with a better pharmacological profile.
Part 2
Regarding the second part of this thesis, it focuses on the synthesis of a photoactivatable α4β2 nAChR full agonist with the purpose to spatiotemporally control its release with light at the specific site of action. To follow this strategy, 8-bromo-7-hydroxy-2-methylquinoline (BHQ) and 8-cyano-7-hydroxy-2-methylquinoline (CyHQ) protecting groups were synthesized and used to cage a previously synthesized full agonist. Subsequently, its release after the irradiation with the UV light at 365 nm was followed using HPLC in order to obtain a full photo- chemical characterization of the caged compounds to get necessary information for in vitro/in vivo experiments.
Book chapters on the topic "Nicotinic partial agonist"
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Coe, Jotham W., Frank R. Busch, and Robert A. Singer. "Varenicline (Chantix): An α4β2 Nicotinic Receptor Partial Agonist for Smoking Cessation." In Modern Drug Synthesis, 225–47. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470768594.ch16.
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"Varenicline: An α4β2 Nicotinic Acetylcholine Receptor Partial Agonist as an Aid to Smoking Cessation." In Medication Treatments for Nicotine Dependence, 231–40. CRC Press, 2006. http://dx.doi.org/10.1201/9781420005431-23.
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Coe, Jotham W., Hans Rollema, and Brian T. O’Neill. "Chapter 4 Case History: Chantix™/Champix™ (Varenicline Tartrate), a Nicotinic Acetylcholine Receptor Partial Agonist as a Smoking Cessation Aid." In Annual Reports in Medicinal Chemistry, 71–101. Elsevier, 2009. http://dx.doi.org/10.1016/s0065-7743(09)04404-2.
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Sudano, Isabella, and Thomas F. Lüscher. "Smoking and Cessation." In Manual of Cardiovascular Medicine, 63–68. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198850311.003.0007.
Full textAbstract:
Tobacco use is not only associated with a high incidence of cancer and vascular disease, such as myocardial infarction, peripheral arterial disease, stroke, and dementia, and impotence among others, but also may cause respiratory diseases such as chronic obstructive pulmonary disease, infections, osteoporosis, gum disease, impaired taste, smell, and sight. Thus, smoking cessation is highly recommended by all guidelines and primarily rests on advice given to patients, (1) ASK; (2) ADVISE; (3) ASSESS; (4) ASSIST, and (5) ARRANGE. In addition, there are pharmacological agents that help in smoking cessation, such as nicotine replacement therapy, partial nicotine receptor agonists, and central acting compounds inhibiting dopamine and adrenaline re-uptake.
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O’Brien, Charles P., and James McKay. "Psychopharmacological Treatments for Substance Use Disorders." In A Guide to Treatments that Work, 145–78. Oxford University Press, 2007. http://dx.doi.org/10.1093/med:psych/9780195304145.003.0005.
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The treatment of substance abuse with pharmacological agents is well established, although most experts agree that, to be successful, medication interventions must be combined with psychosocial therapies. A large number of Type 1 and Type 2 controlled trials have shown that the use of nicotine replacement therapy to induce and maintain smoking cessations significantly increases the abstinence rate. Bupropion, which is also an antidepressant, has been found in controlled trials to significantly increase the smoking abstinence rate measured at intervals up to 12 months after beginning of treatment. Trials with novel agents such as the cannabinoid receptor antagonist rimonabant and varenicline, a nicotine receptor partial agonist, have been reported at meetings but have not yet appeared in print. The treatment of alcoholism can now be enhanced by three totally different types of medications: disulfiram, which works when compliance is assured; naltrexone, which reduces alcohol reward via the endogenous opioid system and results in decreased alcohol craving and reduced drinking in most randomized clinical trials; and acamprosate, which reduces post-alcohol excitability and has been effective in European trials but less so in U.S. trials. A depot version of the opiate antagonist naltrexone was approved by the FDA in 2006. It gives therapeutic blood levels for at least 30 days and should greatly improve compliance, thus making naltrexone more useful for the treatment of both opiate addiction and alcoholism. Methadone maintenance treatment for heroin dependence has consistently shown efficacy, and the treatment options have been increased by the availability of the partial opiate agonist buprenorphine. Buprenorphine is unique in that it can be used for the treatment of opiate addiction by qualified physicians in their offices rather than requiring enrollment in a highly regulated methadone treatment program. There are as yet no FDA-approved medications for the treatment of stimulant addiction, which includes cocaine and methamphetamine. There are recent double-blind, placebo-controlled clinical trials of several medications that have been found effective against cocaine addiction and are currently in multisite trials to confirm efficacy.