Pub Date : 1998-09-01DOI: 10.1111/J.1527-3458.1998.TB00072.X
A. Šulcová
{"title":"The 7th Biennial Meeting of the European Behavioral Pharmacology Society (EBPS'98), a Joint Meeting with the Behavioral Pharmacology Society Brno, Czech Republic, September 2–6, 1998","authors":"A. Šulcová","doi":"10.1111/J.1527-3458.1998.TB00072.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.1998.TB00072.X","url":null,"abstract":"","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"2016 1","pages":"301-305"},"PeriodicalIF":0.0,"publicationDate":"1998-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88907252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1998-09-01DOI: 10.1111/J.1527-3458.1998.TB00065.X
X. Guitart, X. Codony, M. Ballarín, A. Dordal, A. Farré
{"title":"E‐5842: A New Potent and Preferential Sigma Ligand. Preclinical Pharmacological Profile","authors":"X. Guitart, X. Codony, M. Ballarín, A. Dordal, A. Farré","doi":"10.1111/J.1527-3458.1998.TB00065.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.1998.TB00065.X","url":null,"abstract":"","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"19 7","pages":"201-224"},"PeriodicalIF":0.0,"publicationDate":"1998-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91496101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1998-09-01DOI: 10.1111/J.1527-3458.1998.TB00067.X
J. Kojima, K. Onodera, M. Ozeki, K. Nakayama
Ipidacrine (NIK-247, 9-amino-2,3,5,6,7,8-hexahydro-1H-cyclopenta[b]quinoline monohydrochloride monohydrate) is a novel substance synthesized by the National Research Center for Biologically Active Compounds in the Russian Federation. Ipidacrine was earlier referred to by the chemical name amiridine (7). This compound contains the structure of 4-aminopyridine and is structurally very similar to tacrine (9-amino-l,2,3,4-tetrahydroacridine hydrochloride hydrate), as is shown in Fig. 1. It has been reported that ipidacrine blocks specific [3H]tacrine binding (43). Tacrine is an antidementia agent that can inhibit acetylcholinesterase (EC 3.1.1.1.7, AChE) (21,26,48,50). Senile dementia has been associated with a loss of cholinergic neurotransmission, which is essential for some cognitive functions (20,53). Degeneration of basal forebrain cholinergic neurons in the nucleus basalis of Meynert (NBM) and deficiencies of acetylcholine and choline acetyltransferase (EC 2.3.1.6.) are known to occur in Alzheimer’s disease (10,72). This cholinergic hypothesis has led to the development of compounds that are capable of improving cholinergic neurotransmission in the brain. Among the various approaches to enhancement of the cholinergic system, inhibition of the degrading enzyme (AChE) is presently the most promising in terms of providing candidate drugs for treatment of patients with dementia (16,32,57,63). Recently, tacrine and E-2020 (1-benzyl-4-[{5,6-dimethoxy1-indanon}-2-yl]methylpiperidine hydrochloride, Eisai Co., Ltd., Tokyo, Japan), a pure AChE inhibitor, won FDA approval for treating Alzheimer’s Disease (Fig. 1) (57). A number of additional AChE inhibitors await approval; however, CI-1002 is not one of them, since it was disqualified in phase I clinical trials. Therefore, we discuss in this paper
{"title":"Ipidacrine (NIK-247): A Review of Multiple Mechanisms as an Antidementia Agent","authors":"J. Kojima, K. Onodera, M. Ozeki, K. Nakayama","doi":"10.1111/J.1527-3458.1998.TB00067.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.1998.TB00067.X","url":null,"abstract":"Ipidacrine (NIK-247, 9-amino-2,3,5,6,7,8-hexahydro-1H-cyclopenta[b]quinoline monohydrochloride monohydrate) is a novel substance synthesized by the National Research Center for Biologically Active Compounds in the Russian Federation. Ipidacrine was earlier referred to by the chemical name amiridine (7). This compound contains the structure of 4-aminopyridine and is structurally very similar to tacrine (9-amino-l,2,3,4-tetrahydroacridine hydrochloride hydrate), as is shown in Fig. 1. It has been reported that ipidacrine blocks specific [3H]tacrine binding (43). Tacrine is an antidementia agent that can inhibit acetylcholinesterase (EC 3.1.1.1.7, AChE) (21,26,48,50). Senile dementia has been associated with a loss of cholinergic neurotransmission, which is essential for some cognitive functions (20,53). Degeneration of basal forebrain cholinergic neurons in the nucleus basalis of Meynert (NBM) and deficiencies of acetylcholine and choline acetyltransferase (EC 2.3.1.6.) are known to occur in Alzheimer’s disease (10,72). This cholinergic hypothesis has led to the development of compounds that are capable of improving cholinergic neurotransmission in the brain. Among the various approaches to enhancement of the cholinergic system, inhibition of the degrading enzyme (AChE) is presently the most promising in terms of providing candidate drugs for treatment of patients with dementia (16,32,57,63). Recently, tacrine and E-2020 (1-benzyl-4-[{5,6-dimethoxy1-indanon}-2-yl]methylpiperidine hydrochloride, Eisai Co., Ltd., Tokyo, Japan), a pure AChE inhibitor, won FDA approval for treating Alzheimer’s Disease (Fig. 1) (57). A number of additional AChE inhibitors await approval; however, CI-1002 is not one of them, since it was disqualified in phase I clinical trials. Therefore, we discuss in this paper","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"16 1","pages":"247-259"},"PeriodicalIF":0.0,"publicationDate":"1998-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81275647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1998-09-01DOI: 10.1111/J.1527-3458.1998.TB00070.X
A. Scriabine
M. Csejtei et al. (Gedeon Richter Ltd., Budapest, Hungary) reported pharmacological studies with RGH-2716 (8-{4,4-bis(4-fluorophenyl)butyl}-3-1,1-dimethylethyl)-4-methylene-1-oxa-3,8-diazaspiro{4,5}decan-2-one), known also as TDN-345. This drug was reported to protect ischemic brain tissue from energy loss in mice at doses ranging from 3 to 30 mg/kg i.p. At 0.1 to 10 μM it blocked veratridine-induced release of [3H]dopamine or [3H]norepinephrine in rat brain slices. It is thought to prevent elevation of intracellular Ca2+ levels and inhibit voltage-gated Na+ channels in neurons. Gedeon Richter Ltd. is developing RGH-2716 as a memory-enhancing and neuroprotective drug in collaboration with Takeda Chemical Industries of Japan. M. Paroczai et al. (Gedeon Richter Ltd., Budapest, Hungary) reported behavioral effects of RGH 5279 ([–]-transapovincaminic acid-[acetoxy]ethyl ester [3β, 16α]) in rats. RGH-5279 was previously reported to have neuroprotective activity and to inhibit lipid peroxidation in animals. It was now found to antagonize learning and memory deficits induced by diazepam or scopolamine in young rats in the water labyrinth test. It was effective in a retrograde amnesia model at doses as low as 3 mg/kg p.o. It was also effective as a cognition enhancer in rats with basal forebrain lesions. K. Iwasaki et al. (Fukuoka Univ., Japan) reported that the muscarinic (M1) partial agonist SB202026A ({R-(Z)}-α-(methoxyimino)-1-azabicyclo{2,2,2}octane-acetonitrile monohydrochloride) improved deficits in spatial cognition induced by scopolamine, pirenzepine, or experimental brain ischemia in rats. At doses as low as 1 μg/kg i.p., SB202026A decreased errors in radial maze task. The drug is under development for the treatment of Alzheimer’s disease.
{"title":"XIIIth International Congress of Pharmacology Munich, Germany, July 26–31, 1998 New Drugs Affecting Central Nervous System","authors":"A. Scriabine","doi":"10.1111/J.1527-3458.1998.TB00070.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.1998.TB00070.X","url":null,"abstract":"M. Csejtei et al. (Gedeon Richter Ltd., Budapest, Hungary) reported pharmacological studies with RGH-2716 (8-{4,4-bis(4-fluorophenyl)butyl}-3-1,1-dimethylethyl)-4-methylene-1-oxa-3,8-diazaspiro{4,5}decan-2-one), known also as TDN-345. This drug was reported to protect ischemic brain tissue from energy loss in mice at doses ranging from 3 to 30 mg/kg i.p. At 0.1 to 10 μM it blocked veratridine-induced release of [3H]dopamine or [3H]norepinephrine in rat brain slices. It is thought to prevent elevation of intracellular Ca2+ levels and inhibit voltage-gated Na+ channels in neurons. Gedeon Richter Ltd. is developing RGH-2716 as a memory-enhancing and neuroprotective drug in collaboration with Takeda Chemical Industries of Japan. M. Paroczai et al. (Gedeon Richter Ltd., Budapest, Hungary) reported behavioral effects of RGH 5279 ([–]-transapovincaminic acid-[acetoxy]ethyl ester [3β, 16α]) in rats. RGH-5279 was previously reported to have neuroprotective activity and to inhibit lipid peroxidation in animals. It was now found to antagonize learning and memory deficits induced by diazepam or scopolamine in young rats in the water labyrinth test. It was effective in a retrograde amnesia model at doses as low as 3 mg/kg p.o. It was also effective as a cognition enhancer in rats with basal forebrain lesions. K. Iwasaki et al. (Fukuoka Univ., Japan) reported that the muscarinic (M1) partial agonist SB202026A ({R-(Z)}-α-(methoxyimino)-1-azabicyclo{2,2,2}octane-acetonitrile monohydrochloride) improved deficits in spatial cognition induced by scopolamine, pirenzepine, or experimental brain ischemia in rats. At doses as low as 1 μg/kg i.p., SB202026A decreased errors in radial maze task. The drug is under development for the treatment of Alzheimer’s disease.","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"94 1","pages":"287-290"},"PeriodicalIF":0.0,"publicationDate":"1998-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90210787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1998-09-01DOI: 10.1111/J.1527-3458.1998.TB00066.X
E. Spack, N. Wehner, J. Winkelhake
The recent approvals of Betaseron, Avonex, and Copaxone have improved treatment options for multiple sclerosis (MS), but these therapeutics delay the progression of disease in only ~30% of the patient population. There remains an unmet need for MS therapeutics, and several new drugs enter clinical testing each year in an attempt to meet this need (37,38). This review summarizes the development of an antigen-specific therapeutic comprised of a solubilized major histocompatibility complex (MHC) molecule bearing an autoantigenic peptide of myelin basic protein, called AG284, and the initiation of its phase I clinical trial in MS. The combination of MHC molecule, peptide, and detergent excipient in AG284 presented several unique challenges in the formulation of this drug and in the analysis of its biodistribution and stability. Furthermore, the considerable polymorphism of MHC molecules complicated preclinical efficacy studies, as well as tests of toxicity and immunogenicity. Other challenges that were also encountered in other recent MS clinical trials included a dearth of simple, sensitive surrogate markers, particularly for tracking T-cell reactivity. The preclinical testing and trial design of AG284 reviewed here illustrate several of the challenges likely to face other antigen-specific therapeutics, and some of the solutions detailed herein may have applications for similar trials in other diseases.
{"title":"Preclinical and Pharmacological Studies of AG284, a Soluble HLA‐DR2:Myelin Basic Protein Peptide Complex for the Treatment of Multiple Sclerosis","authors":"E. Spack, N. Wehner, J. Winkelhake","doi":"10.1111/J.1527-3458.1998.TB00066.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.1998.TB00066.X","url":null,"abstract":"The recent approvals of Betaseron, Avonex, and Copaxone have improved treatment options for multiple sclerosis (MS), but these therapeutics delay the progression of disease in only ~30% of the patient population. There remains an unmet need for MS therapeutics, and several new drugs enter clinical testing each year in an attempt to meet this need (37,38). This review summarizes the development of an antigen-specific therapeutic comprised of a solubilized major histocompatibility complex (MHC) molecule bearing an autoantigenic peptide of myelin basic protein, called AG284, and the initiation of its phase I clinical trial in MS. The combination of MHC molecule, peptide, and detergent excipient in AG284 presented several unique challenges in the formulation of this drug and in the analysis of its biodistribution and stability. Furthermore, the considerable polymorphism of MHC molecules complicated preclinical efficacy studies, as well as tests of toxicity and immunogenicity. Other challenges that were also encountered in other recent MS clinical trials included a dearth of simple, sensitive surrogate markers, particularly for tracking T-cell reactivity. The preclinical testing and trial design of AG284 reviewed here illustrate several of the challenges likely to face other antigen-specific therapeutics, and some of the solutions detailed herein may have applications for similar trials in other diseases.","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"22 1","pages":"225-246"},"PeriodicalIF":0.0,"publicationDate":"1998-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81122554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1998-09-01DOI: 10.1111/J.1527-3458.1998.TB00071.X
L. Köles
This symposium was organized by P. Illes (Univ. Leipzig, Germany), A. Reichenbach (Paul-Flechsig Institute for Brain Research, Leipzig, Germany) and H. Zimmermann (Univ. Frankfurt/Main, Germany). More than 150 experts on purinergic transmission met at a historical building of the University of Leipzig in the center of the town. The symposium consisted of 32 twenty-minute-long lectures by invited speakers from eleven countries. In addition, 50 posters were presented in two poster sessions. After an informal gathering of speakers, participants and guests on Friday evening, the official scientific program of the conference began on Saturday by the opening addresses of T. Butz (Univ. Leipzig) and P. Illes. The first session was chaired by E. A. Barnard (Royal Free Hospital School of Medicine, London, UK) and G. Burnstock (from the same institution). The first speaker of this session was one of the chairmen, G. Burnstock. He gave an outstanding lecture on the current status of purinergic signalling in the nervous system. He reviewed the history of purinergic transmission, from the early 1970s until now. The “purinergic nerve” hypothesis was proposed in 1972, with evidence to suggest that ATP is a neurotransmitter in some non-adrenergic, non-cholinergic nerves. Later it became evident that ATP is a cotransmitter with classical transmitters in autonomic and sensory-motor nerves. In 1978, receptors to purines were shown to belong to two main subtypes: P1 purinoceptors, which are selective for adenosine, and P2 purinoceptors, which are selective for ATP and ADP. Subsequently, subtypes of P1 purinoceptors: A1, A2a, A2b, and A3 were identified. Burnstock and colleagues proposed the subclassification of P2 purinoceptors into P2X and P2Y receptors. Further investigations revealed that the P2X receptors, which are ligand-gated cation channels, can be subclassified to at least seven subtypes, while the P2Y receptor family (G protein-coupled receptors) consists of at least 10 subtypes. G. Burnstock mentioned some new aspects of the purinergic research field at the end of his excellent presentation. P2X and P2Y receptors are present on sensory nerves, and might play an important role in mechanoception and nociception. There is rapidly expanding interest in purinergic signalling in the brain and spinal cord. The plasticity of purinergic cotransmission has a remarkable role in some pathophysiological conditions (e.g., interstitial cystitis, outflow obstruction of the bladder, hypertension). Apart from “fast” purinergic signalling in the nervous system, nucleotides play long-term (trophic) roles in development and degeneration.
{"title":"Nucleotides and their receptors in the nervous system, Leipzig, Germany, August 1-2, 1998","authors":"L. Köles","doi":"10.1111/J.1527-3458.1998.TB00071.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.1998.TB00071.X","url":null,"abstract":"This symposium was organized by P. Illes (Univ. Leipzig, Germany), A. Reichenbach (Paul-Flechsig Institute for Brain Research, Leipzig, Germany) and H. Zimmermann (Univ. Frankfurt/Main, Germany). More than 150 experts on purinergic transmission met at a historical building of the University of Leipzig in the center of the town. The symposium consisted of 32 twenty-minute-long lectures by invited speakers from eleven countries. In addition, 50 posters were presented in two poster sessions. After an informal gathering of speakers, participants and guests on Friday evening, the official scientific program of the conference began on Saturday by the opening addresses of T. Butz (Univ. Leipzig) and P. Illes. The first session was chaired by E. A. Barnard (Royal Free Hospital School of Medicine, London, UK) and G. Burnstock (from the same institution). The first speaker of this session was one of the chairmen, G. Burnstock. He gave an outstanding lecture on the current status of purinergic signalling in the nervous system. He reviewed the history of purinergic transmission, from the early 1970s until now. The “purinergic nerve” hypothesis was proposed in 1972, with evidence to suggest that ATP is a neurotransmitter in some non-adrenergic, non-cholinergic nerves. Later it became evident that ATP is a cotransmitter with classical transmitters in autonomic and sensory-motor nerves. In 1978, receptors to purines were shown to belong to two main subtypes: P1 purinoceptors, which are selective for adenosine, and P2 purinoceptors, which are selective for ATP and ADP. Subsequently, subtypes of P1 purinoceptors: A1, A2a, A2b, and A3 were identified. Burnstock and colleagues proposed the subclassification of P2 purinoceptors into P2X and P2Y receptors. Further investigations revealed that the P2X receptors, which are ligand-gated cation channels, can be subclassified to at least seven subtypes, while the P2Y receptor family (G protein-coupled receptors) consists of at least 10 subtypes. G. Burnstock mentioned some new aspects of the purinergic research field at the end of his excellent presentation. P2X and P2Y receptors are present on sensory nerves, and might play an important role in mechanoception and nociception. There is rapidly expanding interest in purinergic signalling in the brain and spinal cord. The plasticity of purinergic cotransmission has a remarkable role in some pathophysiological conditions (e.g., interstitial cystitis, outflow obstruction of the bladder, hypertension). Apart from “fast” purinergic signalling in the nervous system, nucleotides play long-term (trophic) roles in development and degeneration.","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"52 1","pages":"291-300"},"PeriodicalIF":0.0,"publicationDate":"1998-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75945109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-09-01DOI: 10.1111/J.1527-3458.1995.TB00284.X
H. Hara, T. Morita, T. Sukamoto, F. M. Cutrer
{"title":"Lomerizine (KB-2796), a New Antimigraine Drug","authors":"H. Hara, T. Morita, T. Sukamoto, F. M. Cutrer","doi":"10.1111/J.1527-3458.1995.TB00284.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.1995.TB00284.X","url":null,"abstract":"","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"46 1","pages":"204-226"},"PeriodicalIF":0.0,"publicationDate":"1995-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81512449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-09-01DOI: 10.1111/J.1527-3458.1995.TB00280.X
B. Vitális, A. Bakonyi, V. Csillik-Perczel, E. Horváth, K. Horváth, I. Máté, J. Székely, T. Yemane, G. Ábrahám, S. Sólyom, L. G. Hársing
{"title":"The Pharmacology of GYKI‐46 903, a New Cognition Enhancer","authors":"B. Vitális, A. Bakonyi, V. Csillik-Perczel, E. Horváth, K. Horváth, I. Máté, J. Székely, T. Yemane, G. Ábrahám, S. Sólyom, L. G. Hársing","doi":"10.1111/J.1527-3458.1995.TB00280.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.1995.TB00280.X","url":null,"abstract":"","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"43 1-2","pages":"129-148"},"PeriodicalIF":0.0,"publicationDate":"1995-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91489428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-09-01DOI: 10.1111/J.1527-3458.1995.TB00282.X
E. Costa, D. M. Thompson, J. Auta, A. Guidotti
{"title":"Imidazenil: A Potent Benzodiazepine Partial Positive Modulator of GABAergic Transmission Virtually Devoid of Tolerance Liability","authors":"E. Costa, D. M. Thompson, J. Auta, A. Guidotti","doi":"10.1111/J.1527-3458.1995.TB00282.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.1995.TB00282.X","url":null,"abstract":"","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"29 1","pages":"168-189"},"PeriodicalIF":0.0,"publicationDate":"1995-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78213476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-09-01DOI: 10.1111/J.1527-3458.1995.TB00286.X
C. Bever
{"title":"4-Aminopyridine: Use in Multiple Sclerosis","authors":"C. Bever","doi":"10.1111/J.1527-3458.1995.TB00286.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.1995.TB00286.X","url":null,"abstract":"","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"113 1","pages":"261-279"},"PeriodicalIF":0.0,"publicationDate":"1995-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80563274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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