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公开(公告)号:US6156794A
公开(公告)日:2000-12-05
申请号:US297803
申请日:1999-09-13
申请人: Morris Faiman , John V. Schloss , Jang-Yen Wu
发明人: Morris Faiman , John V. Schloss , Jang-Yen Wu
IPC分类号: C07D295/20 , A61K31/145 , A61K31/16 , A61K31/27 , A61K31/397 , A61K31/40 , A61K31/4453 , A61K31/55 , A61P9/10 , A61P25/04 , A61P25/08 , A61P25/14 , A61P25/22 , A61P25/28 , A61P25/34 , A61P37/04 , C07C381/14 , C07D277/34 , C07D277/36 , C07D279/06 , A61K31/325
CPC分类号: A61K31/16 , A61K31/145 , A61K31/27 , C07D277/36 , C07D279/06
摘要: A method of using a compound of formula (I) wherein R.sup.1, R.sup.2, R.sup.3, X and n have any of the meanings defined in the specification, to antagonize glutamate binding, or to treat glutamate-related disorders is provided. Novel compounds, intermediates and pharmaceutical compositions are also provided.
摘要翻译: PCT No.PCT / US97 / 20308 Sec。 371日期1999年9月13日 102(e)1999年9月13日PCT 1997年11月6日PCT公布。 第WO98 / 19676号公报 日期1998年5月14日提供了使用其中R1,R2,R3,X和n具有本说明书中定义的任何含义以拮抗谷氨酸结合或治疗谷氨酸相关病症的式(I)化合物的方法。 还提供了新颖的化合物,中间体和药物组合物。
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公开(公告)号:US20050037975A1
公开(公告)日:2005-02-17
申请号:US10626923
申请日:2003-07-25
申请人: Morris Faiman , John Schloss , Jang-Yen Wu
发明人: Morris Faiman , John Schloss , Jang-Yen Wu
IPC分类号: A61K31/145 , A61K31/16 , A61K31/27 , A61K38/05 , A61K31/325
CPC分类号: A61K31/27 , A61K31/145 , A61K31/16
摘要: Disclosed are novel compounds and novel pharmaceutical compositions for use in medical therapy, as well as intermediates and processes for preparing such compounds. Therapeutic methods for preventing or treating glutamate-related disorders in a mammal and methods to inhibit or prevent glutamate binding in mammalian tissue are also disclosed.
摘要翻译: 公开了用于医学治疗的新型化合物和新型药物组合物,以及用于制备这些化合物的中间体和方法。 还公开了用于预防或治疗哺乳动物组织中谷氨酸相关病症的治疗方法和抑制或预防哺乳动物组织中谷氨酸结合的方法。
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公开(公告)号:US20130259824A1
公开(公告)日:2013-10-03
申请号:US13853183
申请日:2013-03-29
IPC分类号: A61K38/19 , A61K31/192 , A61K31/27
CPC分类号: A61K31/27 , A61K31/192 , A61K38/193 , A61K2300/00
摘要: Granulocyte colony-stimulating factor (G-CSF; a stem cell enhancer and facilitator), DETC-MeSO (a glutamate receptor partial antagonist and anti-excitotoxicity agent), and sulindac (a potent anti-oxidant and anti-inflammatory agent) each can protect brain tissue exposed to a cerebral ischemia/reperfusion injury, and minimize the size of infarcts that develop as a result of the injury. When administered in combination, these agents are effective at protecting brain tissue and minimizing the size of an infarct resulting from the injury at much lower concentrations compared to using a single agent.
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公开(公告)号:US07723302B2
公开(公告)日:2010-05-25
申请号:US12113723
申请日:2008-05-01
申请人: Jang-Yen Wu , Dipnarine Maharaj
发明人: Jang-Yen Wu , Dipnarine Maharaj
IPC分类号: A61K38/19 , C07K14/535
CPC分类号: A61K38/16
摘要: The invention relates to the discovery that in an animal model of Parkinson's disease (PD), administration of granulocyte colony-stimulating factor (G-CSF) to rodents having 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD restored the function of dopamine neurons. In these animals, G-CSF treatment increased the number of dopamine neurons in the substantia nigra (SN), G-CSF treatment partially restored the nigrostriatal pathway, and G-CSF restored the function of dopamine to the level before MPTP treatment. The invention also relates to the discovery that treatment of a human patient with corticobasilar ganglionic degeneration, a rare progressive neurological disorder characterized by Parkinsonism and coritcal dysfunction, with G-CSF resulted in a significant improvement in the patient's Unified Parkinson's Disease Rating Scale evaluations as well as measures of activity of daily living. The invention further relates to the discovery that G-CSF treatment of a patient who had suffered an acute stroke resulted in a significant improvement in neurological function, the patient having minimal observable disability seven years later. The methods described herein can be used to treat PD in a mammalian subject (e.g., rodent, human) as well as other neurodegenerative diseases such as Alzheimer's disease, spinal cord injury, and stroke.
摘要翻译: 本发明涉及在帕金森病(PD)的动物模型中发现,向具有1-甲基-4-苯基-1,2,3,6-四氢吡啶的啮齿类动物施用粒细胞集落刺激因子(G-CSF) (MPTP)诱导的PD恢复多巴胺神经元的功能。 在这些动物中,G-CSF治疗增加黑质(SN)中多巴胺神经元的数量,G-CSF治疗部分恢复了黑质纹状体途径,G-CSF将多巴胺的功能恢复到MPTP治疗前的水平。 本发明还涉及以下发现:用G-CSF治疗患有皮质基底神经节变性的人类患者,其是以帕金森综合征和角膜功能障碍为特征的罕见进行性神经障碍,导致患者的统一帕金森氏病评定量表评估的显着改善 作为日常生活活动的措施。 本发明进一步涉及发现患有急性中风的患者的G-CSF治疗导致神经功能的显着改善,该患者在七年后几乎没有可观察到的残疾。 本文所述的方法可用于治疗哺乳动物受试者(例如啮齿动物,人)以及其它神经变性疾病如阿尔茨海默病,脊髓损伤和中风中的PD。
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公开(公告)号:US20080300176A1
公开(公告)日:2008-12-04
申请号:US12113723
申请日:2008-05-01
申请人: Jang-Yen Wu , Dipnarine Maharaj
发明人: Jang-Yen Wu , Dipnarine Maharaj
CPC分类号: A61K38/16
摘要: The invention relates to the discovery that in an animal model of Parkinson's disease (PD), administration of granulocyte colony-stimulating factor (G-CSF) to rodents having 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD restored the function of dopamine neurons. In these animals, G-CSF treatment increased the number of dopamine neurons in the substantia nigra (SN), G-CSF treatment partially restored the nigrostriatal pathway, and G-CSF restored the function of dopamine to the level before MPTP treatment. The invention also relates to the discovery that treatment of a human patient with corticobasilar ganglionic degeneration, a rare progressive neurological disorder characterized by Parkinsonism and coritcal dysfunction, with G-CSF resulted in a significant improvement in the patient's Unified Parkinson's Disease Rating Scale evaluations as well as measures of activity of daily living. The invention further relates to the discovery that G-CSF treatment of a patient who had suffered an acute stroke resulted in a significant improvement in neurological function, the patient having minimal observable disability seven years later. The methods described herein can be used to treat PD in a mammalian subject (e.g., rodent, human) as well as other neurodegenerative diseases such as Alzheimer's disease, spinal cord injury, and stroke.
摘要翻译: 本发明涉及在帕金森病(PD)的动物模型中发现,向具有1-甲基-4-苯基-1,2,3,6-四氢吡啶的啮齿类动物施用粒细胞集落刺激因子(G-CSF) (MPTP)诱导的PD恢复多巴胺神经元的功能。 在这些动物中,G-CSF治疗增加黑质(SN)中多巴胺神经元的数量,G-CSF治疗部分恢复了黑质纹状体途径,G-CSF将多巴胺的功能恢复到MPTP治疗前的水平。 本发明还涉及以下发现:用G-CSF治疗患有皮质基底神经节变性的人类患者,其是以帕金森综合征和角膜功能障碍为特征的罕见进行性神经障碍,导致患者的统一帕金森氏病评定量表评估的显着改善 作为日常生活活动的措施。 本发明进一步涉及发现患有急性中风的患者的G-CSF治疗导致神经功能的显着改善,该患者在七年后几乎没有可观察到的残疾。 本文所述的方法可用于治疗哺乳动物受试者(例如啮齿动物,人)以及其它神经变性疾病如阿尔茨海默病,脊髓损伤和中风中的PD。
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