CP-101,606: An NR2B-Selective NMDA Receptor Antagonist.
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Stephen A. Williams | F. Menniti | K. Wilner | W. White | B. Chenard | Ajit K. Shah | W. White | W. White | Ajit K. Shah | Stephen A. Williams | Keith D. Wilner | Bertrand L. Chenard
[1] F. Menniti,et al. CP-101,606, an NR2B subunit selective NMDA receptor antagonist, inhibits NMDA and injury induced c-fos expression and cortical spreading depression in rodents , 2000, Neuropharmacology.
[2] K. Wilner,et al. A Double‐Blind, Placebo‐Controlled Study of the Safety, Tolerability and Pharmacokinetics of CP‐101,606 in Patients with a Mild or Moderate Traumatic Brain Injury , 1999, Annals of the New York Academy of Sciences.
[3] K. Wilner,et al. An Open‐Label Study of CP‐101,606 in Subjects with a Severe Traumatic Head Injury or Spontaneous Intracerebral Hemorrhage , 1999, Annals of the New York Academy of Sciences.
[4] D. Lynch,et al. An NR2B point mutation affecting haloperidol and CP101,606 sensitivity of single recombinant N-methyl-D-aspartate receptors. , 1998, The Journal of pharmacology and experimental therapeutics.
[5] W. White,et al. Effects of the NMDA antagonist CP-98,113 on regional cerebral edema and cardiovascular, cognitive, and neurobehavioral function following experimental brain injury in the rat , 1998, Brain Research.
[6] P D Leeson,et al. Effect of plasma protein binding on in vivo activity and brain penetration of glycine/NMDA receptor antagonists. , 1997, Journal of medicinal chemistry.
[7] R. Bullock,et al. Effect of CP101,606, a novel NR2B subunit antagonist of the N-methyl-D-aspartate receptor, on the volume of ischemic brain damage off cytotoxic brain edema after middle cerebral artery occlusion in the feline brain. , 1997, Stroke.
[8] Hui-Sheng Huang,et al. The NR2B-specific Interactions of Polyamines and Protons with theN-Methyl-d-aspartate Receptor* , 1997, The Journal of Biological Chemistry.
[9] E. Aizenman,et al. Functional consequences of NR2 subunit composition in single recombinant N-methyl-D-aspartate receptors. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[10] F. Menniti,et al. CP-101,606, a potent neuroprotectant selective for forebrain neurons. , 1997, European journal of pharmacology.
[11] A. Schousboe,et al. Association of c‐fos mRNA expression and excitotoxicity in primary cultures of mouse neocortical and cerebellar neurons , 1997, Journal of neuroscience research.
[12] R. Bullock,et al. The neuroprotective effect of the forebrain-selective NMDA antagonist CP101,606 upon focal ischemic brain damage caused by acute subdural hematoma in the rat. , 1997, Journal of neurotrauma.
[13] Eric A. Barnard. Ionotropic glutamate receptors: new types and new concepts. , 1997, Trends in pharmacological sciences.
[14] L. Carlock,et al. NMDA Receptor Overstimulation Triggers a Prolonged Wave of Immediate Early Gene Expression: Relationship to Excitotoxicity , 1997, Experimental Neurology.
[15] W. White,et al. Effects of the novel NMDA antagonists CP-98,113, CP-101,581 and CP-101,606 on cognitive function and regional cerebral edema following experimental brain injury in the rat. , 1997, Journal of neurotrauma.
[16] M. Waterfield,et al. Characterization of p150, an Adaptor Protein for the Human Phosphatidylinositol (PtdIns) 3-Kinase , 1997, The Journal of Biological Chemistry.
[17] J. T. Greenamyre,et al. Bioenergetics and glutamate excitotoxicity , 1996, Progress in Neurobiology.
[18] Greenamyre Jt,et al. Bioenergetics and glutamate excitotoxicity. , 1996 .
[19] C. Sotak,et al. The role of spreading depression in focal ischemia evaluated bv dffusion mapping , 1996, Annals of neurology.
[20] T. Obrenovitch,et al. Inhibition of cortical spreading depression by L‐701,324, a novel antagonist at the glycine site of the N‐methyl‐D‐aspartate receptor complex , 1996, British journal of pharmacology.
[21] A. Schousboe,et al. Sustained c-fos expression is associated with excitotoxicity during the development of neuronal cells in vitro. , 1996, Biochemical Society transactions.
[22] T A Gennarelli,et al. Neuropathological sequelae of traumatic brain injury: relationship to neurochemical and biomechanical mechanisms. , 1996, Laboratory investigation; a journal of technical methods and pathology.
[23] R. Bullock,et al. Massive persistent release of excitatory amino acids following human occlusive stroke. , 1995, Stroke.
[24] M. Mishina,et al. Structure and function of the NMDA receptor channel , 1995, Neuropharmacology.
[25] R. Bullock,et al. Evidence for Prolonged Release of Excitatory Amino Acids in Severe Human Head Trauma , 1995, Annals of the New York Academy of Sciences.
[26] M. Collins,et al. (1S,2S)-1-(4-hydroxyphenyl)-2-(4-hydroxy-4-phenylpiperidino)-1-propanol: a potent new neuroprotectant which blocks N-methyl-D-aspartate responses. , 1995, Journal of medicinal chemistry.
[27] C. Meredith,et al. Excitatory amino acid-induced cytotoxicity in primary cultures of mouse cerebellar granule cells correlates with elevated, sustained c-fos protoncogene expression , 1995, Neuroscience Letters.
[28] S. Heinemann,et al. Control of proton sensitivity of the NMDA receptor by RNA splicing and polyamines. , 1995, Science.
[29] N. Belluardo,et al. NMDA receptor-dependent and -independent immediate early gene expression induced by focal mechanical brain injury , 1995, Neurochemistry International.
[30] K. Lees,et al. Clinical experience with excitatory amino acid antagonist drugs. , 1995, Stroke.
[31] K. Williams. Pharmacological properties of recombinant N-methyl-d-aspartate (NMDA) receptors containing the ϵ4 (NR2D) subunit , 1995, Neuroscience Letters.
[32] J. Grotta. Why do all drugs work in animals but none in stroke patients? 2 Neuroprotective therapy , 1995, Journal of internal medicine.
[33] D. Attwell,et al. Triggering and execution of neuronal death in brain ischaemia: two phases of glutamate release by different mechanisms , 1994, Trends in Neurosciences.
[34] M. Aftabuddin,et al. Induction of N-methyl-D-asparate receptor mediated c-fos protein in the rat brain by incomplete ischaemia. , 1994, The Indian journal of medical research.
[35] B. Siesjö. Calcium‐Mediated Processes in Neuronal Degeneration a , 1994, Annals of the New York Academy of Sciences.
[36] F. Stephenson,et al. Molecular characterization of N-methyl-D-aspartate receptors expressed in mammalian cells yields evidence for the coexistence of three subunit types within a discrete receptor molecule. , 1994, The Journal of biological chemistry.
[37] F. Sharp,et al. MK-801 inhibits the induction of immediate early genes in cerebral cortex, thalamus, and hippocampus, but not in substantia nigra following middle cerebral artery occlusion , 1994, Neuroscience Letters.
[38] P. Mailleux,et al. Homolateral cerebrocortical increase of immediate early gene and neurotransmitter messenger RNAs after minimal cortical lesion: Blockade by N-methyl-d-aspartate antagonist , 1994, Neuroscience.
[39] Y. Jan,et al. Changing subunit composition of heteromeric NMDA receptors during development of rat cortex , 1994, Nature.
[40] T. Christensen,et al. Impairment of Fos protein formation in the rat infarct borderzone by MK‐801, but not by NBQX , 1993, Acta neurologica Scandinavica.
[41] K. Williams,et al. Developmental switch in the expression of NMDA receptors occurs in vivo and in vitro , 1993, Neuron.
[42] D. G. Herrera,et al. Spreading depression induces c-fos-like immunoreactivity and NGF mRNA in the rat cerebral cortex , 1993, Brain Research.
[43] T. Wieloch,et al. NMDA-receptor blockers but not NBQX, an AMPA-receptor antagonist, inhibit spreading depression in the rat brain. , 1992, Acta physiologica Scandinavica.
[44] K. Sakimura,et al. Molecular diversity of the NMDA receptor channel , 1992, Nature.
[45] Bert Sakmann,et al. Heteromeric NMDA Receptors: Molecular and Functional Distinction of Subtypes , 1992, Science.
[46] R. Albin,et al. Alternative excitotoxic hypotheses , 1992, Neurology.
[47] J. Olney,et al. NMDA antagonist neurotoxicity: mechanism and prevention. , 1991, Science.
[48] J. Garthwaite,et al. Excitatory amino acid neurotoxicity and neurodegenerative disease. , 1990, Trends in pharmacological sciences.
[49] D. Graham,et al. Ischemic brain damage in a model of acute subdural hematoma. , 1990, Neurosurgery.
[50] P. Rosenberg,et al. Hundred-fold increase in neuronal vulnerability to glutamate toxicity in astrocyte-poor cultures of rat cerebral cortex , 1989, Neuroscience Letters.
[51] D. Choi,et al. Glutamate neurotoxicity and diseases of the nervous system , 1988, Neuron.
[52] R. Dingledine,et al. Requirement for glycine in activation of NMDA-receptors expressed in Xenopus oocytes. , 1988, Science.
[53] D. Choi,et al. Pharmacology of glutamate neurotoxicity in cortical cell culture: attenuation by NMDA antagonists , 1988, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[54] M. Mayer,et al. The physiology of excitatory amino acids in the vertebrate central nervous system , 1987, Progress in Neurobiology.
[55] J. Olney,et al. Excitotoxity and the NMDA receptor , 1987, Trends in Neurosciences.
[56] P. Ascher,et al. Glycine potentiates the NMDA response in cultured mouse brain neurons , 1987, Nature.
[57] D. Choi. Ionic dependence of glutamate neurotoxicity , 1987, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[58] J. Penney,et al. Glutamate dysfunction in Alzheimer's disease: an hypothesis , 1987, Trends in Neurosciences.
[59] J. Greenamyre. The role of glutamate in neurotransmission and in neurologic disease. , 1986, Archives of neurology.
[60] L. Pitts,et al. Rat middle cerebral artery occlusion: evaluation of the model and development of a neurologic examination. , 1986, Stroke.
[61] Jianhong Luo,et al. The majority of N-methyl-D-aspartate receptor complexes in adult rat cerebral cortex contain at least three different subunits (NR1/NR2A/NR2B). , 1997, Molecular pharmacology.
[62] C. Meredith,et al. Excitatory amino acid-induced cytotoxicity in primary cultures of mouse cerebellar granule cells correlates with elevated, sustained c-fos proto-oncogene expression. , 1995, Neuroscience letters.
[63] K. Williams. Pharmacological properties of recombinant N-methyl-D-aspartate (NMDA) receptors containing the epsilon 4 (NR2D) subunit. , 1995, Neuroscience letters.
[64] J. Mcculloch. Glutamate receptor antagonists in cerebral ischaemia. , 1994, Journal of neural transmission. Supplementum.
[65] W. Schmidt. Behavioural effects of NMDA-receptor antagonists. , 1994, Journal of neural transmission. Supplementum.
[66] J. Kemp,et al. The glycine site of the NMDA receptor--five years on. , 1993, Trends in pharmacological sciences.
[67] R. Bullock,et al. Prevention of post-traumatic excitotoxic brain damage with NMDA antagonist drugs: a new strategy for the nineties. , 1992, Acta neurochirurgica. Supplementum.
[68] H. Goldman,et al. Cerebrovascular changes in a rat model of moderate closed-head injury. , 1991, Journal of neurotrauma.
[69] M. Mattson. Excitatory amino acids, growth factors, and calcium: a teeter-totter model for neural plasticity and degeneration. , 1990, Advances in experimental medicine and biology.
[70] Y. Ben-Ari. Excitatory Amino Acids and Neuronal Plasticity , 1990, Advances in Experimental Medicine and Biology.
[71] Yoji Yoshida,et al. Experimental studies of ischemic brain edema , 1986 .