87 results about "N-Methyl-D-aspartic acid" patented technology

The preparation method of medicine for curing dementia, N-methyl-D-aspartic acid (NMDA) receptor antagonist memantine hydrochloride includes the following steps: using polybasic alcohol as solvent; making 1-bromo-3,5-dimethyl adamantane and urea according to the mole ratio of 1:0.25-10 react for 0.5-48 hr. at 20-200 deg.C; after the reaction is completed, adding sodium hydroxide into the reactionsolution according to that the mole ratio of 1-bromo-3,5-dimethyl adamantane and sodium hydroxide is 1:0.1-10, making alcoholysis at 50-200 deg.C, chloroform extraction, concentration, acidification with hydrochloric acid and salt-forming so as to obtain the invented menantine hydrochloride. It features safe and simple operation and low cost, etc.

Pain associated with primary and secondary dysmenorrhea is relieved in a human suffering there from by administering to the human a pain relieving amount of a synergistically acting sub-therapeutic combination of a nontoxic N-methyl-D-aspartate receptor antagonist such as dextromethorphan, magnesium, dextrorphan, ketamine or pharmaceutically acceptable salt thereof, tramadol or its analog such as recemic tramadol or an analogously acting molecular entity or pharmaceutically acceptable salt thereof, and an anticonvulsant and / or a tricyclic anti-depressant or pharmaceutically acceptable salt thereof, and optionally in sustained release dosage form.

A method of inhibiting the binding between N-methyl-D-aspartate receptors and neuronal proteins in a neuron the method comprising administering to the neuron an effective inhibiting amount of a peptide replacement agent for the NMDA receptor or neuronal protein interaction domain that effect said inhibition of the NMDA receptor neuronal protein. The method is of value in reducing the damaging effect of injury to mammalian cells. Postsynaptic density-95 protein (PSD-95) couples neuronal N-methyl-D-aspartate receptors (NMDARs) to pathways mediating excitotoxicity and ischemic brain damage. This coupling was disrupted by transducing neurons with peptides that bind to modular domains on either side of the PSD-95 / NMDAR interaction complex. This treatment attenuated downstream NMDAR signaling without blocking NMDAR activity, protected cultured cortical neurons from excitotoxic insults and dramatically reduced cerebral infarction volume in rats subjected to transient focal cerebral ischemia. The treatment was effective when applied either before, or one hour after, the onset of excitotoxicity in vitro and cerebral ischemia in vivo. This approach prevents negative consequences associated with blocking NMDAR activity and constitutes practical therapy for stroke.

A method of evaluating memory / learning functions with the use of a model with glutamic acid N-methyl-D-aspartate (NMDA) type receptor hypofunction as an animal model for schizophrenia and with the use of reference memory task, wherein there has been found concrete means for detecting any differences in activity between typical anti-psychosis drugs and atypical anti-psychosis drugs is found.An in vivo animal model for screening of a therapeutic agent for improving cognitive dysfunction by schizophrenia is provided.

Disclosed are compounds of the formulaor a pharmaceutically acceptable salt or solvate thereof, whereinR1 isR is —C(O)—N(R27)(R28) orand the remaining variables are as defined in the specification.Also disclosed are pharmaceutical compositions comprising the compounds of formula I.Also disclosed are methods of treating cognitive or neurodegenerative diseases such as Alzheimer's disease.Also disclosed are pharmaceutical compositions and methods of treating cognitive or neurodegenerative diseases comprising the compounds of formula I in combination with a β-secretase inhibitor other than those of formula I, an HMG-CoA reductase inhibitor, a gamma-secretase inhibitor, a non-steroidal anti-inflammatory agent, an N-methyl-D-aspartate receptor antagonist, a cholinesterase inhibitor or an anti-amyloid antibody.

The invention pertains to a method of treating Parkinson's disease (PD) in a mammal, comprising administering a first pharmaceutical agent and a second pharmaceutical agent, wherein the first pharmaceutical agent is an antagonist of the adenosine receptor 2 (A2A) and the second pharmaceutical agent is an antagonist of the N-methyl-D-aspartate (NMDA) receptor subtype NR2B.

The present invention relates to a microRNA-based short hairpin RNA for gene silencing the genetic expression of NR1 subunit of N-methyl-D-aspartate receptor comprises a single strand RNA fragment comprising a first fragment, a second fragment and a connecting fragment, wherein the first fragment and the second fragment are complementary to each other, and are spaced and connected by the connecting fragment, with the connecting fragment being randomly arranged nucleotides, with the first fragment having a Drosha recognized cleavage site, a silencing site and a Dicer recognized cleavage site, with the Drosha recognized cleavage site and the Dicer recognized cleavage site being spaced and connected by the silencing site, with the silencing site encoding homologous nucleotides corresponding to NR1 subunit of subcutaneous N-methyl-D-aspartate receptor.

The invention discloses a preparation method of a medicament-carrying biological membrane, which comprises the following steps: preparing type I collagen into a porous and degradable collagen spongy carrier by a freeze-drying process by temperature cross-linking; according to the pharmacokinetics of the selected medicaments, adding medicaments with a certain concentration, such as antibiotics, antiepileptic medicaments, nerve growth factors, NMDA (N-methyl-D-aspartic acid) receptor stimulants, NMDA receptor antagonists and the like, into the liquid medicine slowly in the preparation process of slurry, or soaking a biological membrane into the liquid medicine with a certain concentration; adsorbing the medicaments for a period of time; freeze-drying; packaging; and sterilizing in a proper sterilizing mode (gamma rays or epoxy ethane) according to the properties of the medicaments to form a medicament-carrying preparation with a slow-release effect. The invention has wide application prospects in the technical fields of infection prevention, nerve growth promotion, NMDA metabolism, epileptic prevention and the like.

A small interfering RNA for gene knockdown of the N-methyl-D-aspartate receptor NR1 subunit comprises 21 to 25 ribonucleic acids, which are homologous to the RNA sequence of N-methyl-D-aspartate receptor NR1 subunit. A method of using the small interfering RNA, applying the small interfering RNA on subcutaneous tissues temporary interfere with the genetic expression of the NMDA receptor NR1 subunit in hypoderm. A use of the small interfering RNA on pharmaceutics, applying the small interfering RNA manufacture into new analgesic drugs for moderating the inflammatory pain or intolerable chronic pain, especially on clinical chronic pain and burn pain patients. An analgesic drug for skin inflammatory pain comprising: the small interfering RNA and a siRNA acceptable vehicle.

Novel heterodimers of tetrahydroacridines and tetrahydroquinolinones are disclosed. The heterodimers are capable of acting as both acetylcholinesterase inhibitors and N-methyl-D-aspartate (NMDA) receptor antagonists. The heterodimers may be used to improve cognitive defects via treatment or prevention in both humans and non-humans.

Disclosed are novel compounds of the formulaor a pharmaceutically acceptable salt or solvate thereof, whereinR1, R2, R3, R4 and X are as defined in the specification.Also disclosed are pharmaceutical compositions comprising the compounds of formula I.Also disclosed are methods of treating cognitive or neurodegenerative diseases such as Alzheimer's disease.Also disclosed are methods of treating a cognitive or neurodegenerative disease comprising administering to a patient I need of such treatment a combination of at least one compound of formula I and at least one compound selected from the group consisting of β-secretase inhibitors other than those of formula I, HMG-CoA reductase inhibitors, gamma-secretase inhibitors, non-steroidal anti-inflammatory agents, N-methyl-D-aspartate receptor antagonists, cholinesterase inhibitors and anti-amyloid antibodies.

Disclosed are novel compounds of the formulaor a pharmaceutically acceptable salt or solvate thereof, whereinR1, R2, R3, n and X are as defined in the specification.Also disclosed are pharmaceutical compositions comprising the compounds of formula I.Also disclosed are methods of treating cognitive or neurodegenerative diseases such as Alzheimer's disease.Also disclosed are methods of treating a cognitive or neurodegenerative disease comprising administering to a patient I need of such treatment a combination of at least one compound of formula I and at least one compound selected from the group consisting of β-secretase inhibitors other than those of formula I, HMG-CoA reductase inhibitors, gamma-secretase inhibitors, non-steroidal anti-inflammatory agents, N-methyl-D-aspartate receptor antagonists, cholinesterase inhibitors and anti-amyloid antibodies.

Compositions comprising skin-permeable pharmaceutically effective amounts of an opioid agonist; an N-methyl-D-aspartate receptor antagonist and an anti-inflammatory may be incorporated into formulations and devices suitable for transdermal delivery of the active ingredients to alleviate pain.

The invention is a manufacturing method of diamante amine hydrochlorate. The invention adopts 1, 3-dimethyl adamantine to reacts with tert-butylchlorine and gets 1-chlorine-3, 5-dimethyl adamantine; then reacts with acetamide directly, the educt from water reacts with sodium hydroxide in ethanediol or glycerine solvent, extracts by acetic ester, condenses, and blow in dry hydrochloride gas and gets the coarse product. There gets the pure product through alcohol-acetic ester recrystallization.

A method of evaluating memory / learning functions with the use of a model with glutamic acid N-methyl-D-aspartate (NMDA) type receptor hypofunction as an animal model for schizophrenia and with the use of reference memory task, wherein there has been found concrete means for detecting any differences in activity between typical anti-psychosis drugs and atypical anti-psychosis drugs is found.An in vivo animal model for screening of a therapeutic agent for improving cognitive dysfunction by schizophrenia is provided.

A method of inhibiting the binding between N-methyl-D-aspartate receptors and neuronal proteins in a neuron is disclosed. The method comprises administering to the neuron an effective inhibiting amount of a peptide replacement agent for the NMDA receptor or neuronal protein interaction domain that effect said inhibition of the NMDA receptor-neuronal protein interaction. The method is of value in reducing the damaging effect of injury to mammalian cells. Postsynaptic density-95 protein (PSD-95) couples neuronal N-methyl-D-aspartate receptors (NMDARS) to pathways mediating excitotoxicity, ischemic and traumatic brain damage. This coupling was disrupted by transducing neurons with peptides that bind to modular domains on either side of the PSD-95 / NMDAR interaction complex. This treatment attenuated downstream NMDAR signaling without blocking NMDAR activity, protected cultured cortical neurons from excitotoxic insults, dramatically reduced cerebral infarction volume in rats subjected to transient focal cerebral ischemia, and traumatic brain injury (TBI) in rats.