http://rdf.ncbi.nlm.nih.gov/pubchem/patent/BR-0303585-A
Outgoing Links
| Predicate | Object |
|---|---|
| assignee | http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_e84399f6b699c9ba6d35a986174731d4 |
| classificationIPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61P25-18 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-495 |
| filingDate | 2003-07-17-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| inventor | http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_8b2f2c940428f9b2b4ab519c3628c8ee |
| publicationDate | 2005-05-10-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| publicationNumber | BR-0303585-A |
| titleOfInvention | Application of flunarizine and cinnarizine in the treatment of psychiatric disorders. |
| abstract | "APPLICATION OF FLUNARIZIN AND CINARIZIN IN TREATMENT OF PSYCHIATRIC DISORDERS". More specifically severe psychiatric disorders such as schizophrenia, schizoaffective disorder and bipolar affective disorder. Based on its moderate affinity for D2 receptors and its long half-life, it can be hypothesized that flunarizine is an atypical long-acting antipsychotic. The mechanisms by which flunarizine favors the treatment of the aforementioned diseases are T, L and N calcium channel blockade, which promotes events such as neurotransmitter release, increased synaptic activity, modulation of various enzymes and induction of cell death. ; Na ^ + ^ channel blockade, a critical mechanism in the action of many anticonvulsants that reduces neuronal depolarization and neurotransmitter release; increased adenosine-mediated actions, which inhibit the release of most neurotransmitters and whose deficit may be involved in the pathophysiology of schizophrenia; neuroprotective effect in models of cerebral ischemia, nerve damage, NGF deprivation and neuronal implantation, which may favor neural plasticity by attenuating the postulated trophic activity deficit and attenuating the vulnerability to excitotoxicity and neurodegeneration in schizophrenia; anticonvulsant action in animals and humans, and schizophrenia is associated with an increased risk of seizures; cognitive effects, since flunarizine causes cognitive performance improvement in humans, which may be relevant for schizophrenia, as cognition is fundamental in the syndrome and accounts for much of the morbidity and functional impairment caused by the disease. The advantages of using flunarizine in the treatment of indicated conditions are the few adverse effects, both acute and long-term, compared to antipsychotics in general, efficacy in negative symptoms, in which only atypical antipsychotics act and simple dosage consisting of 1 tablet per day but may be administered at intervals of 1 to 2 weeks for flunarizine. |
| priorityDate | 2003-07-17-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| type | http://data.epo.org/linked-data/def/patent/Publication |
Incoming Links
Total number of triples: 21.