Details
Stereochemistry | RACEMIC |
Molecular Formula | C17H20N2O.ClH |
Molecular Weight | 304.814 |
Optical Activity | ( + / - ) |
Defined Stereocenters | 0 / 1 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
Cl.CC(CC1=CC=CC=C1)(NC(=O)CN)C2=CC=CC=C2
InChI
InChIKey=HYQMIUSWZXGTCC-UHFFFAOYSA-N
InChI=1S/C17H20N2O.ClH/c1-17(19-16(20)13-18,15-10-6-3-7-11-15)12-14-8-4-2-5-9-14;/h2-11H,12-13,18H2,1H3,(H,19,20);1H
DescriptionSources: https://www.ncbi.nlm.nih.gov/pubmed/12519561 | https://www.ncbi.nlm.nih.gov/pubmed/12519561Curator's Comment: description was created based on several sources, including:
https://www.ncbi.nlm.nih.gov/pubmed/11502903 | https://www.ncbi.nlm.nih.gov/pubmed/11391123
Sources: https://www.ncbi.nlm.nih.gov/pubmed/12519561 | https://www.ncbi.nlm.nih.gov/pubmed/12519561
Curator's Comment: description was created based on several sources, including:
https://www.ncbi.nlm.nih.gov/pubmed/11502903 | https://www.ncbi.nlm.nih.gov/pubmed/11391123
Remacemide is a low-affinity noncompetitive NMDA receptor antagonist with sodium channel blocking properties. It has been studied for a number of conditions including acute ischemic stroke, epilepsy, Parkinsons Disease, and Huntington's disease. It was concluded, that was unlikely that remacemide would be further developed as an antiepileptic drug. As for other conditions, there no any information in the literature, why remacemide is no longer being developed for them.
CNS Activity
Originator
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
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Target ID: CHEMBL2094124 Sources: https://www.ncbi.nlm.nih.gov/pubmed/7486610 |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
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Primary | remacemide Approved UseUnknown |
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Preventing | remacemide Approved UseUnknown |
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Primary | remacemide Approved UseUnknown |
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Primary | remacemide Approved UseUnknown |
Cmax
Value | Dose | Co-administered | Analyte | Population |
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86.8 ng/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/12160664 |
600 mg 1 times / day multiple, oral dose: 600 mg route of administration: Oral experiment type: MULTIPLE co-administered: |
AR-R12495 plasma | Homo sapiens population: UNHEALTHY age: ADULT sex: FEMALE / MALE food status: UNKNOWN |
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458 ng/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/12160664 |
600 mg 1 times / day multiple, oral dose: 600 mg route of administration: Oral experiment type: MULTIPLE co-administered: |
REMACEMIDE plasma | Homo sapiens population: UNHEALTHY age: ADULT sex: UNKNOWN food status: UNKNOWN |
AUC
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
439.5 ng × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/12160664 |
600 mg 1 times / day multiple, oral dose: 600 mg route of administration: Oral experiment type: MULTIPLE co-administered: |
AR-R12495 plasma | Homo sapiens population: UNHEALTHY age: ADULT sex: FEMALE / MALE food status: UNKNOWN |
|
1288 ng × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/12160664 |
600 mg 1 times / day multiple, oral dose: 600 mg route of administration: Oral experiment type: MULTIPLE co-administered: |
REMACEMIDE plasma | Homo sapiens population: UNHEALTHY age: ADULT sex: UNKNOWN food status: UNKNOWN |
Sample Use Guides
acute ischemic stroke: Groups of 8 patients (6 active, 2 placeboes) were planned to receive twice-daily treatment, with l00 mg, 200 mg, 300 mg, 400 mg, 500 mg, or 600 mg remacemide hydrochloride given as 2 intravenous infusions followed by 6 days' oral treatment. The maximum well-tolerated dose for remacemide hydrochloride in acute stroke is 400 mg BID.
Epilepsy: Two parallel group trials were included representing 514 individuals. Daily doses of 300, 600, 800 and 1200 mg of remacemide were tested. Regression models did, however, suggest a significant effect for 800-1200mg remacemide per day
Route of Administration:
Other
In Vitro Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/8769858
remacemide and its anticonvulsant metabolite 1,2-diphenyl-2-propylamine monohydrochloride (desglycinyl remacemide; DGR) a low-affinity NMDA receptor antagonist, were investigated using primary rat cortical neuronal cultures. Exposure of cortical cultures to NMDA (100 microM) for 15 min killed 85% of the neurons during the next 24 h. This neurotoxicity was blocked in a concentration-dependent manner by adding DGR (5-20 microM), but not its remacemide precursor (10-100 microM), to the cultures during the time of NMDA exposure. This suggests that the neuroprotective, as well as the anticonvulsant, the activity of remacemide is mediated by DGR.
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NCI_THESAURUS |
C78272
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CHEMBL25843
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I1ST2B6HIM
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AA-40
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m9520
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111686-79-4
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C152184
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DBSALT002016
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60510
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C067553
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DTXSID9045683
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118754-06-6
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SUPERSEDED |
ACTIVE MOIETY
SUBSTANCE RECORD