Darodipine

Chemical compound From Wikipedia, the free encyclopedia

Darodipine is an experimental calcium channel blocker that based on animal models may reduce neuronal cytoskeletal alterations during aging and in neurodegenerative disorders. Studies performed on rats have shown darodipine to have an effect on brain serotonergic systems. Darodipine increased the 5-HIAA/5-HT ratio within various parts of the brain.[1] Darodipine has also been shown to impair memory and learning processes on mice.[2]

Quick facts Names, Identifiers ...
Darodipine
Names
Preferred IUPAC name
Diethyl 4-(2,1,3-benzoxadiazol-4-yl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylate
Other names
4-(2,1,3-Benzoxadiazol-7-yl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylic acid diethyl ester
Identifiers
3D model (JSmol)
ChEMBL
ChemSpider
UNII
  • InChI=1/C19H21N3O5/c1-5-25-18(23)14-10(3)20-11(4)15(19(24)26-6-2)16(14)12-8-7-9-13-17(12)22-27-21-13/h7-9,16,20H,5-6H2,1-4H3
    Key: QERUYFVNIOLCHV-UHFFFAOYAW
  • O=C(OCC)\C3=C(\N\C(=C(\C(=O)OCC)C3c1cccc2nonc12)C)C
Properties
C19H21N3O5
Molar mass 371.393 g·mol−1
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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The longterm effect of darodipine was tested in the rats and it shows that there is no significant change in their body and brain weight values but, there is a significant change in their alkaline phosphate reactive capillary profile values. Alkaline phosphate enzymes plays an important role in the functioning of the cerebral capillary activities.[3] The effect of darodipine on plasma concentration was also tested on a group of healthy male human volunteers. The result showed that darodipine resulted in the change in heart rate and diastolic blood pressure which is related to the plasma concentration.[4]

Darodipine (50–500 nM), the sensitivity of DMPO‐COO.− adduct decreased by more than that of the DMPO‐OH adduct and the concentration-dependent drop in signal intensity. It has additional preventive effects, because of its calcium antagonistics, against free-radical mediated electrophysiological alterations; it is likely because of the trapping of such radical molecules.

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