| Stereochemistry | ABSOLUTE |
| Molecular Formula | C17H21NO.ClH |
| Molecular Weight | 291.816 |
| Optical Activity | ( - ) |
| Defined Stereocenters | 1 / 1 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
Cl.CNCC[C@@H](OC1=C(C)C=CC=C1)C2=CC=CC=C2
InChI
InChIKey=LUCXVPAZUDVVBT-UNTBIKODSA-N
InChI=1S/C17H21NO.ClH/c1-14-8-6-7-11-16(14)19-17(12-13-18-2)15-9-4-3-5-10-15;/h3-11,17-18H,12-13H2,1-2H3;1H/t17-;/m1./s1
| Molecular Formula | C17H21NO |
| Molecular Weight | 255.3547 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ABSOLUTE |
| Additional Stereochemistry | No |
| Defined Stereocenters | 1 / 1 |
| E/Z Centers | 0 |
| Optical Activity | UNSPECIFIED |
| Molecular Formula | ClH |
| Molecular Weight | 36.461 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
Atomoxetine is indicated for the treatment of Attention-Deficit/Hyperactivity Disorder. The precise mechanism by which atomoxetine produces its therapeutic effects in Attention-Deficit/Hyperactivity Disorder (ADHD) is unknown, but is thought to be related to selective inhibition of the pre-synaptic norepinephrine transporter. Most common adverse reactions are: nausea, vomiting, fatigue, decreased appetite, abdominal pain, and somnolence, constipation, dry mouth, dizziness, erectile dysfunction, and urinary hesitation. Atomoxetine is a substrate for CYP2D6 and hence concurrent treatment with CYP2D6 inhibitors such as bupropion (Wellbutrin) or fluoxetine (Prozac) is not recommended, as this can lead to significant elevations of plasma atomoxetine levels.
CNS Activity
Originator
Approval Year
Overview
OverviewOther
| Other Inhibitor | Other Substrate | Other Inducer |
|---|---|---|
Drug as perpetrator
Drug as victim
Tox targets
Sourcing
PubMed
Patents
Sample Use Guides
Atomoxetine should be initiated at a total daily dose of approximately 0.5 mg/kg and increased after a minimum of 3 days to a target total daily dose of approximately 1.2 mg/kg administered either as a single daily dose in the morning or as evenly divided doses in the morning and late afternoon/early evening. No additional benefit has been demonstrated for doses higher than 1.2 mg/kg/day.
Route of Administration:
Oral
Electrophysiological recordings was performed with the extracellular standard solution at different membrane potentials ranging from -80 mV to +40 mV while the concentration of the agonists (100 uM NMDA/10 uM glycine) and the antagonist (25 uM atomoxetine) were kept constant. The inhibitory effect was clearly voltage-dependent, so that the inhibition was attenuated by depolarization.
Showing 1 to 5 of 11 entries