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Details

Stereochemistry ACHIRAL
Molecular Formula C18H22N2.C2HF3O2
Molecular Weight 380.404
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of DESIPRAMINE TRIFLUOROACETATE

SMILES

OC(=O)C(F)(F)F.CNCCCN1C2=CC=CC=C2CCC3=CC=CC=C13

InChI

InChIKey=UFQHEQUKRIFMOM-UHFFFAOYSA-N
InChI=1S/C18H22N2.C2HF3O2/c1-19-13-6-14-20-17-9-4-2-7-15(17)11-12-16-8-3-5-10-18(16)20;3-2(4,5)1(6)7/h2-5,7-10,19H,6,11-14H2,1H3;(H,6,7)

HIDE SMILES / InChI

Molecular Formula C2HF3O2
Molecular Weight 114.0233
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

Molecular Formula C18H22N2
Molecular Weight 266.3807
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

Description

Desipramine is a tricyclic antidepressant that was approved by the FDA in 1964. It was derived from imipramine, which was the first tricyclic antidepressant to be manufactured. Desipramine is one of many tricyclic antidepressants, and this type of antidepressant gets its name due to its three-ring chemical structure. Desipramine, a secondary amine tricyclic antidepressant, is structurally related to both the skeletal muscle relaxant cyclobenzaprine and the thioxanthene antipsychotics such as thiothixene. It is the active metabolite of imipramine, a tertiary amine TCA. The acute effects of desipramine include inhibition of noradrenaline re-uptake at noradrenergic nerve endings and inhibition of serotonin (5-hydroxy tryptamine, 5HT) re-uptake at the serotoninergic nerve endings in the central nervous system. Desipramine exhibits greater noradrenergic re-uptake inhibition compared to the tertiary amine TCA imipramine. In addition to inhibiting neurotransmitter re-uptake, desipramine down-regulates beta-adrenergic receptors in the cerebral cortex and sensitizes serotonergic receptors with chronic use. The overall effect is increased serotonergic transmission. Antidepressant effects are typically observed 2 - 4 weeks following the onset of therapy though some patients may require up to 8 weeks of therapy prior to symptom improvement. Patients experiencing more severe depressive episodes may respond quicker than those with mild depressive symptoms. Desipramine is marketed under the trade name Norpramin, indicated for the treatment of depression.

CNS Activity

Originator

Approval Year

Targets

Primary TargetPharmacologyConditionPotency
1.5 nM [IC50]
163.0 nM [Ki]

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
NORPRAMIN

Cmax

ValueDoseCo-administeredAnalytePopulation
21.8 ng/mL
50 mg single, oral
DESIPRAMINE plasma
Homo sapiens

AUC

ValueDoseCo-administeredAnalytePopulation
656 ng × h/mL
50 mg single, oral
DESIPRAMINE plasma
Homo sapiens

T1/2

ValueDoseCo-administeredAnalytePopulation
21 h
50 mg single, oral
DESIPRAMINE plasma
Homo sapiens

Funbound

ValueDoseCo-administeredAnalytePopulation
9.78%
DESIPRAMINE plasma
Homo sapiens

Doses

AEs

OverviewOther

Other InhibitorOther SubstrateOther Inducer






Drug as perpetrator​

Drug as victim

Tox targets

PubMed

Sample Use Guides

In Vivo Use Guide
Usual Adult Dose for Depression 100 to 200 mg orally per day Maximum dose: 300 mg orally per day Comments: -Dosage should be initiated at a lower level and increased according to tolerance and clinical response. -In severely ill patients, dosage may be further increased to 300 mg per day if needed. -Treatment of patients requiring as much as 300 mg should generally be initiated in hospitals. Usual Geriatric Dose for Depression 25 to 100 mg orally per day Maximum dose: 150 mg orally per day
Route of Administration: Oral
In Vitro Use Guide
Neuronal uptake 1 inhibitor desipramine (100 nM) decreased NE in 60-min hypothermic ischemia in isolated perfused guinea pig hearts.
Substance Class Chemical
Record UNII
5T6XJJ77M3
Record Status Validated (UNII)
Record Version