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    Venlafaxine molecular structure

    Venlafaxine Stats & Data

    Efexor Effexor Effexor xr
    NPS DataHub
    MW277.41
    FormulaC17H27NO2
    CAS93413-69-5
    IUPAC1-[2-dimethylamino-1-(4-methoxyphenyl)ethyl]cyclohexan-1-ol
    SMILESCOc1ccc(cc1)C(CN(C)C)C1(O)CCCCC1
    InChIKeyPNVNVHUZROJLTJ-UHFFFAOYSA-N
    Phenethylamines; Others; 2020/1. Von 2-Phenethylamin abgeleitete Verbindungen; 2021/1. Von 2-Phenethylamin abgeleitete Verbindungen; 2022/1. Von 2-Phenethylamin abgeleitete Verbindungen
    Chemical Class medicine

    Pharmacology

    DrugBank
    Half-life 5 hours State Solid

    Description

    Venlafaxine (Effexor) is an antidepressant within the serotonin-norepinephrine reuptake inhibitor (SNRI) class of medications. It exerts its effects primarily by blocking the transporters involved in the reuptake of the neurotransmitters serotonin and norepinephrine, therefore leaving more active neurotransmitter in the synapse. Venlafaxine is officially approved for use in the management of major depressive disorder (MDD), generalized anxiety disorder (GAD), social anxiety disorder, and panic disorder. As of 2014, Canadian clinical practice guidelines recommend venlafaxine as a first-line option for treatment of generalized anxiety, social anxiety, panic disorder, major depressive disorder (MDD), and consider it a second-line option for management of obsessive-compulsive disorder (OCD) . Venlafaxine is also used off-label for prophylaxis of migraine headaches , for reduction of vasomotor symptoms associated with menopause , and for management of neuropathic pain (although there is only minimal evidence of efficacy for this condition) .

    Mechanism of Action

    The exact mechanism of action of venlafaxine is unknown, but appears to be associated with the potentiation of neurotransmitter activity in the CNS. Venlafaxine and its active metabolite, O-desmethylvenlafaxine (ODV), inhibit the reuptake of both serotonin and norepinephrine with a potency greater for the 5-HT than for the NE reuptake process . Both venlafaxine and the ODV metabolite have weak inhibitory effects on the reuptake of dopamine but, unlike the tricyclics and similar to SSRIs, they are not active at histaminergic, muscarinic, or alpha(1)-adrenergic receptors.

    Pharmacodynamics

    The mechanism of venlafaxine's (and its metabolite, O-desmethylvenlafaxine (ODV)) antidepressant effect is believed to be due to their potentiation of neurotransmitter activity in the central nervous system through the inhibition of the reuptake of serotonin and norepinephrine from within the synapse. Venlafaxine has also been shown to weakly inhibit dopamine reuptake. Neither venlafaxine nor ODV bind to muscarinic, histaminergic, or alpha-1 adrenergic receptors; pharmacologic activity at these receptors is hypothesized to be associated with the various anticholinergic, sedative, and cardiovascular effects seen with other psychotropic drugs. Hyponatremia has also been shown to occur as a result of treatment with SNRIs, and is associated with the development of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) FDA Label, A177244. Venlafaxine also demonstrates a clinically significant and dose-related effect on blood pressure, likely due to its potentiation of norepinephrine FDA Label, A177250.

    Metabolism

    Undergoes extensive first pass metabolism in the liver to its major, active metabolite, O-desmethylvenlafaxine ODV, and two minor, less active metabolites, N-desmethylvenlafaxine and N,O-didesmethylvenlafaxine. Formation of ODV is catalyzed by cytochrome P450 (CYP) 2D6, whereas N-demethylation is catalyzed by CYP3A4, 2C19 and 2C9. ODV possesses antidepressant activity that is comparable to that of venlfaxine.

    Absorption

    Venlafaxine is well absorbed, with at least 92% of a single dose absorbed on the basis of mass balance studies . Food does not affect the absorption of venlafaxine or its subsequent metabolism into ODV. Bioavailability is 45% following oral administration. Time to steady state = 3 days.

    Toxicity

    Overdose of venlafaxine is typically associated with mild symptoms. However, severe toxicity is reported with the most common symptoms being CNS depression, serotonin toxicity, seizure, or cardiac conduction abnormalities. Venlafaxine's toxicity appears to be higher than other SSRIs, with a fatal toxic dose closer to that of the tricyclic antidepressants than the SSRIs. Doses of 900 mg or more are likely to cause moderate toxicity. Deaths have been reported following large doses.

    Indication

    Venlafaxine is indicated in the management of major depressive disorder (MDD), generalized anxiety disorder (GAD), social anxiety disorder (social phobia), and panic disorder with or without agoraphobia. Venlafaxine is also used off-label for prophylaxis of migraine headaches , for reduction of vasomotor symptoms associated with menopause , and for management of neuropathic pain (although there is only minimal evidence of efficacy for this condition) . It is also considered a second-line option for management of obsessive-compulsive disorder (OCD) .

    Protein Binding

    The degree of binding of venlafaxine to human plasma is 27% ± 2% at concentrations ranging from 2.5 to 2215 ng/mL. The degree of ODV binding to human plasma is 30% ± 12% at concentrations ranging from 100 to 500 ng/mL. Protein-binding-induced drug interactions with venlafaxine are not expected.

    Elimination

    Renal elimination of venlafaxine and its metabolites is the primary route of excretion. Approximately 87% of a venlafaxine dose is recovered in the urine within 48 hours as either unchanged venlafaxine (5%), unconjugated ODV (29%), conjugated ODV (26%), or other minor inactive metabolites (27%).

    Volume of Distribution

    * 7.5 ± 3.7 L/kg venlafaxine * 5.7 ± 1.8 L/kg O-desmethylvenlafaxine(active metabolite)

    Clearance

    Steady state plasma clearance, venlafaxine = 1.3 ± 0.6 L/h/kg; Steady state plasma clearance, ODV = 0.4 ± 0.2 L/h/kg.

    Tolerance & Pharmacokinetics

    drugs.wiki

    Tolerance Decay

    Full tolerance 3d Half tolerance 8d Baseline ~14d

    Experience Report Analysis

    Erowid
    155 Reports
    2001–2025 Date Range
    38 With Age Data
    29 Effects Detected

    Demographics

    Gender Distribution

    Age Distribution

    Reports Over Time

    Effect Analysis

    Erowid

    Effects aggregated from 155 experience reports (155 Erowid)

    155 Reports
    29 Effects Detected
    8 Positive
    14 Adverse
    7 Neutral

    Effect Sentiment Distribution

    Confidence Distribution

    Positive Effects 8

    Stimulation 36.8% 70%
    Euphoria 17.4% 70%
    Empathy 16.1% 70%
    Focus Enhancement 16.1% 70%
    Music Enhancement 12.9% 70%
    Color Enhancement 10.3% 70%
    Tactile Enhancement 7.7% 70%
    Body High 3.9% 70%

    Adverse Effects 14

    Anxiety 55.5% 70%
    Confusion 27.1% 70%
    Nausea 22.6% 70%
    Increased Heart Rate 9.7% 70%
    Pupil Dilation 9.0% 70%
    Sweating 8.4% 70%
    Seizure 8.4% 70%
    Muscle Tension 6.5% 70%
    Appetite Suppression 5.2% 70%
    Jaw Clenching 5.2% 70%
    Psychosis 5.2% 70%
    Memory Suppression 4.5% 70%
    Headache 3.2% 70%
    Motor Impairment 2.6% 70%

    Dosage Distribution

    Dose distribution from experience reports

    Median: 150.0 mg IQR: 75.0–200.0 mg n=105

    Real-World Dose Distribution

    62K Doses

    From 173 individual dose entries

    Oral (n=169)

    Median: 150.0mg 25th: 75.0mg 75th: 225.0mg 90th: 300.0mg
    mg/kg median: 1.945 mg/kg 75th: 2.806

    Common Combinations

    Most co-occurring substances in experience reports

    Form / Preparation

    Most common forms and preparations reported

    Body-Weight Dosing

    Dose relative to body weight from reports with weight data

    Median: 1.946 mg/kg IQR: 1.103–2.757 mg/kg n=104

    Redose Patterns

    Redosing behavior across 143 reports

    2.8% Redosed
    1.0 Avg Doses
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