Desvenlafaxine

263.38

263.38

200-659-6

N06AX23|N - Nervous system

2922509090

43.7

2.6

Solid

1.1±0.1 g/cm3

208-213°C

403.8°C at 760 mmHg

9℃

1.573

H2O: soluble

-20°C Freezer

6.8X10-8 mm Hg at 25 deg C (est)

Henry's Law constant = 4.35X10-15 atm-cu m/mol at 25 °C (est)

pKa1 = 9.45 (amine); pKa2 = 10.66 (phenol) (est)

166.7 Ų [M+H]+ [CCS Type: TW, Method: Major Mix IMS/Tof Calibration Kit (Waters)]|166.9 Ų [M+H]+

White to off-white powder; soluble in water (pH dependent); log Kow = 0.21 at pH 7.0 /Desvenlafaxine succinate monohydrate/|Hydroxyl radical reaction rate constant = 1.41X10-10 cu cm/molec-sec at 25 °C (est)

UN1230 - class 3 - PG 2 - Methanol, solution

3

11-23/24/25-39/23/24/25-36

7-16-36/37-45-26

GV8872620

F,T,Xi

P210-P260-P280-P301 + P310-P311

H225-H301 + H311 + H331-H370

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.|SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including desvenlafaxine succinate, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Desvenlafaxine succinate/

|Warning|H319 (95.35%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]|P264, P280, P305+P351+P338, and P337+P313|Aggregated GHS information provided by 45 companies from 8 notifications to the ECHA C&L Inventory.

Desvenlafaxine is excreted in breast milk and as a result, nursing mothers must either stop the drug or stop breast feeding depending on the risks and benefit to mother and child.

Liver test abnormalities have been reported to occur in less than 1% of patients on venlafaxine or desvenlafaxine, and elevations are usually modest and usually do not require dose modification or discontinuation. Rare instances of acute, clinically apparent episodes of liver injury with marked liver enzyme elevations with or without jaundice have been reported in patients on both venlafaxine but not desvenlafaxine, perhaps because of less overall use of the more recently approved agent. The onset of injury is usually within 1 to 3 months. The patterns of serum enzyme elevation have varied from cholestatic to hepatocellular. All cases have been self-limiting and resolved within a few months. Autoimmune (autoantibodies) and immunoallergic features (rash, fever, eosinophilia) are uncommon or mild. The estimated frequency is 1 per 5000 patients years of exposure.

Desvenlafaxine does not inhibit or induce the CYP3A4 isoenzyme in vitro. Concurrent administration of desvenlafaxine (400 mg daily; 8 times the recommended dosage) and midazolam (single 4-mg dose), a CYP3A4 substrate, decreased the AUC and peak plasma concentrations of midazolam by approximately 31 and 16%, respectively. The manufacturer states that concurrent use of desvenlafaxine with a drug metabolized by CYP3A4 can result in lower exposures to that drug.|Selective serotonin-reuptake inhibitors (SSRIs) and selective serotonin and norepinephrine reuptake inhibitor (SNRIs), including desvenlafaxine, may increase the risk of bleeding events. Concurrent administration of aspirin, nonsteroidal anti-inflammatory agents, warfarin, and other anticoagulants may add to this risk. Case reports and epidemiologic studies have demonstrated an association between the use of drugs that interfere with serotonin reuptake and the occurrence of GI bleeding. Bleeding events related to SSRI and SNRI use have ranged from ecchymoses, hematomas, epistaxis, and petechiae to life-threatening hemorrhages. The manufacturer recommends that patients be advised of the risk of bleeding associated with the concomitant use of desvenlafaxine and aspirin or other nonsteroidal anti-inflammatory agents, warfarin, or other drugs that affect coagulation or bleeding.|Desvenlafaxine minimally inhibits the cytochrome P-450 (CYP) 2D6 isoenzyme. In a study in healthy adults, concurrent administration of desvenlafaxine (100 mg daily) and desipramine (single 50-mg dose), a CYP2D6 substrate, increased peak plasma concentrations and AUCs of desipramine by approximately 25 and 17%, respectively. The manufacturer states that concomitant use of desvenlafaxine with a drug metabolized by CYP2D6 can result in higher plasma concentrations of that drug.|In a clinical study, desvenlafaxine did not increase impairment of mental and motor skills caused by alcohol. However, the manufacturer recommends avoiding concomitant alcohol consumption during desvenlafaxine therapy.|For more Interactions (Complete) data for Desvenlafaxine (11 total), please visit the HSDB record page.

Increases in blood pressure and small increases in heart rate were reported in clinical studies. Desvenlafaxine has not been systematically evaluated in patients with a recent history of myocardial infarction, unstable cardiovascular disease, uncontrolled hypertension, or cerebrovascular disease; patients with these diagnoses, except for cerebrovascular disease, were excluded from clinical studies. Therefore, the manufacturer advises using desvenlafaxine with caution in patients with cardiovascular, cerebrovascular, or lipid metabolism disorders.|In patients with moderate or severe renal impairment or end-stage renal disease (ESRD) the clearance of Pristiq was decreased, thus prolonging the elimination half-life of the drug. As a result, there were potentially clinically significant increases in exposures to Pristiq. Dosage adjustment (50 mg every other day) is necessary in patients with severe renal impairment or ESRD. The doses should not be escalated in patients with moderate or severe renal impairment or ESRD.|Activation of mania and hypomania reported in approximately 0.1% of desvenlafaxine-treated patients during clinical studies for major depressive disorder and vasomotor symptoms. Use with caution in patients with a personal or family history of mania or hypomania.|Mydriasis has been reported in association with desvenlafaxine therapy. Therefore, patients with elevated intraocular pressure or those at risk of angle-closure glaucoma should be monitored during treatment with the drug.

Protein binding is 30% and this is independent of drug concentration.

Desvenlafaxine's production and use in pharmaceutical formulations(1) may result in its release to the environment through various waste streams(SRC). Desvenlafaxine is the major active metabolite of venlafaxine, a prescribed antidepressant(2).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1700(SRC), determined from a structure estimation method(2), indicates that desvenlafaxine is expected to have low mobility in soil(SRC). Estimated values for pKa1 of 9.45 (amine) and pKa2 of 10.66 (phenol)(3) indicate that this compound will exist almost entirely in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization from moist soil is not expected because the compound exists as an cation and cations do not volatilize. Desvenlafaxine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 6.8X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(5). Biodegradation data in soil were not available(SRC, 2012).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1700(SRC), determined from a structure estimation method(2), indicates that desvenlafaxine is expected to adsorb to suspended solids and sediment(SRC). Estimated values for pKa1 of 9.45 (amine) and pKa2 of 10.66 (phenol)(3) indicate desvenlafaxine will exist almost entirely in the cation form at pH values of 5 to 9 and therefore volatilization from water surfaces is not expected to be an important fate process(SRC). According to a classification scheme(4), an estimated BCF of 24(SRC), from an estimated log Kow of 2.72(5) and a regression-derived equation(6), suggests the potential for bioconcentration in aquatic organisms is moderate(SRC). Biodegradation data in water were not available(SRC, 2012).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), desvenlafaxine, which has an estimated vapor pressure of 6.8X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase desvenlafaxine is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 1 hour(SRC), calculated from its rate constant of 1.4X10-10 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase desvenlafaxine may be removed from the air by wet or dry deposition(SRC). Desvenlafaxine does not contain chromophores that absorb at wavelengths >290 nm(4), and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

The rate constant for the vapor-phase reaction of desvenlafaxine with photochemically-produced hydroxyl radicals has been estimated as 1.4X10-10 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about one hour at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Desvenlafaxine is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Desvenlafaxine does not contain chromophores that absorb at wavelengths >290 nm(2), and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 24 was calculated in fish for desvenlafaxine(SRC), using an estimated log Kow of 2.72(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is moderate(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of desvenlafaxine can be estimated to be 1700(SRC). According to a classification scheme(2), this estimated Koc value suggests that desvenlafaxine is expected to have low mobility in soil. Estimated values for pKa1 of 9.45 (amine) and pKa2 of 10.66 (phenol)(3) indicate that this compound will exist almost entirely in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

Estimated values for pKa1 of 9.45 (amine) and pKa2 of 10.66 (phenol) indicate desvenlafaxine will exist almost entirely in the cation form at pH values of 5 to 9 and therefore volatilization from water and moist soil surfaces is not expected to be an important fate process. Desvenlafaxine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 6.8X10-8 mm Hg(SRC), determined from a fragment constant method(3).

While data specific to desvenlafaxine were not located(SRC, 2012), the literature suggests that some pharmaceutically active compounds originating from human and veterinary therapy are not eliminated completely in municipal sewage treatment plants and are therefore discharged into receiving waters(1). Wastewater treatment processes often were not designed to remove them from the effluent(2). Selected organic waste compounds may be degrading to new and more persistent compounds that may be released instead of or in addition to the parent compound(2).

Women participating in a prospective investigation of perinatal pharmacokinetics from January 2001 through July 2006 who were treated with venlafaxine and who chose to continue venlafaxine during lactation were included in the analysis. Breast milk samples were collected via breast pump from foremilk to hindmilk from a single breast to determine the excretion gradient, and serial samples were collected over 24 hours to determine the time course of excretion. Paired maternal/infant plasma samples were also collected. Venlafaxine and desvenlafaxine concentrations were determined using high-performance liquid chromatography with ultraviolet detection. Statistical analyses of breast milk and infant plasma concentrations and their determinants were conducted. Thirteen women and their nursing infants participated, providing 106 breast milk samples. The mean milk/plasma ratio was 275.3% (95% CI = 144.8% to 405.7%). There were statistically significant time courses of excretion for venlafaxine (R = 0.36, F = 6.82, P < 0.02), desvenlafaxine (R = 0.48, F = 4.41, P < 0.009), and combined venlafaxine/desvenlafaxine (R = 0.51, F = 5.16, P < 0.004), with the highest venlafaxine and desvenlafaxine concentrations in the breast milk occurring 8 hours after maternal ingestion. Infant plasma concentrations for combined venlafaxine/desvenlafaxine were 37.1% of maternal plasma concentrations. The theoretical infant venlafaxine/desvenlafaxine dose was 0.208 mg/kg/d, and the relative infant venlafaxine/desvenlafaxine dose was 8.1%. The theoretical and relative infant doses for desvenlafaxine were 197% and 224% higher, respectively, than those for venlafaxine.|This study characterizes the extent of desvenlafaxine transfer into milk and provides data on infant exposure to desvenlafaxine via breast milk in ten women with postnatal depression and their breastfed infants. Desvenlafaxine concentration in milk and plasma was measured chromatographically in milk and in maternal and infant plasma collected at steady state. Theoretic and relative infant doses via milk were estimated and the per cent drug in infant versus mother's plasma was calculated. Theoretic infant dose via milk was 85 (53-117) ug kg(-1) day(-1) (mean and 95% confidence interval) and relative infant dose was 6.8% (5.5-8.1%). The ratio of drug in infant/maternal plasma also gave an infant exposure estimate of 4.8% (3.5-6.2%) for all ten infants and 5.3% (4.2-5.7%) in the eight infants who were exclusively breastfed. ... The relative infant dose was similar to that for previous studies using venlafaxine and was supported by a separate exposure measure using the ratio of drug in the infant's plasma relative to that in the mother's plasma. The theoretic infant dose of desvenlafaxine was 41-45% of that for venlafaxine and its metabolite desvenlafaxine in previous studies, reflecting the lower recommended maternal dose for desvenlafaxine. ...

Occupational exposure to desvenlafaxine may occur through inhalation and dermal contact with this compound at workplaces where desvenlafaxine is produced or used. Exposure to desvenlafaxine among the general population may be limited to those administered the drug Pristiq, an antidepressant. (SRC)

Desvenlafaxine is indicated for the treatment of major depressive disorder in adults.|FDA Label

Venlafaxine is a serotonin and norepinephrine reuptake inhibitor widely used as an antidepressant. Venlafaxine therapy can be associated with transient asymptomatic elevations in serum aminotransferase levels and has been linked to rare instances of clinically apparent acute liver injury.

Antidepressant Agents

O-Desvenlafaxine has known transformation products that include N,O-Didesvenlafaxine.

Antidepressive Agents; Neurotransmitter Uptake Inhibitors|Used to treat major depressive, generalized anxiety, social anxiety and panic disorders /Desvenlafaxine succinate monohydrate/|Like some other selective serotonin and norepinephrine reuptake inhibitors (SNRIs) and selective serotonin-reuptake inhibitors (SSRIs), desvenlafaxine succinate has been studied for the management of vasomotor symptoms in postmenopausal women. /NOT included in US product labeling/|Desvenlafaxine succinate is used in the treatment of major depressive disorder in adults. /Included in US product labeling/|Recent reviews have questioned whether the serotonin-norepinephrine reuptake inhibitor (SNRI) desvenlafaxine succinate offers any practical clinical advantages over existing SNRIs. The following case is one instance where it appears that this SNRI offers unique safety and benefit. Presented is a case report of a patient with Gilbert's syndrome, longstanding social phobia, and more recent depressive disorder not otherwise specified, who was found to have elevated liver transaminases when prescribed both duloxetine and venlafaxine. The patient subsequently responded to desvenlafaxine but without liver abnormalities. In this patient with Gilbert's Syndrome, desvenlafaxine's lack of metabolism through the cytochrome P450 (CYP) 2D6 pathway may explain the avoidance of these abnormalities and thus suggests a possible therapeutic role for this SNRI in similarly susceptible patients.

/BOXED WARNING/ WARNING: SUICIDAL THOUGHTS AND BEHAVIORS. Antidepressants increased the risk of suicidal thoughts and behavior in children, adolescents, and young adults in short-term studies. These studies did not show an increase in the risk of suicidal thoughts and behavior with antidepressant use in patients over age 24; there was a reduction in risk with antidepressant use in patients aged 65 and older. In patients of all ages who are started on antidepressant therapy, monitor closely for worsening, and for emergence of suicidal thoughts and behaviors. Advise families and caregivers of the need for close observation and communication with the prescriber. Pristiq is not approved for use in pediatric patients.|In patients with moderate or severe renal impairment or end-stage renal disease (ESRD) the clearance of Pristiq was decreased, thus prolonging the elimination half-life of the drug. As a result, there were potentially clinically significant increases in exposures to Pristiq. Dosage adjustment (50 mg every other day) is necessary in patients with severe renal impairment or ESRD. The doses should not be escalated in patients with moderate or severe renal impairment or ESRD.|Sustained increases in blood pressure have been reported. In controlled studies, sustained hypertension occurred in 0.7-2.3% of patients receiving desvenlafaxine dosages from 50-400 mg daily, with a suggestion of a higher incidence (2.3%) in those receiving 400 mg of the drug daily. In addition, some cases of elevated blood pressure requiring immediate treatment have been reported with desvenlafaxine. Sustained blood pressure increases could have adverse consequences in patients receiving the drug. Therefore, the manufacturer recommends that preexisting hypertension be controlled before initiating desvenlafaxine therapy and that regular blood pressure monitoring be performed in patients receiving the drug. Desvenlafaxine should be used cautiously in patients with preexisting hypertension or other underlying conditions that may be compromised by increases in blood pressure. Dosage reduction or drug discontinuance should be considered in patients who experience a sustained increase in blood pressure during therapy.|Treatment with selective serotonin-reuptake inhibitors (SSRIs) and selective serotonin and norepinephrine reuptake inhibitor (SNRIs), including desvenlafaxine, may result in hyponatremia.In many cases, hyponatremia appears to be due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Cases with serum sodium concentrations lower than 110 mmol/L have been reported. Geriatric individuals and patients receiving diuretics or who are otherwise volume depleted may be at greater risk of developing hyponatremia. Signs and symptoms of hyponatremia include headache, difficulty concentrating, memory impairment, confusion, weakness, and unsteadiness, which may lead to falls; more severe and/or acute cases have been associated with hallucinations, syncope, seizures, coma, respiratory arrest, and death. Initiate appropriate medical intervention and consider drug discontinuance in patients with symptomatic hyponatremia.|For more Drug Warnings (Complete) data for Desvenlafaxine (20 total), please visit the HSDB record page.

Desvenlafaxine is a selective serotonin and norepinephrine reuptake inhibitor. It lacks significant activity on muscarinic-cholinergic, H₁-histaminergic, or α₁-adrenergic receptors in vitro. Desvenlafaxine does not appear to exert activity against calcium, chloride, potassium and sodium ion channels and also lacks monoamine oxidase (MAO) inhibitory activity. It was also shown to lack significant activity again the cardiac potassium channel, hERG, in vitro. Compared to other SNRIs, desvenlafaxine undergoes simple metabolism, has a low risk of drug-drug interactions and does not have to be extensively titrated to reach a therapeutic dose.

Drugs that selectively block or suppress the plasma membrane transport of SEROTONIN and NORADRENALINE into axon terminals and are used as ANTIDEPRESSIVE AGENTS. (See all compounds classified as Serotonin and Noradrenaline Reuptake Inhibitors.)|Mood-stimulating drugs used primarily in the treatment of affective disorders and related conditions. Several MONOAMINE OXIDASE INHIBITORS are useful as antidepressants apparently as a long-term consequence of their modulation of catecholamine levels. The tricyclic compounds useful as antidepressive agents (ANTIDEPRESSIVE AGENTS, TRICYCLIC) also appear to act through brain catecholamine systems. A third group (ANTIDEPRESSIVE AGENTS, SECOND-GENERATION) is a diverse group of drugs including some that act specifically on serotonergic systems. (See all compounds classified as Antidepressive Agents.)

Oral bioavailability is approximately 80% and is unaffected by food. Peak plasma concentration is reached in 7.5 hours.|Desvenlafaxine is mainly excreted in the urine. 45% of the dose is unchanged in the urine, 19% is excreted as a glucuronide metabolite, and <5% is excreted as N,O-didesmethylvenlafaxine. No dosage adjustment is necessary for gender, ethnicity, food, or combination with other psychotropics.|3.4L/kg.|The plasma protein binding of desvenlafaxine is low (30%) and is independent of drug concentration. The desvenlafaxine volume of distribution at steady-state following intravenous administration is 3.4 L/kg, indicating distribution into nonvascular compartments.|The absolute oral bioavailability of Pristiq after oral administration is about 80%. Mean time to peak plasma concentrations (Tmax) is about 7.5 hours after oral administration.|Approximately 45% of desvenlafaxine is excreted unchanged in urine at 72 hours after oral administration. Approximately 19% of the administered dose is excreted as the glucuronide metabolite and < 5% as the oxidative metabolite (N,O-didesmethylvenlafaxine) in urine|Desvenlafaxine is excreted into human milk.|For more Absorption, Distribution and Excretion (Complete) data for Desvenlafaxine (6 total), please visit the HSDB record page.

Desvenlafaxine also undergoes oxidative N-demethylation via cytochrome P450 3A4 to a minor extent. CYP2D6 is not involved with the metabolism of desvenlafaxine.|Desvenlafaxine is primarily metabolized by conjugation (mediated by UGT isoforms) and, to a minor extent, through oxidative metabolism. CYP3A4 is the cytochrome P450 isozyme mediating the oxidative metabolism (N-demethylation) of desvenlafaxine. The CYP2D6 metabolic pathway is not involved, and after administration of 100 mg, the pharmacokinetics of desvenlafaxine was similar in subjects with CYP2D6 poor and extensive metabolizer phenotype. ... Approximately 19% of the administered dose is excreted as the glucuronide metabolite and < 5% as the oxidative metabolite (N,O-didesmethylvenlafaxine) in urine

The mean terminal half life is 11.1 hours and may be prolonged in patients with renal and/or moderate to severe hepatic impairment.|The mean half life changed from approximately 10 hours in healthy subjects and subjects with mild hepatic impairment to 13 and 14 hours in moderate and severe hepatic impairment, respectively.|The mean terminal half-life, is approximately 11 hours.

Desvenlafaxine, the active metabolite of venlafaxine, is a selective serotonin and norepinephrine reuptake inhibitor. Desvenlafaxine inhibits neurotransmitter reuptake in serotonin, norepinephrine, and dopamine transporters. Desvenlafaxine inhibits serotonin transporters with 10 times the affinity of norepinephrine transporters, and dopamine transporters with the lowest affinity. In vitro, desvenlafaxine has no inhibition of monoamine oxidase, and almost no affinity for muscarinic, cholinergic, H1-histaminergic, and alpha1-adrenergic receptors.|The exact mechanism of antidepressant action of desvenlafaxine has not been fully elucidated but appears to be associated with the drug's potentiation of serotonergic and noradrenergic activity in the CNS. Like venlafaxine and duloxetine, desvenlafaxine is a potent inhibitor of neuronal serotonin and norepinephrine reuptake; however, inhibition of dopamine reuptake at concentrations that inhibit serotonin and norepinephrine reuptake appears unlikely in most patients. The drug does not inhibit monoamine oxidase (MAO) and has not demonstrated significant affinity for muscarinic cholinergic, H1-histaminergic, alpha1-adrenergic, dopaminergic, gamma-aminobutyric acid (GABA), glutamate, and opiate receptors in vitro.

Treatment should consist of those general measures employed in the management of overdosage with any SSRI/SNRI /selective serotonin-reuptake inhibitor / selective serotonin and norepinephrine reuptake inhibitor/. Ensure an adequate airway, oxygenation, and ventilation. Monitor cardiac rhythm and vital signs. General supportive and symptomatic measures are also recommended. Gastric lavage with a large-bore orogastric tube with appropriate airway protection, if needed, may be indicated if performed soon after ingestion or in symptomatic patients. Activated charcoal should be administered. Induction of emesis is not recommended. Because of the moderate volume of distribution of this drug, forced diuresis, dialysis, hemoperfusion, and exchange transfusion are unlikely to be of benefit. No specific antidotes for desvenlafaxine are known.|/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/|For more Antidote and Emergency Treatment (Complete) data for Desvenlafaxine (8 total), please visit the HSDB record page.

/SIGNS AND SYMPTOMS/ Potential pharmacologic interaction (potentially serious, sometimes fatal serotonin syndrome or Neuroleptic Malignant Syndrome (NMS)-like reactions) if used concurrently with antipsychotic agents or other dopamine antagonists. If serotonin syndrome or NMS signs and symptoms occur, immediately discontinue treatment with desvenlafaxine and any concurrently administered antidopaminergic or serotonergic agents and initiate supportive and symptomatic treatment.|/CASE REPORTS/ A case is presented of the occurrence of an episode of mania apparently induced by desvenlafaxine, in a patient with a history of major depressive disorder and no apparent history of previous mania or hypo-mania. ...|/CASE REPORTS/ A 70-year-old Caucasian male with alcohol and opioid dependence in remission, was started on 50 mg of desvenlafaxine for a moderate depressive episode. After 10 weeks, he developed an ecchymosis of the right upper extremity, in the absence of past or family history of bleeding disorder. He had a prolonged activated partial thromboplastin time (74.5 s) not corrected on performing mixing study, decreased Factor VIII activity (< 1%) and detectable Factor VIII inhibitor (30 Bethesda units) confirming a diagnosis of AHA /acquired hemophilia A/. After all other causes were ruled out, desvenlafaxine was discontinued and the patient was infused with Factor VIIa followed by a 6-week prednisone taper with which he achieved remission.|/OTHER TOXICITY INFORMATION/ Potential pharmacologic interaction (increased risk of bleeding) if used concurrently with aspirin or other nonsteroidal anti-inflammatory agents, warfarin, or other drugs that affect coagulation or bleeding; use with caution. Altered anticoagulant effects, including increased bleeding, have been reported when selective serotonin-reuptake inhibitors (SSRIs) or selective serotonin and norepinephrine reuptake inhibitor (SNRIs) were concurrently administered with warfarin or other anticoagulants. The manufacturer recommends carefully monitoring patients receiving warfarin during initiation and discontinuance of desvenlafaxine therapy.

2-(1-hydroxycyclohexyl)-2-((4-hydroxyphenyl)ethyl)dimethylammonium 3-carboxypropanoate monohydrate

Oral: Tablet, extended-release, film-coated 50 mg (of desvenlafaxine), Pristiq, (Wyeth); 100 mg (of desvenlafaxine), Pristiq, (Wyeth). /Desvenlafaxine succinate/

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Pharmaceuticals -> Nervous System -> Psycholeptics -> Antidepressants -> Transformation products