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Desvenlafaxine | CAS No: 93413-62-8 | GMP-certified suppliers
A medication that treats major depressive disorder in adults by restoring neurotransmitter balance through serotonin and norepinephrine reuptake inhibition, with low potential for drug interactions.
Therapeutic categories
Primary indications
- Desvenlafaxine is indicated for the treatment of major depressive disorder in adults
- It has also been used off-label to treat hot flashes in menopausal women
Product Snapshot
- Desvenlafaxine is available as oral extended-release tablets and capsules
- It is primarily indicated for treating major depressive disorder in adults
- The product is approved and marketed in key regulatory regions including the US and Canada
Clinical Overview
Pharmacologically, desvenlafaxine selectively inhibits the reuptake of serotonin and norepinephrine, with approximately tenfold greater affinity for serotonin transporters relative to norepinephrine transporters. Dopamine transporter inhibition is minimal by comparison. The compound does not exhibit significant activity at muscarinic-cholinergic, histaminergic H1, or alpha-1 adrenergic receptors, nor does it inhibit monoamine oxidase. It also shows no relevant interactions with cardiac ion channels including hERG and does not produce QT interval prolongation based on clinical electrocardiographic data.
Following oral administration, desvenlafaxine undergoes conjugation primarily via UDP-glucuronosyltransferases (UGT) rather than metabolism by cytochrome P450 enzymes, notably CYP2D6, reducing its potential for drug-drug interactions compared to venlafaxine. The drug is mainly eliminated renally. Safety profiles have been generally consistent with those observed for other SNRIs, with considerations including the risk for serotonergic syndrome and potential to increase heart rate. Off-label uses, such as management of menopausal hot flashes, have been reported but are not formally approved indications.
Desvenlafaxine is sourced as a cyclohexanol derivative with specific stereochemistry and purity standards critical for pharmaceutical formulation. Quality control measures in API procurement should focus on confirming identity, assay, impurity profile, and compliance with regulatory guidelines to ensure consistent pharmacological activity and safety. Given its metabolic pathway, attention to potential conjugation-related impurities and solvent residues is also recommended.
Identification & chemistry
| Generic name | Desvenlafaxine |
|---|---|
| Molecule type | Small molecule |
| CAS | 93413-62-8 |
| UNII | NG99554ANW |
| DrugBank ID | DB06700 |
Pharmacology
| Summary | Desvenlafaxine is a selective serotonin and norepinephrine reuptake inhibitor (SNRI) primarily targeting sodium-dependent serotonin and norepinephrine transporters, with lower affinity for dopamine transporters. Its antidepressant effects are attributed to potentiation of serotonin and norepinephrine neurotransmission in the central nervous system. Desvenlafaxine lacks significant activity at muscarinic, histaminergic, adrenergic receptors, ion channels, and monoamine oxidase enzymes. |
|---|---|
| Mechanism of action | The exact mechanism of the antidepressant action of desvenlafaxine is unknown but is thought to be related to the potentiation of serotonin and norepinephrine in the central nervous system, through inhibition of their reuptake. Particularly, desvenlafaxine has been found to inhibit the serotonin, norepinephrine, and dopamine transporters with varying degrees of affinity. Desvenlafaxine inhibits serotonin transporters with 10 times the affinity of norepinephrine transporters, and dopamine transporters with the lowest affinity. |
| Pharmacodynamics | Desvenlafaxine is a selective serotonin and norepinephrine reuptake inhibitor. It lacks significant activity on muscarinic-cholinergic, H<sub>1</sub>-histaminergic, or α<sub>1</sub>-adrenergic receptors <i>in vitro</i>, or inhibitory activity against monoamine oxidase. 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 against the cardiac potassium channel, hERG, <i>in vitro</i>. Electrocardiograms were obtained from 1,492 desvenlafaxine treated patients with major depressive disorder and 984 placebo-treated patients in clinical studies lasting up to 8 weeks. No clinically relevant differences were observed between desvenlafaxine treated and placebo-treated patients for QT, QTc, PR, and QRS intervals. In a thorough QTc study with prospectively determined criteria, desvenlafaxine did not cause QT prolongation. No difference was observed between placebo and desvenlafaxine treatments for the QRS interval. |
Targets
| Target | Organism | Actions |
|---|---|---|
| Sodium-dependent noradrenaline transporter | Humans | inhibitor |
| Sodium-dependent serotonin transporter | Humans | inhibitor |
| Sodium-dependent dopamine transporter | Humans | inhibitor |
ADME / PK
| Absorption | The absolute oral bioavailability of desvenlafaxine after oral administration is about 80%. The time to reach maximal concentration (T<sub>max</sub>) is estimated to be 7.5 hours after oral administration. The AUC in a 24 h dosing interval at steady state with a 100 mg dose was also calculated to be 6747 ng*h/mL, and the C<sub>max</sub> 376 ng/mL. Ingestion of a high-fat meal (800 to 1000 calories) increased desvenlafaxine C<sub>max</sub> about 16% and had no effect on AUC. |
|---|---|
| Half-life | The mean terminal half-life is 11.1 hours and may be prolonged in patients with renal and/or moderate to severe hepatic impairment. |
| Protein binding | The plasma protein binding of desvenlafaxine is 30% and is independent of drug concentration. |
| Metabolism | Desvenlafaxine is primarily metabolized by conjugation (mediated by UGT isoforms) and, to a minor extent, through oxidative metabolism. O-glucuronide conjugation is likely be catalyzed by UGT1A1, UGT1A3, UGT2B4, UGT2B15, and UGT2B17. CYP3A4 and potentially CYP2C19 mediates the oxidative metabolism (N-demethylation) of desvenlafaxine to N,O-didesmethyl venlafaxine. The CYP2D6 metabolic pathway is not involved. The pharmacokinetics of desvenlafaxine was similar in subjects with CYP2D6 poor and extensive metabolizer phenotype. |
| Route of elimination | Desvenlafaxine is mainly excreted in the urine. 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-didesmethyl venlafaxine) in urine. |
| Volume of distribution | The steady-state volume of distribution of desvenlafaxine is 3.4 L/kg. |
| Clearance | Following the administration of 100 mg of desvenlafaxine in healthy subjects from 18 to 45 years of age, the renal clearance was calculated to be 222 ± 82 mL/min. |
Formulation & handling
- Desvenlafaxine is a small molecule oral API formulated predominantly as extended-release tablets and capsules.
- It exhibits moderate water solubility and lipophilicity (LogP 2.29), supporting sustained-release oral delivery.
- The API absorption is not affected by food, but co-administration with alcohol and St. John's Wort should be avoided.
Regulatory status
| Lifecycle | The active pharmaceutical ingredient (API) has patent protections in Canada and the United States that expired between February and March 2022, with an additional patent in the US valid until July 2027. This indicates early to mid-stage market maturity in these regions. |
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| Markets | Canada, US |
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Supply Chain
| Supply chain summary | Desvenlafaxine is marketed primarily in North American markets, including Canada and the US, with multiple branded product variants available. The presence of several patents, some expiring in early 2022 and others extending to mid-2027, indicates both existing and potential upcoming opportunities for generic competition. Originator companies play a key role in maintaining branded product exclusivity within these regions. |
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Safety
| Toxicity | Published epidemiological studies of pregnant women exposed to the parent compound venlafaxine have not reported a clear association with major birth defects or miscarriage. Methodological limitations of these observational studies include possible exposure and outcome misclassification, lack of adequate controls, adjustment for confounders, and confirmatory studies; therefore, these studies cannot establish or exclude any drug-associated risk during pregnancy. Retrospective cohort studies based on claims data have shown an association between venlafaxine use and preeclampsia, compared to depressed women who did not take an antidepressant during pregnancy. One study that assessed venlafaxine exposure in the second trimester or first half of the third trimester and preeclampsia showed an increased risk compared to unexposed depressed women (adjusted (adj) RR 1.57, 95% CI 1.29 to 1.91). Preeclampsia was observed at venlafaxine doses equal to or greater than 75 mg/day and a duration of treatment >30 days. Another study that assessed venlafaxine exposure in gestational weeks 10 to 20 and preeclampsia showed an increased risk at doses equal to or greater than 150 mg/day. Available data are limited by possible outcome misclassification and possible confounding due to depression severity and other confounders. Retrospective cohort studies based on claims data have suggested an association between venlafaxine use near the time of delivery or through delivery and postpartum hemorrhage. One study showed an increased risk for postpartum hemorrhage when venlafaxine exposure occurred through delivery, compared to unexposed depressed women (adj RR 2.24, 95% CI 1.69 to 2.97). There was no increased risk in women who were exposed to venlafaxine earlier in pregnancy. Limitations of this study include possible confounding due to depression severity and other confounders. Another study showed an increased risk for postpartum hemorrhage when SNRI exposure occurred for at least 15 days in the last month of pregnancy or through delivery, compared to unexposed women (adj RR 1.64 to 1.76). The results of this study may be confounded by the effects of depression. Neonates exposed to SNRIs or SSRIs, late in the third trimester have developed complications requiring prolonged hospitalization, respiratory support, and tube feeding. Such complications can arise immediately upon delivery. Reported clinical findings have included respiratory distress, cyanosis, apnea, seizures, temperature instability, feeding difficulty, vomiting, hypoglycemia, hypotonia, hypertonia, hyperreflexia, tremor, jitteriness, irritability, and constant crying. These features are consistent with either a direct toxic effect of SSRIs and SNRIs or, possibly, a drug discontinuation syndrome. It should be noted that, in some cases, the clinical picture is consistent with serotonin syndrome. Antidepressants, such as desvenlafaxine, increase the risk of suicidal thoughts and behaviors in pediatric patient. Of the 4,158 patients in pre-marketing clinical studies with desvenlafaxine, 6% were 65 years of age or older. No overall differences in safety or efficacy were observed between these patients and younger patients; however, in the short-term placebo-controlled studies, there was a higher incidence of systolic orthostatic hypotension in patients ≥65 years of age compared to patients <65 years of age treated with desvenlafaxine. For elderly patients, possible reduced renal clearance of desvenlafaxine should be considered when determining dose. SSRIs and SNRIs, including desvenlafaxine, have been associated with cases of clinically significant hyponatremia in elderly patients, who may be at greater risk for this adverse event. There is limited clinical trial experience with desvenlafaxine succinate overdosage in humans. However, desvenlafaxine is the major active metabolite of venlafaxine. Overdose experience reported with venlafaxine (the parent drug of desvenlafaxine) is presented below; the identical information can be found in the Overdosage section of the venlafaxine package insert. In post-marketing experience, overdose with venlafaxine (the parent drug of desvenlafaxine) has occurred predominantly in combination with alcohol and/or other drugs. The most commonly reported events in overdosage include tachycardia, changes in level of consciousness (ranging from somnolence to coma), mydriasis, seizures, and vomiting. Electrocardiogram changes (e.g., prolongation of QT interval, bundle branch block, QRS prolongation), sinus and ventricular tachycardia, bradycardia, hypotension, rhabdomyolysis, vertigo, liver necrosis, serotonin syndrome, and death have been reported. Published retrospective studies report that venlafaxine overdosage may be associated with an increased risk of fatal outcomes compared to that observed with SSRI antidepressant products, but lower than that for tricyclic antidepressants. Epidemiological studies have shown that venlafaxine-treated patients have a higher pre-existing burden of suicide risk factors than SSRI-treated patients. The extent to which the finding of an increased risk of fatal outcomes can be attributed to the toxicity of venlafaxine in overdosage, as opposed to some characteristic(s) of venlafaxine-treated patients, is not clear. No specific antidotes for desvenlafaxine are known. In managing over dosage, consider the possibility of multiple drug involvement. In case of overdose, call Poison Control Center at 1-800-222-1222 for latest recommendations. Desvenlafaxine succinate administered by oral gavage to mice and rats for 2 years did not increase the incidence of tumors in either study. Mice received desvenlafaxine succinate at dosages up to 500/300 mg/kg/day (dosage lowered after 45 weeks of dosing). The AUC exposure at 300 mg/kg/day dose is estimated at 10 times the AUC exposure at an adult human dose of 100 mg per day. Rats received desvenlafaxine succinate at dosages up to 300 mg/kg/day (males) or 500 mg/kg/day (females). The AUC exposure at the highest dose is estimated at 11 (males) or 26 (females) times the AUC exposure at an adult human dose of 100 mg per day. Desvenlafaxine was not mutagenic in the in vitro bacterial mutation assay (Ames test) and was not clastogenic in an in vitro chromosome aberration assay in cultured CHO cells, an in vivo mouse micronucleus assay, or an in vivo chromosome aberration assay in rats. Additionally, desvenlafaxine was not genotoxic in the in vitro CHO mammalian cell forward mutation assay and was negative in the in vitro BALB/c-3T3 mouse embryo cell transformation assay. When desvenlafaxine succinate was administered orally to male and female rats, fertility was reduced at the high dose of 300 mg/kg/day, which is 10 (males) and 19 (females) times the AUC exposure at an adult human dose of 100 mg per day. There was no effect on fertility at 100 mg/kg/day, which is 3 (males) or 5 (females) times the AUC exposure at an adult human dose of 100 mg per day. These studies did not address reversibility of the effect on fertility. The relevance of these findings to humans is not known. |
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- Overdose may result in cardiovascular and neurological toxicity including tachycardia, seizures, QT interval prolongation, and altered consciousness
- No specific antidote is available
Desvenlafaxine is a type of Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs)
Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs) belong to a vital subcategory of pharmaceutical active pharmaceutical ingredients (APIs) that have gained significant popularity in the treatment of various medical conditions. SNRIs work by modulating the levels of two essential neurotransmitters in the brain, namely serotonin and norepinephrine.
These APIs are commonly prescribed for managing a range of mental health disorders, including depression, anxiety disorders, and certain chronic pain conditions. By inhibiting the reuptake of serotonin and norepinephrine, SNRIs enhance their availability in the brain, leading to improved mood, increased energy levels, and reduced pain perception.
SNRIs exhibit a unique dual mechanism of action, making them distinct from other classes of antidepressant medications. By targeting both serotonin and norepinephrine reuptake, SNRIs provide a broader spectrum of therapeutic effects, making them effective in treating patients who do not respond well to other medications.
Due to their widespread usage and effectiveness, SNRIs have become a preferred choice for healthcare professionals. Some commonly prescribed SNRIs include duloxetine, venlafaxine, and desvenlafaxine. These APIs are typically available in oral formulations and are well-tolerated by most patients, with a favorable side effect profile.
In summary, SNRIs represent a significant subcategory of pharmaceutical APIs that play a crucial role in the management of mental health disorders and chronic pain conditions. Their unique dual mechanism of action and effectiveness make them a valuable treatment option for healthcare providers, ensuring improved patient outcomes and quality of life.
Desvenlafaxine (Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs)), classified under Antidepressants
Antidepressants are a category of pharmaceutical Active Pharmaceutical Ingredients (APIs) widely used in the treatment of depression and other mood disorders. These medications work by balancing the levels of certain chemicals in the brain called neurotransmitters, such as serotonin, norepinephrine, and dopamine.
There are several types of antidepressants available, each with its own mechanism of action and efficacy. Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed as a first-line treatment for depression. They prevent the reabsorption of serotonin, resulting in increased serotonin levels in the brain. Examples of popular SSRIs include fluoxetine, sertraline, and escitalopram.
Tricyclic antidepressants (TCAs) are another class of antidepressants that work by blocking the reuptake of both serotonin and norepinephrine. They are generally used when SSRIs are ineffective or not well-tolerated. Amitriptyline, nortriptyline, and imipramine are commonly prescribed TCAs.
Other antidepressants include serotonin-norepinephrine reuptake inhibitors (SNRIs), atypical antidepressants, and monoamine oxidase inhibitors (MAOIs). SNRIs, such as venlafaxine and duloxetine, inhibit the reuptake of both serotonin and norepinephrine. Atypical antidepressants, including bupropion and mirtazapine, have diverse mechanisms of action, targeting multiple neurotransmitters. MAOIs, such as phenelzine and tranylcypromine, work by inhibiting the enzyme monoamine oxidase, which breaks down neurotransmitters.
It is important to note that antidepressants may have various side effects and require close monitoring by healthcare professionals. Dosages and treatment duration vary based on individual needs and response. Antidepressants are typically prescribed as part of a comprehensive treatment plan that may include psychotherapy and lifestyle modifications.
In conclusion, antidepressants are a vital category of pharmaceutical APIs used to manage depression and related mood disorders. They act on neurotransmitters in the brain to alleviate symptoms and improve overall well-being. It is crucial to consult with a healthcare provider to determine the most suitable antidepressant and monitor its effects.
Desvenlafaxine API manufacturers & distributors
Compare qualified Desvenlafaxine API suppliers worldwide. We currently have 7 companies offering Desvenlafaxine API, with manufacturing taking place in 1 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| Atilus Pharma | Producer | India | India | BSE/TSE, CEP, CoA, FDA, GMP, HALAL, Kosher, MSDS | 11 products |
| Global Pharma Tek | Distributor | India | India | BSE/TSE, CoA, FDA, GMP, ISO9001, MSDS | 484 products |
| Gonane Pharma | Producer | India | India | BSE/TSE, CoA, GMP, MSDS | 166 products |
| Lupin | Producer | India | India | CoA, GMP, USDMF, WC | 155 products |
| MSN Life Sciences | Producer | India | India | CoA, USDMF, WC | 46 products |
| Mylan | Producer | India | India | CoA, GMP, WC | 201 products |
| Sun Pharma | Producer | India | India | CoA, USDMF | 219 products |
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