Serotonin-norepinephrine reuptake inhibitor ( SNRIs ) is a class of antidepressant drugs that treat major depressive disorders (MDDs) and can also treat anxiety disorders, obsessive-compulsive disorder (OCD), attention hyperactivity disorder (ADHD), chronic neuropathic pain, fibromyalgia syndrome (FMS), and menopausal symptoms.
SNRI is a monoamine reuptake inhibitor; In particular, they inhibit reuptake of serotonin and norepinephrine. These neurotransmitters play an important role in mood. SNRI can be contrasted with the more widely used selective serotonin reuptake inhibitor (SSRI), which works only on serotonin.
The human serotonin transporter (SERT) and norepinephrine (NET) transporter is a membrane transport protein responsible for reuptake of serotonin and norepinephrine. The double inhibition of serotonin and norepinephrine reuptake can offer advantages over other antidepressant drugs by treating a wider variety of symptoms.
SNRI, along with selective serotonin reuptake inhibitors (SSRIs) and norepinephrine reuptake inhibitors (NRIs), are second generation antidepressants. Over the past two decades, second generation antidepressants have gradually replaced first generation antidepressants, such as tricyclic antidepressants (TCA) and monoamine oxidase inhibitors (MAOIs), as the drug of choice for MDD treatment because of better tolerability and safety. Profile.
A closely related type of drug is a serotonin-norepinephrine release agent (SNRA), for example the appetite suppressant of phenfluramine/phentermine (Fen-Phen) appetite. SNRAs primarily induce release rather than inhibit reuptake of serotonin and norepinephrine.
Video Serotonin-norepinephrine reuptake inhibitor
Type
- Atomoxetine - a dominant norepinephrine SNRI used in the treatment of ADHD and, off-label, severe depression. Approved by the FDA in 2002. It was initially thought of as a selective norepinephrine reuptake inhibitor, but later studies revealed that it significantly inhibited serotonin reuptake in clinical doses as well.
- Desvenlafaxine - active metabolite of venlafaxine. It is believed to work in the same way, although some evidence suggests a lower response rate than venlafaxine and duloxetine. Introduced by Wyeth in May 2008 and later became the third approved SNRI. Duloxetine was approved for the treatment of depression and neuropathic pain in August 2004. Duloxetine is contraindicated in patients with heavy alcohol use or chronic liver disease, as duloxetine may increase certain liver enzyme levels that may cause acute hepatitis or other diseases in at-risk patients certain. Currently, the risk of liver damage appears to be only for already at risk patients, unlike the antidepressant nefazodon, which, although rare, can spontaneously cause liver failure in healthy patients. Duloxetine is also approved for major depressive disorder (MDD), generalized anxiety disorder (GAD), diabetic neuropathy, chronic musculoskeletal pain, including chronic osteoarthritis pain and low chronic low back pain.
- Levomilnacipran - levorotating milnaciprane isomers. In the development for the treatment of depression in the United States and Canada, it was approved by the FDA for the treatment of MDD in July 2013.
- Milnacipran - proven to be very effective in the treatment of depression and fibromyalgia. The Food and Drug Administration (FDA) approved a milnacipran for the treatment of fibromyalgia in the United States in January 2009, but is currently not approved for depression in the country. Milnacipran has been commercially available in Europe and Asia for several years. It was first introduced in France in 1996.
- Sibutramine - a SNRI, which, instead of being developed for the treatment of depression, is widely marketed as an appetite suppressant for weight loss purposes. Sibutramine is the first drug for obesity treatment approved in 30 years. This has been associated with increased cardiovascular events and stroke and has been withdrawn from markets in several countries and regions including the United States in 2010.
- Weak tramadol - opioid and SNRI. It was approved by the FDA in 1995, although it has been marketed in Germany since 1977. It is used to treat acute and chronic pain. This has shown effectiveness in the treatment of fibromyalgia, although not specifically approved for this purpose. The drug is also being investigated as an antidepressant and for the treatment of neuropathic pain. This is related in chemical structure to venlafaxine.
- Venlafaxine - the first and most commonly used SNRI. It was introduced by Wyeth in 1994. The reuptake effect of venlafaxine is dose-dependent. At low doses (& lt; 150 mg/day), it only works on serotonergic transmission. In moderate doses (& gt; 150mg/day), it acts on the serotonergic and noradrenergic system, whereas at high doses (& gt; 300 mg/day), it also affects the dopaminergic neurotransmission.
Maps Serotonin-norepinephrine reuptake inhibitor
History
In 1952, iproniazid, an antimicrobacterial agent, was found to have psychoactive properties while being investigated as a possible treatment for tuberculosis. Researchers noted that patients given iproniazid become cheerful, more optimistic, and more physically active. Immediately after its development, iproniazide and related substances are shown to slow the enzymatic breakdown of serotonin, dopamine, and norepinephrine by inhibition of the monoamine oxidase enzyme. For this reason, this class of drugs is known as monoamine oxidase inhibitors, or MAOIs. During this time the development of different antidepressant agents was also investigated. Imipramine is the most clinically useful tricyclic antidepressant (TCA). Imipramine is found to affect many neurotransmitter systems and to block the reuptake of norepinephrine and serotonin from synapses, thereby increasing the levels of these neurotransmitters. The use of MAOI and TCA provides great advances in the treatment of depression but its use is limited by unpleasant side effects and significant safety and toxicity issues.
Throughout the 1960s and 1970s, the hypothesis of the catecholamine hypothesis and its association with depression was of widespread interest and that decreased levels of certain neurotransmitters, such as norepinephrine, serotonin, and dopamine may play a role in the pathogenesis of depression. This led to the development of fluoxetine, the first SSRI. The enhanced safety and tolerability profile of SSRIs in patients with MDD, compared with TCA and MAOI, represents another significant advance in the treatment of depression.
Since the late 1980s, SSRIs have dominated the antidepressant drug market. Currently, there is an increased interest in antidepressant drugs with a broader mechanism of action that can offer fewer efficacy and side effects. In 1993, a new drug was introduced to the US market called venlafaxine, a reuptake inhibitor of serotonin-norepinephrine. Venlafaxine is the first compound described in a new class of antidepressive agents called phenylethylamines. These substances are not associated with other TCAs and SSRIs. Venlafaxine blocks the reuptake of neuronal serotonin, noradrenaline, and, to a lesser extent, dopamine in the central nervous system. In contrast to some other antidepressant drugs, venlafaxine can cause rapid onset mainly due to subsequent inhibition of norepinephrine reuptake. See the timeline in Figure 1.
Action mechanism
Monoamines are linked to the pathophysiology of depression. Symptoms occur because the concentration of neurotransmitters, such as norepinephrine and serotonin, is insufficient. Drugs for depression affect the transmission of serotonin, norepinephrine, and dopamine. Older and less selective antidepressants such as TCA and MAOI inhibit reuptake or norepinephrine and serotonin metabolism in the brain, resulting in higher concentrations of neurotransmitters. Antidepressants that have double action mechanisms inhibit reuptake of serotonin and norepinephrine and, in some cases, inhibit with the weak effects of dopamine reuptake. Antidepressants affect variable neuronal receptors such as muscarinic-cholinergic ,? 1 - and? 2 -adrenergic, and H - histopathic receptors, and sodium channels in the heart muscle, leading to decreased cardiac conduction and cardiotoxicity. The selectivity of antidepressant agents is based on neurotransmitters that are thought to affect the symptoms of depression. Drugs that selectively block reuptake of serotonin and norepinephrine effectively treat depression and are better tolerated than TCA. TCA has a comprehensive effect on various neurotransmitter receptors, leading to a lack of tolerability and increased risk of toxicity. Tricyclic antidepressants
TCA is the first drug to have multiple action mechanisms. The mechanism of action of secondary tricyclic amidum antidepressants is only partially understood. TCA has a dual inhibitory effect on the reuptake of the norepinephrine transporter and the serotonin reuptake transporter. Increased norepinephrine and serotonin concentrations are obtained by inhibiting these two carrier proteins. TCA has a much greater affinity for the norepinephrine reuptake protein than the SSRI. This is due to the formation of a secondary amine metabolite TCA.
In addition, TCA interacts with adrenergic receptors. This interaction appears to be important for the increased availability of norepinephrine at or near the synaptic cleft. Tricyclic antidepressant measures such as imipramine have complex, secondary adaptations for initial and ongoing action as norepinephrine transport inhibitors and variable blockade of serotonin transport. Norepinephrine interacts with postsinaps? and? subtypes of adrenergic and presinaptic receptors? 2 autoreceptors. The receptor " 2 includes presinaptic autoreceptors that limit neurofisiologic neuron noradrenergic activity in the central nervous system.The formation of norepinephrine is reduced by autoreptor by enzyme that limits the rate of tyrosine hydroxylase, the effect mediated by decreased activation of cyclic AMP-mediated enzyme phosphorylation. 2 receptors also cause decreased intracellular cyclic AMP expression resulting in smooth muscle relaxation or decreased secretion.TCA activates a negative feedback mechanism by its effect on presinaptic receptors One possible explanation for the effect on decreasing the release of neurotransmitters is that, when the receptor activates, inhibition of neurotransmitter release occurs (including voltage-gated suppression of Ca 2 current and activation of protein-coupled-G receptors operates current K ). this leads to inhibition of the release of neurotransmitters, but p repeated TCA bills eventually cause a decrease in response by the 2 receptor. Desensitization of this response may be due to increased endogenous norepinephrine exposure or from prolonged occupation of the norepinephrine transport mechanism (via allosteric effects). Adaptation allows the synthesis of presynaptic and norepinephrine secretions to return to, or even exceed, the normal level of norepinephrine in the synaptic cleft. Overall, inhibition of norepinephrine-induced reuptake by TCA results in decreased firing rates of neurons (mediated via 2 autoreceptors), metabolic activity, and neurotransmitter release.
TCA does not block dopamine transport directly, but it can facilitate dopaminergic effects indirectly by inhibiting dopamine transport to the noradrenergic terminal of the cerebral cortex. Because they affect so many different receptors, TCA has adverse effects, poor tolerability, and an increased risk of toxicity.
Selective serotonin reuptake inhibitor
Selective Serotonin Reuptake Inhibitors (SSRIs) selectively inhibit serotonin reuptake and are a widely used group of antidepressants. With increased receptor selectivity compared to TCA, undesirable effects such as poor tolerability are avoided. Serotonin is synthesized from an amino acid called L -tryptophan. The active transport system regulates the absorption of tryptophan in the blood-brain barrier. Serotonergic pathways are classified into two main ways in the brain; the projection rises from the medial and dorsal rapia as well as the decreased projection of the caudal raphe to the spinal cord.
Selective norepinephrine reuptake inhibitor
Noradrenergic neurons are located in two major regions of the brain. These areas are locus coeruleus and lateral tegmental. With selective NRI administration, neuronal activity in the koeruleus locus region is induced by increased norepinephrine concentrations in the synaptic cleft. This results in activation of adrenergic receptors? 2 , as discussed earlier.
Test has shown that selective NRI has an insignificant tendency for mACh ,? 1 and? 2 adrenergic, or H 1 receptor.
Dual serotonin and norepinephrine reuptake inhibitor
Agents with double serotonin and inhibition of norepinephrine reuptake (SNRI) are sometimes called non-tricyclic serotonin and norepinephrine reuptake inhibitors. Clinical studies show that compounds that increase concentrations in the synaptic cleft of both norepinephrine and serotonin are more successful than single acting agents in the treatment of depression. Double reuptake inhibitors have a low affinity in neuronal receptors from other neurotransmitters, which have a low side effect compared to TCA. Nontricyclic antidepressants have increased potential and accelerated action of onset in antidepressant response than SSRI alone, suggesting that synergism is an efficient property in mediating antidepressant activity.
The non-tricyclic SNRIs have several important differences based on pharmacokinetics, metabolism for active metabolites, inhibition of CYP isoforms, drug-drug interaction effects, and the beak of nontricyclic SNRI.
The combination of action mechanisms in a single active agent is an important development in psychopharmacology. Aryloxypropanamine scaffold
Some reuptake inhibitors contain aryloxypropanamine scaffolds. This structural motif has a high affinity bond potential for biogenic amine transport. Drugs containing aryloxypropanamine scaffolds have a selectivity profile for norepinephrine and serotonin transporters that depend on the aryloxy ring substitution pattern. Selective NRI contains the substituent in position 2 'of the aryloxy ring but the SSRI contains a substituent in position 4' of the aryloxy ring. Atomoxetine, nisoxetine and reboxetine all have substitution groups in position 2 'and are selective NRIs while compounds with substitution groups in positions 4' (such as fluoxetine and paroxetine) are SSRIs. Duloxetine contains a phenyl group attached at the 2 'and 3' positions, therefore it has a selective inhibition effect of the norepinephrine reagent and serotonin double and has the same potential for both transporters. The nature of the aromatic substituent also has a significant effect on the activity and selectivity of the compound as a serotonin inhibitor or norepinephrine transporter.
Cycloalkanol ethylamine scaffold
Venlafaxine and desvenlafaxine contain the cycloalkanol ethylamine scaffold. Increasing the electron withdrawal properties of the aromatic ring provides a stronger inhibitory effect of norepinephrine uptake and increases the selectivity for norepinephrine above the serotonin transporter. The effect of substitution of chloro, methoxy and trifluoromethyl in cycloalkanol ethylamine scaffold aromatic ring was tested. The results indicate that the strongest electron withdrawal m -trifluoromethyl shows the strongest inhibitory effect of norepinephrine and the highest selectivity of serotonin uptake. WY-46824, a strain containing piperazine, has shown inhibition of norepinephrine reuptake and dopamine. Further synthesis and testing identify WAY-256805, a powerful norepinephrine reuptake inhibitor that exhibits excellent and efficacious selectivity in animal models of depression, pain, and thermoregulation dysfunction.
Milnacipran
Milnacipran is structurally different from other SNRIs. The milnacipran derivative SAR at the transporter level is still unclear and based on in vivo efficacy reported in 1987. N -methylation of milnacipran in the substituent group R 4 and R 5 reduces the activity of norepinephrine and serotonin. Research on different secondary amides in the substitution group R 6 and R 7 show it? electrons play an important role in the interaction between the carrier and the ligand. A phenyl group in the substituent R 6 shows the effect on the norepinephrine transporter. Substituent groups in R 6 and R 7 with double allic binding showed significant improvement effects on norepinephrine and serotonin transporters. Studies show that introducing 2-methyl groups in the substituent R 3 , the potential of norepinephrine and serotonin transporters is almost eliminated. The methyl group in the substituent group R 1 and R 2 also abolished the potential of norepinephrine and serotonin transporters. The researchers found that replacing one of the milnacipran ethyl groups with one part alil increased the potency of norepinephrine. Farmakofora milnacipran derivatives remains unclear.
Milnacipran conformation is an important part of pharmacofores. Changing SAR in milnacipran alters the stereochemistry of the compound and affects the concentrations of norepinephrine and serotonin. Milnacipran is marketed as a racemic mixture. The milnacipran effect is in (1 S , 2 R ) - the isomers and substitutions of the phenyl group in (1 S , 2 R ) - isomers have a negative impact on norepinephrine concentration. Milnacipran has low molecular weight and low lipophilicity. Because of these traits, milnacipran represents the ideal pharmacokinetics in humans such as high bioavailability, low inter-subject variability, limited liver enzyme interactions, moderate tissue distribution and long elimination half-life. The lack of interaction of Milnacipran drugs through the P450 cytochrome enzyme is considered to be an attractive feature since many central nervous system drugs are highly lipophilic and are primarily eliminated by liver enzymes.
Future SAR development
The application of aryloxypropanamine scaffolds has resulted in a number of powerful MAOIs. Prior to the development of duloxetine, the exploration of aryloxypropanamine SAR resulted in the identification of fluoxetine and atomoxetine. The same motif can be found in reboxetine where it is limited in the morfoline ring system. Several studies have been conducted in which oxygen in reboxetine is replaced by sulfur to produce arytitiomethyl morphol. Some arylthiomethyl morpholine derivatives maintain a potent level of serotonin and inhibition of norepinephrine reuptake. Inhibition of serotonin and double norepinephrine reuptake resides in different enantiomers for the arylthiomethyl morpholine scaffold. Possible drug candidates with serotonin and norepinephrine reuptake inhibitory activity have also been derived from piperazine, 3-amino-pyrrolidine and benzylamine templates.
Clinical test
Several studies have shown that antidepressant drugs that combine serotonergic and noradrenergic activity are generally more effective than SSRIs, which act on serotonin reuptake by themselves. Serotonergic-noradrenergic antidepressant drugs may have a modest efficacy advantage compared with SSRIs in treating major depressive disorder (MDD), but slightly less well tolerated. Further research is needed to examine the possible efficacy differences in specific MDD subpopulations or for specific MDD symptoms, among these antidepressant drug classes.
Data from clinical trials show that SNRI may have pain-relieving properties. Although the perception and transmission of excitatory pain in the central nervous system has not been fully explained, extensive data support the role of serotonin and norepinephrine in pain modulation. Findings from human clinical trials have shown these antidepressants can reduce pain and functional impairment in conditions of central and neuropathic pain. This SNRI properties can be used to reduce the dosage of other painkillers and decrease the frequency of safety, limited efficacy and tolerability issues. Clinical research data have been shown in patients with GAD that duloxetine SNRI is significantly more effective than placebo in relieving symptoms associated with GAD pain, after short and long term treatment. However, the findings indicate that such physical pain symptoms reoccur in a relapse situation, which indicates the need for ongoing care in patients with GAD and painful physical symptoms simultaneously.
Indication
SNRI has been approved for the treatment of the following conditions:
- Major depressive disorder (MDD)
- Posttraumatic stress disorder (PTSD)
- Generalized anxiety disorder (GAD)
- Social anxiety disorder (SAD)
- Panic disorder
- Neuropathic pain
- Fibromyalgia
- Chronic musculoskeletal pain
Pharmacology
Administrative route
SNRI is delivered orally, usually in capsule form. The drugs themselves are usually a fine crystalline powder that diffuses into the body during digestion.
Dose
The dose fluctuates depending on the SNRI used because of the various potential drugs as well as some strengths for each drug.
Action mode
A condition most of which is indicated by SNRI, major depressive disorder, is thought to be primarily due to a decrease in serotonin and norepinephrine levels in the synaptic cleft, which causes erratic signals. Because of the hypothesis of monoamine depression, which confirms that decreased concentrations of monoamine neurotransmitters lead to depressive symptoms, the following relationships are determined: "Norepinephrine may be related to alertness and energy and anxiety, attention, and interest in life; [lack of serotonin to anxiety, obsessions, and compulsions; and dopamine to attention, motivation, pleasure, and appreciation, and interest in life. "SNRI works by inhibiting the reuptake of serotonin neurotransmitters and norepinephrine. This results in increased concentrations of extracellular serotonin and norepinephrine and, therefore, an increase in neurotransmission. Most SNRIs include venlafaxine, desvenlafaxine, and duloxetine, several times more selective for serotonin than norepinephrine, while milnacipran is three times more selective for norepinephrine than serotonin. Increased norepinephrine levels are considered necessary for antidepressants to be effective against neuropathic pain, a property shared with older tricyclic antidepressants (TCA), but not with SSRIs.
Recent studies have shown that depression may be associated with increased inflammatory responses, so efforts to find additional mechanisms for SNRI have been made. Studies have shown that SNRI and SSRI have significant anti-inflammatory action on microglia in addition to its effect on serotonin and norepinephrine levels. Thus, it is possible that the additional mechanisms of these drugs that act in combination with previously understood mechanisms exist. The implications behind these findings suggest the use of SNRI as a potential anti-inflammation after a brain injury or another disease in which brain swelling is a problem. Regardless of the mechanism, however, the efficacy of these drugs in treating the disease that has been indicated has been proven, both clinically and in practice.
Pharmacodynamics
Most SNRIs function with primary metabolites and secondary metabolites to inhibit reuptake of serotonin, norepinepherine, and the amount of marginal dopamine. For example, venlafaxine works in addition to its primary metabolite O -desmethylvenlafaxine to greatly inhibit serotonin and norepinephrine reuptake in the brain. The evidence also suggests that dopamine and norepinepherine behave in a mode of transport, due to the inactivation of dopamine by norepinephrine reuptake in the frontal cortex, an area of ​​the brain that is severely lacking in dopamine transport. This SNRI effect results in increased dopamine neurotransmission, in addition to increased serotonin and norepinephrine activity. Furthermore, since SNRIs are highly selective, they have no measurable effects on other unwanted receptors, in contrast to monoamine oxidase inhibition. Pharmaceutical tests have determined that the use of SNRI or SSRI can produce significant anti-inflammatory action in microglia as well.
Activity profile
Pharmacokinetics
The normal half-life of the SNRI is 5 hours, with the patient achieving peak efficacy ~ 4 hours after consumption.
Contraindications
Due to the effect of increased norepinephrine levels and, therefore, higher noradrenergic activity, pre-existing hypertension should be controlled before treatment with SNRI and blood pressure is regularly monitored during treatment. Duloxetine has also been associated with cases of liver failure and should not be prescribed for patients with chronic alcohol use or liver disease. Patients suffering from coronary artery disease should avoid using SNRI. In addition, due to some SNRI measures on obesity, patients with major eating disorders such as anorexia nervosa or bulimia should not be prescribed SNRI. Duloxetine and milnaciprane are also contraindicated in patients with uncontrolled narrow-angle glaucoma, as they have been shown to increase the incidence of midriasis.
SNRI should be taken with caution when using St. John's Wort, because the combination can cause a fatal serotonin syndrome. There is also a significant risk when combining SNRI with dextromethorphan, tramadol, cyclobenzaprine, meperidine/pethidine, and propoxyphene. They should not be taken within 24 hours of other antidepressants, especially with monoamine oxidase inhibitors (MAOIs), as a combination of SNRI with MAOIs can cause hyperthermia, rigidity, myoclonus, autonomic instability with vital signs fluctuations, and mental status changes that include extreme agitation developed into delirium and coma.
Side effects
Because SNRI and SSRIs act in the same way to increase serotonin levels, they share many side effects, albeit to varying degrees. The most common side effects include loss of appetite, weight, and sleep, drowsiness, dizziness, fatigue, headache, increased suicidal thoughts, nausea/vomiting, sexual dysfunction, and urinary retention. There are two common sexual side effects: decreased sex interest (libido) and difficulty reaching climax (anorgasmia), which is usually milder with SNRI than with SSRIs. Increased levels of norepinephrine can sometimes cause anxiety, a slightly elevated beat, and an increase in blood pressure. However, the selective norepinephrine antidepressants, such as reboxetine and desipramine, have successfully treated anxiety disorders. People at risk of developing hypertension and heart disease should monitor their blood pressure.
Precautions
Starting the SNRI regimen
Due to the extreme changes in noradrenergic activity resulting from inhibition of norepinephrine reuptake and serotonin, patients who are just starting the SNRI regimen are usually given a lower dose than the expected final dose to allow the body to adjust to the effects of the drug. When the patient continues to walk with low doses without side effects, the dose increases gradually until the patient sees symptomatic improvement without adverse side effects.
Termination syndrome
Like SSRIs, the sudden termination of SNRI usually leads to withdrawal, or "termination syndrome", which may include anxiety and other symptoms. Therefore, it is recommended that users seeking to stop the SNRI slowly reduce the dose under the supervision of a professional. The cessation syndrome has been reported to be very poor for venlafaxine when compared with other SNRIs. Thus, as tramadol is associated with venlafaxine, the same conditions apply. This may be because the half-life is relatively short and therefore clearance is fast at the time of termination.
Overdose
Cause
Overdose in SNRI can be caused by a combination of drugs or an excessive amount of the drug itself. Venlafaxine is slightly more toxic in overdose than duloxetine or SSRI.
Symptoms
Symptoms of an overdose of SNRI, whether mixed or drug-only interactions, vary in intensity and occurrence based on the amount of drug taken and the individual's sensitivity to the treatment of SNRI. Possible symptoms include:
- Somnolen
- Comes
- Serotonin syndrome
- Seizures
- Sync
- Tachycardia
- Hypotension
- Hypertension
- Hyperthermia
- Vomit
Management
Overdose is usually treated symptomatically, especially in the case of serotonin syndrome, which requires treatment with ciproheptadine and temperature control based on the development of serotonin toxicity. Patients are often monitored for vital signs and cleared airways to ensure that they receive adequate oxygen levels. Another option is to use activated carbon in the digestive tract to absorb excess neurotransmitters. It is important to consider drug interactions when dealing with overdosed patients, as separate symptoms may appear.
Comparison with SSRI
Since SNRI is developed more recently than SSRIs, there are relatively few of them. However, SNRI is one of the most widely used antidepressants today. In 2009, Cymbalta and Effexor were the 11th and 12th most-prescribed brand drugs in the United States. This translates to the most common 2 and 3 common antidepressants, behind Lexapro (# 5), escitalopram SSRI. In some studies, SNRI showed slightly higher antidepressant efficacy than SSRIs (response rate 63.6% versus 59.3%). However, in one study, escitalopram had a superior efficacy profile for venlafaxine.
See also
- Monoamine reuptake inhibitor
References
Source of the article : Wikipedia
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