The antidepressant efficacy of VALDOXAN has been confirmed in four trials versus placebo, three over the short term and one over the long term. The antidepressant efficacy of VALDOXAN is significantly superior to that of placebo, as mentioned in the Valdoxan SPC, whatever the symptom intensity, including the more severely depressed patients.
VALDOXAN demonstrated a significantly higher global clinical improvement compared with venlafaxine as early as the first week, at 6 weeks, and 6 months of treatment (CGI).
VALDOXAN also demonstrated a higher antidepressant efficacy compared with sertraline after 6 weeks of treatment (HAM-D₁₇ and CGI). In particular, Valdoxan’s antidepressant efficacy has been illustrated by a significantly higher responder rate as early as the second week of treatment, as well as in the long term (at 6 months).

The maintenance of antidepressant efficacy was demonstrated in a relapse prevention study. Patients responding to 8 to 10 weeks of acute treatment with open-label Valdoxan 25 to 50 mg once daily were randomized to either Valdoxan 25 to 50 mg once daily or placebo for a further 6 months.
Valdoxan 25-50 mg once daily demonstrated a statistically significant superiority compared with placebo (P=0.0001) on the primary outcome measure, the prevention of depressive relapse, as measured by time to relapse. The incidence of relapse during the 6-month double-blind follow-up period was 22% and 47% for Valdoxan and placebo, respectively.
This long-term antidepressant efficacy of Valdoxan has recently been confirmed over 10 months of treatment.

Mood disorders are closely linked to circadian rhythm disturbances. This is why, unlike healthy subjects, depressed patients present alterations in the circadian pattern of mood.
Another clinical manifestation of circadian rhythm disturbances in depressed patients is sleep- wake disturbances. Your patients often report difficulties in falling asleep, early-morning awakening, and altered quality of sleep.
All these complaints from your depressed patients concern core symptoms of depression. The restoration of disturbed circadian rhythms is an innovative approach in depression treatment.
Through the results of clinical trials, VALDOXAN has demonstrated that its innovative approach offers significant antidepressant efficacy, also demonstrated in more severely depressed patients.

Valdoxan’s mode of action is totally innovative. VALDOXAN is an agonist at MT₁ and MT₂ melatonergic receptors and an antagonist at 5-HT_2c receptors.
Valdoxan has no affinity for other receptors, no effect on monoamine uptake, and no influence on extracellular levels of serotonin.
Thanks to its unique receptor profile, VALDOXAN resynchronizes circadian rhythms and offers a significant antidepressant efficacy also demonstrated in more severely depressed patients.

VALDOXAN is a first in its class. Indeed, it is the first melatonergic antidepressant: Valdoxan is both a melatonergic agonist (MT₁ and MT₂ receptors) and an antagonist at 5-HT_2c receptors.
Thanks to its unique receptor profile, Valdoxan resynchronizes circadian rhythms and therefore represents a major innovation in depression treatment, and offers a significant antidepressant efficacy also demonstrated in more severely depressed patients.

VALDOXAN is very well tolerated. The most common adverse reactions are nausea and dizziness. Adverse reactions are usually mild or moderate and occur within the first 2 weeks of treatment.
These adverse reactions are usually transient and do not generally lead to cessation of therapy.

No. Because VALDOXAN has no interactions with α-2 adrenergic or cholinergic receptors, there are no changes in biological and cardiovascular parameters during short-term and long-term treatment with VALDOXAN.
Valdoxan had no effects on heart rate and blood pressure in clinical studies. Therefore no precaution is necessary with prescription of VALDOXAN.

As with any psychotropic drug, clinical and neurological examinations should be carried out to confirm the diagnosis of depression, and laboratory test should be performed to monitor the treatment.
Because an elevation in transaminases has been observed with an incidence of 1.1% for Valdoxan compared with 0.7% for placebo, transaminases tests should be performed in all patients: at initiation of treatment, and then periodically after around 6 weeks (end of acute phase), 12 weeks, and 24 weeks (end of maintenance phase), and thereafter, when clinically indicated.

Any patient who develops increased serum transaminases should have his/her liver function tests repeated within 48 hours.
Then, if the increase in ASAT and/or ALAT exceeds 3 ULN, Valdoxan therapy should be discontinued and laboratory tests should be performed regularly until serum transaminases return to normal values.
In any case, the decision to continue blood sample monitoring should be defined based on the patient’s clinical picture.
In clinical studies, elevations of serum transaminases (>3 times the upper limit of the normal range) have been particularly observed in patients treated with Valdoxan at the dose of 50 mg. When Valdoxan was discontinued in these patients, the serum transaminases usually returned to normal levels.

Clinical trials have shown that the therapeutic dosage of VALDOXAN for most patients is one tablet of 25 mg once daily at bedtime.
The recommended dose is 25 mg once daily taken orally at bedtime. In the rare cases of no improvement of symptoms after 2 weeks of treatment, the dose may be increased to two 25 mg tablets taken together at bedtime.

VALDOXAN has to be taken in a daily single dose at bedtime to maximize the agonist effect on melatonergic receptors.
VALDOXAN is an agonist at MT₁ and MT₂ melatonergic receptors and an antagonist at 5-HT_2c receptors. Thanks to its unique receptor profile, VALDOXAN resynchronizes circadian rhythms, and offers a significant antidepressant efficacy also demonstrated in more severely depressed patients.

The recommended duration of treatment with VALDOXAN is at least 6 months to ensure that patients are free of symptoms.