• Embed Doc
  • Readcast
  • Collections
  • CommentGo Back
Download
 
Page 1AgomelatineJune 2009London New Drugs Group APC/DTC
Briefing
 
T
HIS
 
IS
 
AN
NHS
DOCUMENT
 
NOT
 
TO
 
BE
 
USED
 
FOR
 
COMMERCIAL
 
AND
 
MARKETING
 
PURPOSES
.P
RODUCED
 
TO
 
INFORM
 
LOCAL
 
DECISION
-
MAKING
 
USING
 
THE
 
BEST
 
AVAILABLE
 
EVIDENCE
 
AT
 
THE
 
TIME
 
OF
 
PUBLICATION
.
June 2009
A
GOMELATINE
 
SummaryThe drug and the review
Agomelatine is a new antidepressant with selective agonist actions at mela-tonin receptors and selective antagonist action at serotonin 5HT-2C recep-tors. It does not affect the uptake of serotonin, noradrenaline or dopa-mine.
Agomelatine was launched in the UK in June 2009.
This review evaluates the evidence supporting agomelatine use in adultswith major depressive episodes and seeks to define agomelatine’s potentialplace in therapy.
Background
NICE Guidance (2004 and draft update 2009) recommends an SSRI antide-pressant (e.g. generic fluoxetine or citalopram) first-line for patients withmoderate to severe depression.
Following first-line treatment failure the evidence for sequencing antide-pressants is inconclusive, choice should therefore be based on the needs of the patient, the profile of the drug and financial considerations.
New NICE Guidelines on the treatment of depression in adults are antici-pated in September 2009.
Literature searched
We searched: Medline (agomelatine.af [Limit to: Humans and English Lan-guage]); Embase (agomelatine.af [Limit to: Human and English Language]and [DEPRESSION/dt [Drug Therapy] or *MAJOR DEPRESSION/dt [DrugTherapy]]); and IDIS ("AGOMELATINE 28160472").
This was supplemented with information from the EMEA website (PublicAssessment Report), NICE guidance, and contact with the manufacturerServier Laboratories.
The study programme was extensive:
1 short-term placebo-controlled dose ranging study (8 weeks)
2 short-term placebo-controlled studies (6 weeks with optional exten-sion for a further 46 weeks)
3 short –term placebo-controlled studies with paroxetine or fluoxetineactive controls (6 weeks and optional extension to 6 months)
2 long-term relapse prevention studies.
1 study vs. venlafaxine (6 weeks with optional extension to 6 months),primary endpoint sleep, secondary endpoint efficacy
1 study vs. venlafaxine (12 weeks with optional extension to 6months), primary endpoint sexual function, secondary endpoint effi-cacy
Contents
Summary 1Background 5Safety 6Efficacy studies 7Short term studies 9Short term studies withactive controls 12Long term/ preventionof relapse 13Absence of discontinuationsymptoms 14Sexual dysfunction 15Sleep disorders 17Rating scales and Sleepassessments 19Cost per 100,000population 20References 21Appendices 24
 
T
HIS
 
IS
 
AN
NHS
DOCUMENT
 
NOT
 
TO
 
BE
 
USED
 
FOR
 
COMMERCIAL
 
AND
 
MARKETING
 
PURPOSES
.P
RODUCED
 
TO
 
INFORM
 
LOCAL
 
DECISION
-
MAKING
 
USING
 
THE
 
BEST
 
AVAILABLE
 
EVIDENCE
 
AT
 
THE
 
TIME
 
OF
 
PUBLICATION
.
London New Drugs Group
APC/DTC Briefing Document
Produced for the
London New Drugs Groupby:
Alexandra Denby,Regional MI ManagerMedicines Information ServiceNorthwick Park HospitalMiddlesexHA1 3UJTel: 020 8869 3551Med.info@nwlh.nhs.ukFurther copies of this documentare available from URL:www.nelm.nhs.uk
 
 
Page 2AgomelatineJune 2009London New Drugs Group APC/DTC
Briefing
 
T
HIS
 
IS
 
AN
NHS
DOCUMENT
 
NOT
 
TO
 
BE
 
USED
 
FOR
 
COMMERCIAL
 
AND
 
MARKETING
 
PURPOSES
.P
RODUCED
 
TO
 
INFORM
 
LOCAL
 
DECISION
-
MAKING
 
USING
 
THE
 
BEST
 
AVAILABLE
 
EVIDENCE
 
AT
 
THE
 
TIME
 
OF
 
PUBLICATION
.
1 study vs. sertraline (6 weeks with extension to 6 months), primary endpoint actigraphy,secondary endpoint efficacy
1 open study in patients with major depressive disorder (6 weeks) looking at the effect onsleep EEG
1 study vs. fluoxetine in patients with severe depression (8 weeks with optional extension to6 months)
1 study on sexual disturbance vs. paroxetine.
Efficacy studies
Antidepressant efficacy is generally determined from 6–8 week RCTs comparing responseagainst placebo or active comparators, or 6–10 month RCTs comparing relapse rate against pla-cebo; depression symptoms are evaluated using rating scales.
All analyses were carried out in the intention-to-treat populations: i.e. analysis was performedaccording to the assigned treatment group regardless of protocol deviations and participantcompliance or withdrawal.
Short-term placebo-controlled
A dose-ranging study (n=711) identified agomelatine 25mg daily as the target dose when com-pared with agomelatine 1mg and 5mg daily
In two 6 week placebo controlled RCTs patients with a HAMD score
22 [moderate to severedepression] were randomised to either agomelatine (25mg initial for 2 weeks increased to50mg in non-responders) or placebo; primary endpoint was mean final HAMD score.
In the first study, 212 patients received agomelatine (n=106) or placebo (n=105). Forthe ITT population the between group difference for the mean final HAMD scores was2.30 (S.E. 1.02), p=0.026.
In the second study, 238 patients received agomelatine (n=118) or placebo (n=120).For the ITT population the between group difference for the mean final HAMD scores was3.44 (S.E. 0.92), p<0.001
3 unpublished placebo-controlled studies in which paroxetine or fluoxetine were used as activecontrols to validate the study design are reported in the EMEA public assessment report (EPAR).The efficacy of agomelatine was not directly compared to that of the active controls.
All 3 studies enrolled patients with moderate to severe depression [HAMD
22] and fol-lowed similar methodologies: initial run-in followed by randomisation to agomelatine,placebo, or active control for 6 weeks with subsequent 18 week extensions.
The option to increase the agomelatine dose from 25mg to 50mg was not included inthese studies.
The primary endpoint of difference in HAMD was compared between active control andplacebo, and between agomelatine and placebo. For the first trial, a statistically signifi-cant difference (
p
=0.008) was seen between active control and placebo at 6 weeks forreduction in HAMD score versus placebo, but not for agomelatine and placebo; Neitherthe second nor third trial showed statistically significant differences between agomelatineor the active control and placebo for any comparison at either 6 or 24 weeks, meaningthat no discernable results could be drawn from these studies. A meta-analysis of agomelatine trials shows that 23.5% of patients require a 50mg dose, which is a reasonwhy agomelatine may have failed to differentiate from placebo in the first study. Thesecond and third studies were associated with high placebo response rates.
Active comparator studies
A 6 week study randomised 313 patients with a HAMD score
22 to agomelatine 25–50mg(n=154) or sertraline 50–100mg (n=159) [for each drug the lower initial dose was increasedafter 2 weeks for non-improved patients]. The primary endpoint of the study was the efficacyon rest-activity circadian rhythms. For the secondary endpoint of an improvement in HAMDscore, the difference in scores after 6 weeks was 1.68, in favour of agomelatine (p=0.031).
There were two studies in patients with moderate to severe depression in which agomelatinewas compared with venlafaxine.
 
Page 3AgomelatineJune 2009London New Drugs Group APC/DTC
Briefing
 
T
HIS
 
IS
 
AN
NHS
DOCUMENT
 
NOT
 
TO
 
BE
 
USED
 
FOR
 
COMMERCIAL
 
AND
 
MARKETING
 
PURPOSES
.P
RODUCED
 
TO
 
INFORM
 
LOCAL
 
DECISION
-
MAKING
 
USING
 
THE
 
BEST
 
AVAILABLE
 
EVIDENCE
 
AT
 
THE
 
TIME
 
OF
 
PUBLICATION
.
In the 12 week study patients were randomised to agomelatine 50mg (n=137) or venla-faxine 150mg (n=140). The primary endpoint of the study was deterioration in sexual func-tion and demonstrated statistically significant differences in favour of agomelatine versusvenlafaxine. For the secondary endpoint of the final MADRS score, agomelatine was shownto be at least as effective as venlafaxine (10.1 vs. 9.8).
In the 6 week study patients were randomised to either agomelatine (n=165) or venlafaxine(n=167). The primary endpoint was the effects on sleep variables and demonstrated statis-tically significant differences in favour of agomelatine versus venlafaxine; final HAMD scorewas the secondary endpoint. The final HAMD scores were similar between the groups, indi-cating similar efficacy for agomelatine and venlafaxine (9.9 vs. 11.0).
A 8 week study randomised 500 outpatients with HAMD score
25 and CGI severity of illness score
4 (severely depressed) to agomelatine 25-50mg (n=247) or fluoxetine 20-40mg (n=257) [foragomelatine the initial lower dose was increased at 2 weeks in non-improved patients, for fluoxet-ine the initial lower dose was increased at 4 weeks]. The primary endpoint was improvement inHAMD score from baseline, the difference in scores at week 8 was 1.49, 95% CI=[0.20;2.77](p=0.024) in favour of agomelatine.
Long-term relapse-prevention
Relapse is classified as the appearance of the symptoms of the index episode soon after medica-tion is stopped, whilst recurrence is the appearance of symptoms in a new episode. Relapse indi-cates that the treatment duration was too short.
A study reported in the EPAR had an 8-week open label phase (n=610) during which response toagomelatine was determined, followed by a 26-week double-blind randomised phase (n=367;agomelatine 25mg, n=187; placebo, n=180).
At the end of the 26 week double-blind phase, a significant effect was not demonstrated forthe primary endpoint of relapse (agomelatine 25.9% vs. placebo 23.5%). The placebo re-lapse rate in this trial was unexpectedly low (approximately half that seen in other studies of similar design). This may be reflective of some methodological aspects e.g. the broad rangeof the severity of depression of patients at inclusion.
169 severely depressed patients (n=89 agomelatine, n=80 placebo) (HAMD >25 and CGI-S
5) continued in an 18 week extension; at the end of this extension there was a statisticallysignificant difference in favour of agomelatine (21.3% vs. 31.3%) p=0.046.
A second (published) study, that included a high proportion of patients with moderate to severedepression reflecting the types of patient generally seen by psychiatrists, had an 8-10 week open-label dose determination phase (n=492) followed by a 24 week double-blind phase (n=390)
For the primary endpoint of relapse, results at 24 weeks were significantly lower (p=0.0001)for agomelatine (21.7%) than for placebo (46.6%); agomelatine reduced relapse risk by54% (HR 0.458; 95% CI 0.305–0.60).
190 patients (n=106 agomelatine, n=84 placebo) continued in double-blind 20 week exten-sion. A statistically significant difference in the time to relapse was detected: at 10 monthstwice as many patients treated with placebo relapsed (49.9%) compared to those treatedwith agomelatine (23.9%) (p<0.0001).
The three short term studies with active controls all had 18 week extensions. In one study therelapse rates were lower with agomelatine (14.3%) and fluoxetine (17.8%) than with placebo(33.3%), p=0.017 and p=0.045 respectively. In the other 2 studies there were no differencesseen between agomelatine or active control and placebo which means no discernable results couldbe drawn.
Safety
Agomelatine does not cause weight gain, has a low risk of sexual dysfunction, low incidence of gastro-intestinal reactions, absence of discontinuation symptoms, no sedation or daytime drowsi-ness and an overall incidence rate of adverse events that is similar to placebo.
Emergent elevations of liver transaminase enzymes more than 3x upper limit of normal (3x ULN)occur rarely (approx. 1% of patients). Overall incidences of elevations >3xULN in all patients (i.e.regardless of their transaminase values at baseline) were 1.1% with agomelatine 25mg and0.72% with placebo (p=not significant). The 0.4% absolute difference with placebo compares to a
of 00

Leave a Comment

You must be to leave a comment.
Submit
Characters: ...
You must be to leave a comment.
Submit
Characters: ...