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Fluoxetine Versus Fluoxetine Plus DU125530 in Major Depressive Disorder

This study has been terminated.
(interim analysis suggested no differences with whole sample)
Sponsor:
Information provided by:
Fundació Institut de Recerca de l'Hospital de la Santa Creu i Sant Pau
ClinicalTrials.gov Identifier:
NCT01119430
First received: May 6, 2010
Last updated: NA
Last verified: May 2010
History: No changes posted
  Purpose

The purpose of this study is to examine whether the speed of the clinical antidepressant action of fluoxetine can be accelerated by administering DU125530 a full 5-HT1A antagonist.


Condition Intervention Phase
Major Depression
 Drug: DU125530
Drug: Placebo
 Phase 2

Study Type: Interventional
Study Design: Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor)
Primary Purpose: Treatment
Official Title: Fluoxetine Versus Fluoxetine Plus DU125530 in Latency of Antidepressant Response Shortening in Major Depressive Disorder

Resource links provided by NLM:

U.S. FDA Resources

Further study details as provided by Fundació Institut de Recerca de l'Hospital de la Santa Creu i Sant Pau:

Primary Outcome Measures:
  • Scores on Hamilton Depression Rating Scale [ Time Frame: 8 time points through 8 weeks ] [ Designated as safety issue: No ]

Enrollment: 50
Study Start Date: May 2004
Study Completion Date: November 2007
Primary Completion Date: November 2007 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
Placebo Comparator: Fluoxetine plus placebo Drug: Placebo
Similar pill as active comparator twice a day
Other Name: Fluoxetine+placebo
Active Comparator: Fluoxetine plus DU125530 Drug: DU125530
20mg/twice a day
Other Name: Fluoxetine+DU

Detailed Description:

SSRI acts by blocking the serotonin transporter (5-HT), increasing the availability of serotonin at the synaptic cleft averting its reuptake. The increment of serotonin activates 5-HT1A presynaptic autoreceptors, resulting in a modulation in the release of serotonin by the presynaptic neuron. It is proposed that 5-HT1A receptor antagonism could accelerate the clinical effect of antidepressants by preventing this negative feedback.Preclinical data obtained with selective 5-HT1A antagonists, such as pindolol, and with mice lacking 5-HT1a receptors supports this hypothesis. Results on partial antagonists (pindolol) are conclusive in accelerating SSRI. It is reasonable to call into question whether a total antagonism of 5-HT1a receptors could imply a more rapid antidepressant response. To test this hypothesis we conducted a double blind, randomised, controlled trial with DU 123550 added to fluoxetine 20 mg/day

  Eligibility

Ages Eligible for Study:   18 Years to 70 Years
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Criteria

Inclusion Criteria:

  • Consecutive eligible patients aged 18 to 70
  • Diagnosis of unipolar major depression using DSM-IV criteria with moderate to severe symptoms (score e 18 on the Hamilton Depression Rating Scale-HDRS- of 17 items).
  • There was a wash-out of 1 week of any antidepressant drug (specifically 28 days for fluoxetine) prior entering the study.
  • Written informed consent was obtained from all participants.

Exclusion Criteria:

  • Concurrent psychiatric disorders (DSM IV axis I, II cluster A or B)
  • Failure to respond to drug treatment in current depressive episode
  • Previous resistance to SSRIs or other antidepressant drug
  • Suicide risk score e 3 on the HDRS.
  • Participation in other drug trials within the previous month
  • Presence of delusions or hallucinations
  • History of substance abuse (including alcohol) in the past three months
  • Pregnancy or lactation
  • Organic brain disease or history of seizures
  • Serious organic illnesses such as hypo or hyperthyroidism,cardiac arrhythmias, asthma, diabetes mellitus.
  • Myocardial infarction in the past 6 month
  • Frequent or severe allergic reactions
  • Concomitant use of other psychotropic drugs (benzodiazepines were allowed), lockers or catecholamine-depleting agents
  • Current structured psychotherapy.
  Contacts and Locations
Please refer to this study by its ClinicalTrials.gov identifier: NCT01119430

Locations
Spain
Hospital de Sant Pau
Barcelona, Spain, 08027
Sponsors and Collaborators
Fundació Institut de Recerca de l'Hospital de la Santa Creu i Sant Pau
Investigators
Principal Investigator: Victor Pérez, MD, PhD Psychiatrist, Hospital de Sant Pau
Principal Investigator: Enric Álvarez, MD, PhD Head of Departement, Psiquiatria, Hospital de Sant Pau
Study Chair: Dolors Puigdemont, MD Psychiatrist, Hospital de Sant Pau
Study Director: Josefina Pérez, MD Psychiatrist, Hospital de Sant Pau
  More Information

No publications provided

Responsible Party: Fundació Institut de Recerca de l'Hospital de la Santa Creu i Sant Pau
ClinicalTrials.gov Identifier: NCT01119430     History of Changes
Other Study ID Numbers: HSP-2003-01
Study First Received: May 6, 2010
Last Updated: May 6, 2010
Health Authority: Spain: Spanish Agency of Medicines

Keywords provided by Fundació Institut de Recerca de l'Hospital de la Santa Creu i Sant Pau:
major depression
DU 125530
Treatment depression
Latency antidepressant

Additional relevant MeSH terms:
Depression
Depressive Disorder
Depressive Disorder, Major
Behavioral Symptoms
Mood Disorders
Mental Disorders
Antidepressive Agents
Fluoxetine
Psychotropic Drugs
Central Nervous System Agents
 Therapeutic Uses
Pharmacologic Actions
Serotonin Uptake Inhibitors
Neurotransmitter Uptake Inhibitors
Neurotransmitter Agents
Molecular Mechanisms of Pharmacological Action
Serotonin Agents
Physiological Effects of Drugs
Antidepressive Agents, Second-Generation

ClinicalTrials.gov processed this record on May 16, 2013