Antidepressant —vilazodone
As many as one in five people will be affected by depression at some point. It has many causes, with contributing factors including brain chemistry, social environment and inherited genes. The drugs available for treating depression operate by trying to restore the balance of contributing chemicals in the brain to more normal levels, notably serotonin, noradrenaline and dopamine.
Early antidepressants have significant side-effects, and so more modern categories of drugs such as selective serotonin reuptake inhibitors (SSRIs) were developed, and the search for further compounds of this class is continuing apace, particularly for drugs that have a more rapid effect. It is believed that selective agonism of post-synaptic 5-HT1A receptors will lead to faster acting drugs. Onset should be quicker because the drugs may not suppress the initial firing activity of 5-HT neurons, making for a much faster increase in neurotransmission.1 The search for these compounds continues, but one that has some of this activity, vilazodone, is a partial agonist at the 5-HT1A receptor and may prove to be more effective than current antidepressant therapies.
Discovered by Merck KGaA and licensed to GlaxoSmithKline, vilazodone is currently in Phase II trials. Positron emission tomography has been used to prove that it acts at the 5-HT1A receptors.2 A randomised, double-blind, placebo-controlled crossover study in 10 healthy males looked at how 20mg of vilazodone affected sleep EEGs. It gave a significant suppression in both the duration and density of REM sleep, and this led to the conclusion that it could have desensitised pre-synaptic 5-HT1A receptors, as well as post-synaptic 5-HT2 receptors, while leaving the function of 5-HT1A unaffected.3
Phase II trials on vilazodone are continuing, it could well prove to be a good antidepressant treatment with fewer side-effects than current options.