Abstract

In the early 1970s, evidence of the role of serotonin (5-hydroxytryptamine or 5-HT) in depression began to emerge and the hypothesis that enhancing 5-HT neurotransmission would be a viable mechanism to mediate antidepressant response was put forward. On the basis of this hypothesis, efforts to develop agents that inhibit the uptake of 5-HT from the synaptic cleft were initiated. These studies led to the discovery and development of the selective serotonin-reuptake inhibitor fluoxetine hydrochloride (Prozac; Eli Lilly), which was approved for the treatment of depression by the US FDA in 1987. Here, we summarize this research and discuss the many challenges that we encountered during the development of fluoxetine hydrochloride, which has now been widely acknowledged as a breakthrough drug for depression.

Author affiliations

1. Department of Psychiatry, Indiana University School of Medicine, Indianapolis 46202, USA.
2. Neuroscience Research Division, Lilly Research Laboratories, Eli Lilly and Company, Lilly Corporate Center, Indianapolis 46285, USA.

Correspondence to: David T. Wong¹ Email: dtwongindy@iquest.net

Published online 24 August 2005

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