Nefazodone

Nefazodone hydrochloride (trade name Serzone) is an antidepressant drug marketed by Bristol-Myers Squibb. Its sale was discontinued in 2003 in some countries, due to the small possibility of hepatic (liver) injury, which could lead to the need for a liver transplant, or even death. The incidence of severe liver damage is approximately one in 250,000 to 300,000 patient-years.^[1] On May 20, 2004, Bristol-Myers Squibb discontinued the sale of Serzone in the United States. Several generic formulations of nefazodone are still available.^[2][3]

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Structure and mode of action

Nefazodone is most closely related to trazodone (trade name Desyrel). Nefazodone is not considered to be an SSRI, MAOI or tricyclic antidepressant. It is not chemically related to either bupropion/amfebutamone or venlafaxine.

It operates by blocking post-synaptic serotonin type-2_A receptors and, to a lesser extent, by inhibiting pre-synaptic serotonin and norepinephrine (noradrenaline) reuptake. Nefazodone is also a relatively potent alpha-1 adrenoceptor antagonist.^[4]

Dosing

Nefazodone doses for adults typically start at 50 mg twice daily uptitrated by 100 mg/day per week to a maximum of 600 mg (300 mg twice daily), according to Food and Drug Administration (FDA) regulations. Some patients with severe depression were treated with more than 600 mg/day. Most patients were treated with 300 mg–600 mg daily.

Side effects

Unlike most other SNRIs and SSRIs, Nefazodone has no negative effects on libido or sexual functioning, and is actually sometimes used as an antidote to SSRI induced impotence and anorgasmia in men.^[5]

Advantages

Nefazodone's claimed advantages over other antidepressants include reduced possibility of disturbed sleep or sexual dysfunction, and ability to treat some patients who did not respond to other antidepressant drugs.

Notes

1. ^ Rxlist.com: "Nefazodone Prescribing Information", accessed 8 January 2007.]
2. ^ FDA Orange Book, accessed 15 January 2006.
3. ^ About.com: "Serzone Pulled from U.S. Market", accessed 15 January 2006.
4. ^ Sanchez, C; J. Hyttel (1999). "Comparison of the Effects of Antidepressants and Their Metabolites on Reuptake of Biogenic Amines and on Receptor Binding". Celular and Molecular Neurobiology 19 (4): 467-89.
5. ^ [1]