This review highlights recent pharmacological and clinical advances in the understanding of the potential use of serotonin 5-HT2receptor antagonists as treatments for a number of psychiatric disorders, namely anxiety, depression and schizophrenia.5-HT2receptor antagonists have not yet been clearly demonstrated to be effective in humans as treatments for anxiety. Some preliminary clinical trials suggest that the 5-HT2receptor antagonist ritanserin may have a beneficial effect in patients with generalised anxiety disorder, but the evidence is far from compelling.Upregulation of central 5-HT2receptors and an accompanying increase in phosphoinositide turnover appear to be predisposing biological factors in depression. A functional interaction between 5-HT1Aand 5-HT2receptors may be of particular importance, since 5-HT2receptor antagonism can ultimately result in a facilitation of 5-HT1Areceptor-mediated neurotransmission and this may be beneficial for the treatment of depression. Ritanserin appears to be more effective than placebo in alleviating the depressive symptoms of dysthymia. Nefazodone is a new antidepressant that combines 5-HT2receptor blockade with serotonin reuptake inhibition. Comparisons with imipramine favour nefazodone in terms of tolerability and suggest that both drugs are equally clinical effective.In schizophrenia, 5-HT2Areceptor function appears to be altered. Modulation of dopaminergic function via 5-HT2Areceptors may provide a viable mechanism for enhancing the effect of antipsychotics. Risperidone, the first post-clozapine agent that has 5-HT2Aand dopamine D2receptor antagonist actions, is at least as effective as haloperidol and perphenazine in reducing acute psychotic symptoms. Its major clinical advantages are a greater efficacy in controlling the secondary negative symptoms and a lower incidence of extrapyramidal symptoms (EPS). The efficacy of ritanserin in alleviating both positive and negative symptoms in acutely psychotic patients seems to support the hypothesis that potent 5-HT2Areceptor antagonism alone may contribute to the therapeutic action of several clinically effective antipsychotics that have reduced liability to induce EPS.