Activity profile<unk>  acts as a full agonist in the frontal cortex and the raphe dorsalis, but only as a partial agonist in the CA3 region of the hippocampus of the 5-HT1A receptor (serotonin receptor) (Ki = 1 nM in cells, but only 15–50 nM in cortex, hippocampus and dorsal raphe) and, with lower affinity, as an antagonist of the 5-HT2A receptor (Ki = 49 nM) and antagonist or very weak partial agonist of the D4 receptor (Ki = 4–24 nM). Despite the much greater affinity of<unk>  for the 5-HT1A receptor, and for reasons that are unknown (although it might be caused by the competition with endogenous serotonin),<unk>  occupies the 5-HT1A and 5-HT2A receptors in vivo with similar percentages.<unk>  also has low affinity for the 5-HT2B receptor (Ki = 89.3 nM) and the 5-HT2C receptor (Ki = 88.3 nM), both of which it behaves as an antagonist of.<unk>  preferentially activates 5-HT1A receptors in the prefrontal cortex, demonstrating regional selectivity, and has been found to increase dopamine and norepinephrine levels and decrease serotonin levels in the rat prefrontal cortex, actions that were determined to be mediated by activation of the 5-HT1A receptor. As such,<unk>  has been described as a norepinephrine–dopamine disinhibitor (NDDI). The proposed mechanism of action refers to the Kinsey dual control model of sexual response. Various neurotransmitters, sex steroids, and other hormones have important excitatory or inhibitory effects on the sexual response. Among neurotransmitters, excitatory activity is driven by dopamine and norepinephrine, while inhibitory activity is driven by serotonin. The balance between these systems is of significance for a normal sexual response. By modulating serotonin and dopamine activity in certain parts of the brain,<unk>  may improve the balance between these neurotransmitter systems in the regulation of sexual response.
Flibanserin
Ketanserin
Nabilone
Adatanserin
Blonanserin
Mianserin
Pimavanserin
Suvorexant