Norcyclobenzaprine (aka desmethylcyclobenzaprine) is one of the major metabolites of cyclobenzaprine which is a muscle relaxant marketed under the brand name Flexeril. Both cyclobenzaprine and norcyclobenzaprine are known to be potent antagonists of the serotonin 2a receptor.

China is one of the most important centers of diversity for Eriobotrya japonica Lindl. in the world. 3-p-coumaroylquinincacid (3-p-CoQA) was identified and quantified in the peel and pulp of the cultivars tested, this compound possessed relatively higher antioxidant activity, and may be excellent sources of phytochemicals and natural antioxidants.

5-(2-Aminopropyl)benzofuran (5-APB) is an empathogenic psychoactive compound of the substituted benzofuran, substituted amphetamine and substituted phenethylamine classes. 5-(2-Aminopropyl)benzofuran is a serotonin–norepinephrine–dopamine reuptake inhibitor and serotonin–norepinephrine–dopamine releasing agent. The toxicity and long-term health effects of recreational 5-APB use do not seem to have been studied in any scientific context and the exact toxic dosage is unknown/ 5-(2-Aminopropyl)benzofuran 's high affinity for the 5-HT2b receptor makes it likely that 5-APB would be cardiotoxic with long-term use, as seen in other 5-HT2B agonists such as fenfluramine and MDMA.

Escin Ia and isoescin Ia have been traditionally used clinically as the chief active ingredients of escin, a major triterpene saponin isolated from horse chestnut (Aesculus hippocastanum) seeds for the treatment of chronic venous insufficiency, hemorrhoids, inflammation and edema. The interconversion of escin Ia and isoescin Ia when given alone indicates that administration of one isomer leads to exposure to the other.

Trifluoromethylphenylpiperazine (TFMPP) acts on serotonin receptors 5-HT1A, 5-HT1B, 5-HT1D, 5-HT2A and 5-HT2C and functions as a full agonist at all sites except the 5-HT2A receptor, where it acts as a weak partial agonist or antagonist. In addition, TFMPP binds to the sodium-dependent serotonin transporter, SERT and evokes the release of serotonin. Besides was shown, that the N-Benzylpiperazine/TFMPP combination produced effects, which crudely mimic those of MDMA, commonly known as ecstasy. The neurophysiological effects of TFMPP in humans was also studied and was shown that TFMPP may affect transmitter systems involved in speeding of interhemispheric communication in the male brain.

Lysergide (LSD) is a semi-synthetic hallucinogen and is one of the most potent drugs known. Recreational use became popular between the 1960s to 1980s, but is now less common. During the 1960s, LSD was investigated for a variety of psychiatric indications, including the following: as an aid in the treatment of schizophrenia; as a means of creating a "model psychosis"; as a direct antidepressant; and as an adjunct to psychotherapy. LSD is listed in Schedule I of the United Nations 1971 Convention on Psychotropic Substances. LSD possesses a complex pharmacological profile that includes direct activation of serotonin, dopamine and norepinephrine receptors. In addition, one of its chief sites of action is that of compound-specific (“allosteric”) alterations in secondary messengers associated with 5HT2A and 5HT2C receptor activation and changes in gene expression. The hallucinogenic effects of LSD are likely due to agonism at 5HT2A and 5HT2C receptors. LSD is also an agonist at the majority of known serotonin receptors, including 5HT1A, 5HT1B, 5HT1D, 5HT5A, 5HT6 and 5HT7 receptors. L-Lysergide (L-LSD) is a non-psychoactive enantiomer of LSD. D-LSD not only completely eradicated the response to 10 muM dopamine in rat hippocampus preparations but also consistently stimulated adenylate cyclase activity. L-LSD (80 muM) was without effect. Also both D- and L-LSD bind to solubilized 5-HT1 sites with comparable high affinities, whereas D-LSD has a markedly higher affinity for the membrane 5-HT1 site. In crude bovine frontal cortical membranes, D-LSD has high affinity for the 5-HT 1 binding site (IC50 = 40 nM), while L-LSD has the very low affinity (IC50 = 10,000 nM versus [3H]5-HT). Solubilized 5-HT1 sites retain high affinity for D-LSD binding site (IC50 = 75 nM). However, L-LSD also has a high affinity for the soluble binding site (IC50 of 200 nM). Thus while the membrane-bound binding site strongly differentiates between D- and L-LSD, both stereoisomers bind to the soluble binding site with relatively high affinity. Lovell and Freedman have suggested that the lone-pair electrons on the 3 nitrogen atoms in D-LSD are oriented downward from the plane of the molecule and form a tripod of electron donor pairs which interact with the 5-HT 1 binding site. This area of attachment of D-LSD would be expected to be much larger than the area of attachment of 5-HT to the binding site, and to overlap or encompass the 5- HT binding region. The lower affinity of L-LSD for the membrane binding site would be due to the fact that one or more of the lone-pair electrons is oriented above the plane of the molecule. The diethylamide group of L-LSD would also be oriented differently. It would therefore either be unavailable for interactions with the binding site or its orientation would be a steric hindrance to binding.

(-)-DDMS (S-Didesmethylsibutramine, (S)-DDMS) is one of sibutramine active metabolites. Sibutramine is widely used in the treatment of obesity. Sibutramine acts by inhibiting the reuptake of serotonin and noradrenaline in synapses, thereby enhancing both satiety and energy expenditure. In preclinical models (S)-Didesmethylsibutramine affected locomotor behavior and the Porsolt test but appeared to be completely inactive on food intake. (S)-enantiomers of didesmethylsibutramine may, to some extent, contribute to sibutramine’s side effect profile.

SDB-006 is a cannabimimetic indole that binds the central cannabinoid (CB1) and peripheral cannabinoid (CB2) receptors with EC50 values of 19 and 134 nM, respectively. SDB-006 was discovered during research of the related compound JWH-018 adamantyl carboxamide, which has been sold illicitly in herbal blends.

MCN-5652W68 is pharmacologically inactive enantiomer of an selective serotonin reuptake MCN-5652. The enantiomers of McN-5652 differed in their ability to inhibit ex vivo binding of paroxetine in rat frontal cortex and hypothalamus, in vitro uptake of 5-HT in rat blood platelets, and 5-HT-induced contraction of rat vascular smooth muscle, with (+)-McN-5652-Z being most active. No difference was observed between the effects of (+)- and (-)-McN-5652-Z on 5-HT metabolism by rat brain monoamine oxidase. MCN-5652, as enantiomeric mixture, is currently being used for positron emission tomography studies.

3,5-Diiodo-L-thyronine (3,5-T2), a potential metabolite of 3,3',5-triiodothyronine (T3), is an active thyroid hormone. It acts as an alternative ligand for thyroid hormone receptor beta. 3,5-Diiodo-L-thyronine has the capacity to stimulate hepatic lipid catabolism but acts by different from T3 molecular mechanisms to achieve this effect.