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. LSD was first synthesized by Albert Hoffman while working for Sandoz Laboratories in Basel in 1938. Some years later, during a re-evaluation of the compound, he accidentally ingested a small amount and described the first ‘trip’. During the 1950s and 1960s, Sandoz evaluated the drug for therapeutic purposes and marketed it under the name Delysid®. It was used for research into the chemical origins of mental illness. Recreational use started in the 1960s and is associated with the ‘psychedelic period’. 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. During the 1960s, LSD was investigated for a variety of psychiatric indications, including the following: as an aid in 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.

Nocodazole is an anti-mitotic drug that has long been used as an experimental tool in cell biology. Nocodazole is known to bind with high affinity to tubulin and to inhibit microtubule assembly. The tubulin molecule is a α/β heterodimer; both α and β exist as various isotypes whose distribution and drug-binding properties are significantly different. Nocodazole has the highest affinity for αβIV and the lowest affinity for αβIII. In addition, nocodazole was investigated as an anticancer drug on xenografts model and it was revealed, that nocodazole possessed a high-affinity for the cancer-related kinases ABL, c-KIT, BRAF, and MEK, and inhibited Abl, Abl(E255K) and Abl(T315I).

Enalkiren (A-64662) is a potent, dipeptide renin inhibitor, mimics the transition state of the human renin substrate, angiotensinogen. The results of clinical trials with enalkiren suggest that renin inhibitors may be safe, useful therapeutic agents in the management of hypertension. In addition, it exerts intraocular pressure lowering pressure. Enalkiren development for the treatment of glaucoma, heart failure, hypertension has been discontinued.

Venritidine [D 16637] is an H2-antagonist which appears to undergo phase I clinical trials in the United Kingdom and preclinical investigation in Germany as a gastric ulcer treatment.

Lusaperidone (R107474) is a potent and relatively selective alpha(2)-adrenoceptor antagonist. It was under clinical evaluation for the treatment of depression, characterized by anergia and lack of drive. However, further clinical development has been stopped. Radiolabeled lusaperidone may be used as a potential radioligand for studying alpha(2)-adrenoceptors using PET.

Hydroxypioglitazone (M-IV) is an active metabolite of the peroxisome proliferator-activated receptor γ (PPARγ) agonist pioglitazone. Experiments in vitro have shown that hydroxypioglitazone was more efficient than the parent drug in stimulating lipid synthesis.

Disoxaril is the antipicornavirus drug. It is an isoxazole heterocyclic compound and a member of the antiviral series commonly referred to as WIN compounds. Disoxaril inhibits enterovirus replication by binding to the hydrophobic pocket within the VP1 coat protein, thus stabilizing the virion and blocking its uncoating. The amino acid sequence of a large VP1 196-258 peptide (disoxaril-binding region) of CVB1/RESISTANT was significantly different from that of the CVB1/SOF (sensitive). Crucially important changes in CVB1/RES were two point mutations, M213H and F237L, both in the ligand-binding pocket. Treatment with disoxaril in newborn mice infected with Coxsackie B1 virus, for 10 days post virus inoculation decreased the virus titer in the mouse brain till day 7.