NO-711 (aka NNC-711) is an anticonvulsant under development by Novo Nordisk. It acts as a gamma-aminobutyric acid (GABA) uptake inhibitor by inhibiting GAT-1. It has been investigated as a potential therapeutic agent for a number of cognitive disorders, as well as the potential to improve normal cognitive functions.

Ellipticine (5,11-dimethyl-6H-pyrido[4,3-b]carbazole), an alkaloid isolated from Apocyanaceae plants (i.e. Ochrosia borbonica, Excavatia coccinea), and several its derivatives exhibit significant antitumor and anti-HIV activities. This compound is one of the simplest naturally occurring alkaloids, having a planar structure. It was first isolated in 1959 from the leaves of the evergreen tree Ochrosia elliptica, which grows wild in Oceania. Ellipticine and its more soluble derivatives (9-hydroxyellipticine, 9-hydroxy-N2-methylellipticinium, 9-chloro-N2 -methylellipticinium and 9-methoxy-N2 -methylellipticinium) exhibit promising results for the treatment of osteolytic breast cancer metastases, kidney cancer, brain tumors and acute myeloblastic leukemia. The main reason for the interest in ellipticine and its derivatives for clinical purposes is their high efficiencies against several types of cancer, their rather limited toxic side effects and their complete lack of hematological toxicity. Nevertheless, the mutagenicity of ellipticines should be evaluated as a potential risk factor for these anticancer agents. Most ellipticines are mutagenic to Salmonella typhimurium Ames tester strains, bacteriophage T4, Neurospora crassa, and mammalian cells and induce prophage lambda in Escherichia coli. The anti-tumor therapeutic ellipticine and its derivatives act as potent anticancer agents via a combined mechanism involving cell cycle arrest and induction of apoptosis. Cell death induced by ellipticine has been shown to engage a p53-dependent pathway, cell cycle arrest, interaction with several kinases and induction of the mitochondrial pathway of apoptotic cell death. Cell cycle arrest was shown to result from DNA damage caused by a variety of tumor chemotherapeutic agents; this is also the case for ellipticines. The prevalent DNA-mediated mechanisms of anti-tumor, mutagenic and cytotoxic activities of ellipticine are (i) intercalation into DNA, (ii) inhibition of DNA topoisomerase II activity, and (iii) covalent binding to DNA in vitro and in vivo after enzymatic activation by cytochrome P450 and/or peroxidase enzymes The mechanism leading to apoptosis by ellipticine is thought to also be associated with DNA damage, by inhibition of topoisomerase II and the covalent modification of DNA. In addition, the formation of ellipticine-DNA adducts ultimately can mutate cancer cells or initiate cell death.

Abietic acid (AA), a diterpene produced by conifer species, such as grand fir and lodgepole pine, has been reported to have anti-inflammatory and immunomodulatory effects and can be used as a wound-healing agent. Its treatment elevates cell migration and tube formation in human umbilical vein vascular endothelial cells by the activation of ERK and p38 MAPKs. In addition was shown, that abietic acid could be used as an antimetastatic agent or as an adjuvant for anticancer therapy. AA acts as a PPARα/γ dual activator to inhibit age-related inflammation by suppressing NF-κB and the MAPK/AP-1 pathway and can be a useful agent for improving skin photoaging.

p-Toluenesulfonic acid (PTSA) is an organic compound with the formula CH3C6H4SO3H. An aromatic sulfonic acid, often used as a strong acid catalyst. p-Toluenesulfonic acid monohydrate has been used as a reducing agent for the reductive amination of ketones and aldehydes. In the presence of p-Toluenesulfonic acid monohydrate novel deazaflavin-cholestane hybrid compounds have been synthesized in a condensation reaction. 2-Phenylethyl alpha-glucoside has also been synthesized in the presence of p-Toluenesulfonic acid monohydrate. p-toluenesulfonic acid esters, are a common class of reagents used in the pharmaceutical industry as alkylating agents, catalysts, and in purification steps of the chemical synthesis of a drug substance.