Tabimorelin is an orally active and selective growth hormone secretagogue (GHS) that was derived from growth hormone-releasing peptide-1(GHRP-1) via ipamorelin by a peptidomimetic approach. Tabimorelin inhibits both on gut and liver CYP3A4 activity. Tabimorelin has been in phase II clinical trials for the treatment of somatotropin deficiency. However, this research has been discontinued because the majority of growth hormone deficient adults did not respond to Tabimorelin.

Rentiapril (SA-446) is an angiotensin-converting-enzyme (ACE) inhibitor that has antihypertensive activity. This compound binds to ACE and blocks the conversion of angtiotensin I to angtiontensin II. Angiotensin II has vasoconstrictive activity, which rentiapril prevents, leading to vasodilation. Rentiapril has been shown to inhibit ADE activity more strongly and for longer periods than two other ACE inhibitors (captopril, and alacepril), and reduces blood pressure more quickly and for a longer time in patients with renovascular hypertension. Because rentiapril also decreases angiotensin II-induced aldosterone secretion by the adrenal cortex, it increases sodium excretion and (subsequently) water outflow.

Diminazene is an aromatic diamidine derived from Surfen C. Diminazene is used as aceturate salt. Diminazene is highly active against both Trypanosoma and Babesia spp. It is also of value in the treatment of theileriosis due to Theileria annulata. Diminazene has become the most commonly used therapeutic agent for trypanosomiasis in animals. It is said to be effective in canine, ovine and bovine babesiosis and, unlike some drugs, is less susceptible to relapse. It may also possess antibacterial properties. Diminazene binds to trypanosomal kDNA. This binding does not occur by intercalation but via specific interaction with sites rich in adenine-thymine (A-T) base pairs. Diminazene specifically inhibits mitochondrial type II topoisomerase in viable trypanosomes. Thus, inhibition of DNA replication may also occur via this interaction. Diminazene is extensively distributed in the body of treated animals. Residues of the compound may persist for several weeks, principally in the liver and kidneys, and also, to a lesser extent, in the gastrointestinal tract, lungs, muscle, brain and fat.

Gimatecan is a topoisomerase I inhibitor that is presently tested in phase II of clinical trials for the treatment of different cancers: glioma, glioblastoma, epithelial ovarian cancer, fallopian tube or peritoneal cancer. The drug recieved orphan designation for the treatment of glioma.

Pelitrexol (also known as AG2037) was developed by Pfizer as a glycinamide ribonucleotide formyltransferase inhibitor. This drug was studied in phase II clinical trials in patients with metastatic non-small cell lung cancer and in patients with metastatic colorectal cancer who failed treatment. In addition, the drug participated in a phase I clinical trial in treating patients who have advanced, metastatic, or recurrent solid tumors. Information about the further development of pelitrexol is not available.

N-(4-Ethylphenyl)-3-(Hydroxymethyl)-N-Isobutyl-4-(Tetrahydro-2h-Pyran-4-Ylmethoxy)Benzenesulfonamide (also known as GSK2981278) is a highly potent and selective inverse agonist of RORγ under development for the topical treatment of psoriasis. Preclinical data showed that GSK2981278 significantly inhibited the production of the Th17 signature cytokines in multiple in vitro and human tissue‐based systems. GSK2981278 may block the transcriptional activity of RORγt, leading to local suppression of cytokine expression and ultimately, improvement in psoriasis. Unfortunately in phase I clinical trial clinical assessment results showed no improvement of psoriatic lesions following treatment with GSK2981278.

Enofelast (BI-L-239) is a potent and selective 5-lipoxygenase inhibitor. It inhibited leukotriene B4 and C4 generation. In animal models, enofelast attenuates bronchoconstriction, leukocyte infiltration, inflammation and hyperresponsiveness that characterize asthma.

Topixantrone (BBR 3576) is a hetero-analog of the anthrapyrazole class of compounds. The mechanism of action of BBR 3576 is similar to that of mitoxantrone in terms of DNA intercalation, DNA affinity, topoisomerase II interaction and formation of single-strand breaks. BBR 3576 showed curative antitumor activity at the maximum tolerated dose (MTD) with a number of long-term survivors and showed greater activity than mitoxantrone and doxorubicin in preclinical studies. BBR 3576 retained a high level of activity across a wide range of doses. In human xenograft studies, equivalent antitumor activity was observed when compared with doxorubicin and mitoxantrone. The compound showed reduced cardiotoxicity when repeatedly administered in rodent models. Topixantrone has a manageable toxicity profile on a 4-week schedule.