Neocinchophen is an analgesic and uricosuric. Cinchophen and neocinchophen (introduced by Chemische Fabrik auf Aktien as Atophan and Novatophan) were being advertised as superior substitutes for salicylates in the treatment of rheumatic fever. Chemically, cinchophen is phenylcinchoninic acid, and neocinchophen is the ethyl ester of its methyl derivative.

Doliracetam possesses activity on the central nervous system. It has cognition enhancing properties and might be useful in the treatment of Alzheimer’s disease and epilepsy

Totrombopag is an orally bioavailable, nonpeptide, small-molecule thrombopoietin receptor agonist. It induces proliferation and differentiation of megakaryocytes and progenitor cells, ultimately increasing the production of platelets. Totrombopag has been investigated in healthy volunteers in a phase 1, single-blind, randomized fashion to cause a dosedependent increase in platelet count with demonstrated safety. There were no serious adverse events, no significant changes in laboratory or cardiovascular safety parameters and there was no observed relationship between the incidence or severity of adverse events and dose. Most adverse events were mild in intensity and self-limiting. Totrombopag was developed for the treatment of immune thrombocytopenic purpura.

Leteprinim is the synthetic purine. It has both anti-excitotoxic neuroprotective properties and enhances the regenerative response of surviving neurons within the central nervous system. Moreover, the experiments in vitro and in vivo reveal that leteprinim can be administered after an excitotoxic event and still produce neuroprotection. This is clearly crucial for any drug designed to treat stroke or any acute central nervous system injury. Therefore, leteprinim has the pharmacological properties required by a drug intended to treat acute stroke as well as a spinal injury. It may be useful in reducing brain injury; it possesses clinical relevance for the treatment of hypoxic-ischemic encephalopathy in the newborn. Leteprinim has the therapeutic potential for use in clinical trials in the treatment of neuronal deterioration in depression.

Mivotilate is an orally active hepatoprotective agent for the treatment of liver cirrhosis and hepatitis-B infection. Mivotilate was shown to exert multiple effects on the hepatic cytochrome P450 system, particularly to inhibit CYP2E1 expression and to up-regulate the CYP1A1 expression. The low oral bioavailability of Mivotilate in rats could be primarily attributed to poor absorption and considerable hepatic and gastrointestinal first-pass effects. The thermal reversible microemulsion system of YH439 greatly enhances the bioavailability of YH439 after oral administration. Mivotilate prevents mutagenesis caused by agents such as benzopyrene and reduces skin tumours induced by these agents.

Vadimezan (5,6-dimethyl(xanthenone-4-acetic acid), ASA404, DMXAA) is a fused tricyclic analogue of flavone acetic acid with potential antineoplastic activity. In pre-clinical mouse tumour models it was demonstrated that administration of Vadimezan rapidly leads to disruption of the existing vasculature in the tumour and consequent haemorrhagic necrosis of the tumour. This was consistent with the finding that a single dose of Vadimezan induced a prolonged reduction in the growth of xenografted tumours in animal models. The ability to disrupt the vasculature in these pre-clinical models has been attributed to a rapid induction of cytokines, particularly TNFα (tumour necrosis factor α), serotonin and nitric oxide, resulting in hemorrhagic necrosis and a decrease in angiogenesis. Despite the fact that the molecular targets for the drug remained unknown, the promising pre-clinical results led to Vadimezan being selected for clinical development. Results of Phase I trials showed some restriction of tumour blood flow within 24 h of treatment, although this was not as dramatic as seen in pre-clinical models. Unlike the animal models, there was also very little evidence for the rapid death of blood vessels or for increases in TNFα levels in human tumors. No difference in antitumour activity, cytokine induction or toxicity was observed between two parallel Phase I trials, one dosed weekly and the other dosed every 3 weeks. Therefore the drug proceeded to Phase II clinical trials, dosed every 21 days in combination with chemotherapeutic agents. These trials indicated the drug had small benefits in the treatment of non-small-cell lung cancer and prostate cancer. However, a subsequent Phase III clinical trial was not able to reproduce this response and clinical development was halted.

Gacyclidine (GK11) is a derivative of phencyclidine with neuroprotective properties. Tritiated gacyclidine and its enantiomers bind to NMDA receptors with binding parameters similar to those of other non‐competitive NMDA receptor antagonists. Beneficial effects of gacyclidine include reduction of lesion size and improvement of functional parameters after injury. In traumatic brain injury models, gacyclidine also improves behavioral parameters and neuronal survival. In an animal model of Amyotrophic lateral sclerosis (ALS), functional alteration of locomotor activity was evident and improved the survival of mice, suggesting that chronic administration of gacyclidine beginning at early symptomatic stage may be beneficial for patients with ALS. Gacyclidine has also been associated with altered mental status and end organ damage in patients.

Sarizotan (also known as EMD-128,130), a chromane derivative that was developed as a selective 5-HT1A receptor agonist and D2 receptor antagonist. Experiments on animal models have shown that the drug effectively suppressed levodopa-induced dyskinesia in primate and rodent models of Parkinson's disease, and tardive dyskinesia in a rodent model. Sarizotan participated in phase II/III clinical trials in the treatment of dyskinesia associated with the dopaminergic treatment of Parkinson's disease. However, further development for this disease was discontinued by Merk, because phase III did not confirm earlier Phase II findings. On July 14, 2015, Newron Pharmaceuticals, research, and development company focused on the novel central nervous system (CNS) and pain therapies, announced that the U.S. Food and Drug Administration (FDA) has granted Orphan Drug Designation to sarizotan for treatment of Rett syndrome. Besides, the drug now is an ongoing clinical trial phase II/III to investigate its the tolerability and efficacy in reducing respiratory abnormalities in Rett Syndrome.

Enecadin (NS 7 or ZK 228326) is a voltage-dependent sodium and calcium channel blocker. Enecadin is a neuroprotective agent demonstrated efficacy in animal models of ischemic injury of brain, spinal cord and retina. Enecadin was undergoing phase II development in stroke with PAION in Germany. Enecadin development has been discontinued.

Salnacedin (also known as G 201) was developed as a topical anti-inflammatory agent; Salnacedin participated in phase II clinical trials in the USA for the treatment of dermatitis, acne, and psoriasis. However, all these studies were discontinued.