7-Methylxanthine is a methyl derivative of xanthine, found occasionally in human urine. 7-Methylxanthine is one of the purine components in urinary calculi. 7-methylxanthine (7-MX) is a metabolite of caffeine and theobromine, and has been shown to have low toxicity and no carcinogenic effects. 7-MX is known as a non-selective adenosine antagonist and has been shown to work against myopia. 7-MX has little effect on the proliferation or apoptosis of human RPE cells; however, 7-MX disturbs the proportion of cells in the G1 stage and inhibits the expression of ADORA1, ADORA2A, and ADORA2B in short-term treatment. 7-MX has been confirmed to reduce the severity of myopia and eye elongation induced by forming deprivation in guinea pigs and to counteract the thinning of the posterior sclera and of collagen fibrils induced by form deprivation. A clinical trial showed that 7-MX reduced eye elongation and myopia progression in childhood myopia.

There is no much available information related to the biological and pharmacological application of imidoline, but this compound has been found to be as potent as chlorpromazine in increasing striatal DOPA accumulation and prolactin secretion in vivo. Imidoline exhibited only weak inhibitory activity towards dopamine-sensitive adenylate cyclase and 3H-spiroperidol binding to striatal membranes in vitro. A proposed active conformation involves intramolecular hydrogen bonding between the protonated dimethylamino group and the oxygen of the imidazolidinone ring. The spatial relationship between the amine nitrogen and phenyl ring in this conformation allows proper fit of imidoline with key dimensions described for the dopamine receptor.

Actinoquinol is sunscreen agent that absorbs Ultraviolet B light. Actinoquinol in combination with hyaluronic acid drops might be helpful for the human eye in the defense against photooxidative and other oxidative processes.

Japan Tobacco developed JTV-519 (known also as K201) as an antiarrhythmic agent. This drug was in Phase II trials for the potential treatment of Atrial Fibrillation, but study was terminated. In experimental myofibrillar overcontraction models, JTV-519 demonstrated greater cardioprotectant effects than propranolol, also, this drug investigated against heart failure, but then these researches have been discontinued. In addition, K201 was in phase II clinical trial for investigation its topical implementation for Atopic Dermatitis. The mechanism of its action is both complex and controversial, known that it is a non-specific blocker of sodium, potassium and calcium channels (multiple-channel blocker). It is believed to stabilize the closed state of the RyR2 (cardiac ryanodine receptor) by increasing its affinity for the FKBP12.6 (12.6 kDa FK506 binding protein), in addition was suggested, that suppression of spontaneous Ca2 release and the activity of RyR2 contributes, at least in part, to the anti-arrhythmic properties of K201.

Procodazole is a non-specific active immunoprotective agent against viral and bacterial infections

3'-C-ethynylcytidine (Ethynylcytidine, TAS-106) is a synthetic cytidine nucleoside containing a covalently bound ethynyl group with potential antineoplastic and radiosensitizing activities. 3'-C-ethynylcytidine is metabolized in tumor cells to ethynylcytidine triphosphate (ECTP), which inhibits RNA synthesis by competitive inhibition of RNA polymerases I, II and III; subsequently, RNase L is activated, resulting in apoptosis. RNase L is a potent antiviral and antiproliferative endoribonuclease that cleaves singled stranded RNA, causes 28s rRNA fragmentation, and activates Janus Kinase (JAK), a mitochondrial-dependent apoptosis signaling molecule. Development of a cytosine derivative of 3'-ethynyl ribonucleoside, TAS-106, as an intravenously administered treatment for solid tumours was discontinued. A phase II trial in patients with head and neck cancer was terminated in the US.

Indibulin is a novel synthetic compound that was identified in a cell-based screening assay to discover cytotoxic drugs. Indibulin destabilizes microtubules and blocks cell cycle transition specifically at the G2-M phase. Indibulin effectively induces apoptosis through Bcl-2 phosphorylation and Bax translocation in human malignant glioma cells in a p53-independent manner. This agent has been shown to be active against multidrug-resistant (MDR) and taxane-resistant tumour cell lines. Indibulin was used in phase I/II clinical trials of patients with advanced solid tumours (metastatic breast cancer). Pharmacokinetic analysis showed a better tolerability underfeeding condition. Dose-limiting toxicities were nausea and vomiting, which seemed to be related to solvent lactic acid.

E7107 is a semisynthetic derivative of the natural product pladienolide B which was originally isolated from Streptomyces platensis. E7107 is the first compound a new class of anti-cancer agents targeting the spliceosome. Specifically E7107 interacts with the Splicing factor 3B subunit 1 (SF3b1) to block the normal splicing of oncogenes. Development of E7107 was suspended after Phase I clinical trials due to an unacceptable profile of adverse events.

Caprindolol, also known as SDZ 21009, is a beta-adrenoceptor blocker with affinity for serotonin (5-HT1A and 5-HT1B receptors.

Funapide (also known as TV 45070; XEN 402) is a small molecule blocker of the voltage-gated sodium channels Nav1.7 (SCN9A) and Nav1.8. Funapide was developed as a potential treatment of pain conditions, including osteoarthritis, neuropathic pain, postherpetic neuralgia, and erythromelalgia, as well as dental pain. In April 2013, the US FDA granted orphan drug designation to funapide for the treatment of pain associated with erythromelalgia (EM). EM is a rare autosomal dominant condition characterized by debilitating spontaneous or easily evoked attacks of symmetrical burning pain in the feet and hands, typically associated with elevated skin temperature and erythema (redness of the skin). Funapide also was involved in phase II clinical trials in patients with post herpetic neuralgia and in participants with primary osteoarthritis (OA) affecting a single knee. On March 7, 2018, Teva Pharmaceutical and Xenon Pharmaceuticals entered into a mutual agreement to terminate the collaborative development and license agreement they entered into in 2012 for the pain drug funapide. The reason was that the top line results of funapide phase 2 study in post-herpetic neuralgia patients failed to meet the primary or secondary endpoints.