Tipentosin is prazosin derivative. It is an angiotensin-converting enzyme inhibitor. Tipentosin was developed as an antihypertensive agent.

Rocastine (AHR-11325) is a potent, nonsedating antihistamine with a rapid onset of action. This H1-antagonist effectively protected guinea pigs challenged with a lethal dose of histamine. It has also been mentioned in patents as a candidate to treat eye conditions and cough/cold mixtures (in which the lack of sedative effects from a non-sedating antihistamine would be especially useful in children, because daytime sedation is especially undesirable in this group). However, information on current use is not available and other second-generation, non-sedative antihistamines are available.

Trimecaine is an amide series local anesthetic with antiarrhythmic activity. It was shown to be capable of eliminating the flutter of atria in dogs simulated by an electric stimulation of the myocardium and atrial fibrillation in cats induced with aconitin and precludes ventricular fibrillation in rats arising due to intoxication with calcium chloride. Trimecaine noticeably mitigates the toxic effect of strophanthin. While depressing the automatism of the sinoatrial node the drug does not affect the conduction function. The combination of epidural trimecaine with morphine after a major urological surgery provides a superior analgesia with fewer side effects when compared to epidurally delivered bupivacaine with fentanyl.

Torcitabine is the beta-L-enantiomer of the natural nucleoside D-cytidine. The drug was under development as an antiviral agent for the treatment of chronic hepatitis B virus infection. Torcitabine has poor oral bioavailability, but its 3’,5’-derivative ester (val-L-dC) and the 3’-monovaline ester, valtorcitabine dihydrochloride, have excellent oral bioavailability and consequently the torcitabine prodrug, valtorcitabine, has replaced torcitabine in clinical development. Torcitabine is active against hepadnaviruses, specifically human hepatitis B virus (HBV), duck hepatitis virus (DHBV) and woodchuck hepatitis virus (WHV). Torcitabine triphosphate is a selective inhibitor of the polymerase enzyme of HBV.

Oxaprotiline (also known as hydroxymaprotiline) is a norepinephrine reuptake inhibitor and blocked the histamine H1 receptor. Oxaprotiline was studied in the treatment of hospitalized depressive patients. However, this drug has never been marketed.

Butinoline (also known as azulone) was used as an antispasmodic drug to treat gastritis.

Spirogermanium [NSC 192965, Spiro-32] is a germanium derivative which was under development by Unimed Pharmaceuticals. Spirogermanium is not a phase or cell cycle specific drug and inhibits DNA, RNA and protein synthesis, the protein synthesis being the most susceptible to this agent. Activity in malignant lymphoma, ovarian cancer, breast cancer, large bowel cancer, and prostatic cancer was reported in the clinical studies. The drug was under clinical investigation against the wide spectrum of solid tumors and malignant lymphomas. Spirogermanium also exhibits antiarthritic and immunoregulatory activities after p.o. administration to rats. Spirogermanium decreased hindleg inflammatory lesions of adjuvant arthritic rats when administered p.o. before or after the development of the arthritic lesions. However, the therapeutic use of spirogermanium has been discontinued because of its high toxicity and the low response rate.

Semapimod (CNI-1493) is a cytokine inhibitor and synthetic guanylhydrazone mitogen-activated protein kinase blocker, is being developed by Cytokine PharmaSciences as a potential treatment for Crohn's disease and other inflammatory conditions. As of December 2001, a phase I study demonstrating the safety of the compound had been completed and phase II trials for psoriasis and Crohn's disease were ongoing. In April 2003, preclinical and early clinical studies were underway for a variety of indications, including congestive heart failure and pancreatitis. Semapimod inhibits activation of p38 MAPK and NF-κB and induction of cyclooxygenase-2 by TLR ligands, but not by IL-1β or stresses. Semapimod inhibits TLR4 signaling (IC50 ≈0.3 umol) and acts by desensitizing cells to LPS; it fails to block responses to LPS concentrations of ≥5 ug/ml. Semapimod had been in phase II clinical trials by Ferring Pharmaceuticals for the treatment of Crohn's disease. However, this research has been discontinued. Semapimod is in phase I clinical trials for the treatment of autoimmune disorders and inflammation.