Seclazone was developed as a non-steroidal anti-inflammatory agent. This compound also possesses analgesic and antipyretic properties. Information about the current use of this compound is not available.

Satigrel (previously known as E5510) was developed as an antithrombotic agent. Satigrel antagonized platelet activation by inhibiting phospholipase C and/or A2, which results in suppression of both phosphatidylinositol breakdown and arachidonic acid release from phospholipids, as well as by inhibiting cyclooxygenase. Satigrel was studied in patients with intermittent claudication due to arteriosclerosis obliterans, where the drug improved the cutaneous circulation and symptoms of patients. In addition, the therapeutic effect of satigrel was studied on biopsy-proven chronic rejection after kidney transplantation. Also was shown that the drug had a clinical benefit over aspirin for the treatment of transient ischemic attacks. However, all these studied were apparently discontinued.

Sanfetrinem cilexetil (formerly known as GV 118819), a beta-lactam antibiotic, is the oral prodrug of sanfetrinem. Experiments on rodents have revealed that sanfetrinem cilexetil had strong antibacterial activity in vitro and good pharmacokinetic behavior in mice. This drug was suitable for the treatment of infections caused by a variety of bacteria and participated in a phase II clinical trial. However, this study was discontinued.

Gliflumide is a compound with a long-lasting hypoglycemic effect. This blood glucose lowering sulfonamide has shown a large decrease of blood glucose levels in healthy volunteers who where administered the drug orally or intravenously. A very similar reaction but delayed and prolonged response was observed for this drug compared to other insulin secretion-stimulating compounds (such as glibenclamide). High affinity of gliflumide to plasma proteins has been suggested to contribute to this delayed activity.

Alovudine (3’ -deoxy-3’ fluorothymidine) is a nucleoside reverse transcriptase inhibitor (NRTI) initially tested in the early 1990s, before the era of combination therapy and before the availability of plasma viral load measurement. Initial toxicity studies showed that the primary target organ of toxicity was the bone marrow. A lack of clear advantages in activity over zidovudine, the only drug approved in the early 1990s, and the potential for bone marrow toxicity caused alovudine development to be stopped [6]. However, later in vitro studies found alovudine to be very effective at suppressing several NRTI-resistant HIV-1 mutants, including isolates with multiple thymidine-associated mutations (TAMs) or multi-NRTI-resistance mutations. Alovudine at a dose of 7.5 mg/day added to a failing antiretroviral combined regimen in patients with isolates resistant to other NRTIs yielded a median viral load decline after a 4-week period in patients not receiving concomitant stavudine. In July 2003, Medivir out-licensed it's HIV antiviral MIV-310 to Boehringer Ingelheim. Under the terms of the agreement, Boehringer Ingelheim will make upfront and milestone payments to Medivir totaling up to 122 million euro in the event that all development and performance milestones are met. In March 2005, Boehringer Ingelheim recently completed a clinical trial of MIV-310 (alovudine) in HIV/AIDS. The efficacy exhibited by MIV-310 at the doses tested showed antiviral activity but did not achieve the target level of efficacy which had previously been defined. Boehringer Ingelheim, therefore, decided to stop the development of this investigational drug.

Mexoprofen was studied as an analgesic agent. This compound has never been marketed.

Clogestone Acetate (AY-11440) is a steroidal progestin that was synthesized in 1964 and was investigated as a progestin-only contraceptive but was never marketed.

Crisnatol is a derivative of arylmethylaminopropanediol with significant antineoplastic activity in a variety of murine and human tumor models. Crisnatol functions as a DNA intercalator, with the presence of additional basic amine groups in the sidechain enhancing binding to DNA due to electrostatic interactions. Crisnatol did not show antitumor efficacy in patients with ovarian carcinoma. In another clinical study, 2 of 26 patients with glioma showed complete long-lasting responses to the drug. The dose-limiting side effect was neurotoxicity.