Cipemastat (Ro 32-3555, tentative trade name Trocade) is a dipeptide, potent, competitive inhibitor of matrix metalloproteinases (MMP) 1, 8 and 13, which was under development by Roche for the potential treatment of rheumatoid arthritis. Cipemastat is a selective inhibitor of metalloproteinases 1, 8 and 13 over the related human matrix metalloproteinases stromelysin 1, and gelatinases A and B. Cipemastat mediated MMP inhibition leads to block the final common event in the destructive cascade resulting in the breakdown of cartilage and bone. Trocade has also been shown to inhibit cartilage destruction in vivo and to prevent structural joint damage in animal models of rheumatoid and osteoarthritis. Cipemastat was in phase II clinical trials for the treatment of rheumatoid arthritis. However, Roche discontinued the development of cipemastat because of an unfavorable risk-benefit profile.

2-(1-Hexyloxyethyl)-2-devinyl pyropheophorbide-a (HPPH), a chlorin-based photosensitize, is used in photodynamic therapy. It has been shown the therapeutic potential of HPPH in phase II clinical trials for the treatment of esophageal cancer. Besides, HPPH participated in clinical trials in treating patients with advanced non-small cell lung cancer that blocks the air passages. However, these studies were terminated.

Fenaftic acid is a choleretic agent.

FIBRACILLIN is a semisynthetic antibacterial agent.

Faropenem medoxomil is an ester prodrug derivative of the beta-lactam antibiotic faropenem. The prodrug form of faropenem offers dramatically improved oral bioavailability and leads to higher systemic concentrations of the drug. Faropenem medoxomil is a broad-spectrum antibiotic that is highly resistant to beta-lactamase degradation. It was under development for the treatment of acute bacterial sinusitis, community-acquired pneumonia, acute exacerbation of chronic bronchitis, and uncomplicated skin and skin structure infections.

Dehydroascorbic acid (DHA) is an oxidized form of ascorbic acid. Ascorbic acid is transported in its oxidized form via GLUT1 across the blood-brain barrier. Dehydroascorbic acid delay low-density lipoprotein (LDL) oxidation when added before the initiation of the process, they accelerate the process if added to minimally oxidized LDL. Dehydroascorbic acid is used as biochemical markers of oxidative stress in clinical investigations. Dehydroascorbic acid has been used as a vitamin C dietary supplement.

Tributyrin is a prodrug of natural butyrate. It is a neutral short-chain fatty acid triglyceride that is likely to overcome the pharmacokinetic drawbacks of natural butyrate as a drug. Tributyrin has potent antiproliferative, proapoptotic and differentiation-inducing effects in neoplastic cells. Compared with butyrate, tributyrin has more favorable pharmacokinetics and is well tolerated. Because it is rapidly absorbed and chemically stable in plasma, tributyrin diffuses through biological membranes and is metabolized by intracellular lipases, releasing therapeutically effective butyrate over time directly into the cell. Tributyrin may, at least in part, exert its growth-reducing and differentiation-inducing effect in Caco-2 cells by an upregulation of the vitamin D receptor; this may provide a useful therapeutic approach in chemoprevention and treatment of colorectal cancer. In phase I study of the orally administered tributyrin there was no consistent increase in hemoglobin F. Peak plasma butyrate concentrations occurred between 0.25 and 3 h after dose. Development of tributyrin as an anticancer agent was discontinued.

Pyroxamide is a potent histone deacetylase (HDAC) inhibitor. Pyroxamide induced terminal differentiation in murine erythroleukemia (MEL) cells and inhibited the growth by cell cycle arrest or apoptosis in a variety of tumor cells. An accumulation of acetylated histones and increased levels of p21/WAF1 expression were detected in cancer cells and in prostate xenografts treated with Pyroxamide.

Carmoxirole is a dopamine D2 receptor agonist with limited central activity that modulates sympathetic activation and subsequently reduces pre-load and afterload in animals. It was shown, that carmoxirole induced beneficial effects on hemodynamic and neurohumoral parameters in heart failure. In addition, experimental evidence showed that carmoxirole lowered blood pressure in various models of hypertension mainly or exclusively through inhibition of noradrenaline release from sympathetic nerve endings. That effect of carmoxirole was mediated by presynaptic dopamine receptors with the characteristic that release inhibition was restricted to low rates of sympathetic nerve discharge.