Cefetrizole is aminocephalosporanic acid derivative with broad antibacterial activity against penicillin-resistant strains patented by Spanish pharmaceutical company Ferrer Internacional S. A.

Cefazaflur (INN) is a semisynthetic first-generation cephalosporin antibiotic patented by Smithkline Corp. For treatment of bacterial infections.

EC-18 (now known as mosedipimod), a synthetic copy of 1-palmitoyl-2-linoleoyl-3-acetyl-rac-glycerol (PLAG) that was developed by Enzychem Lifescience for oral administration for the treatment of immune and inflammatory related diseases, including psoriasis, rheumatoid arthritis, asthma, atopic dermatitis, and sepsis. The US Food and Drug Administration (FDA) has granted Orphan Drug Designation to EC-18 for the treatment of Acute Radiation Syndrome (ARS) and for the for the neutropenia treatment. Besides, the EC-18 is participating in phase II clinical trials to investigate the efficacy and safety of the agent for chemoradiation-induced oral mucositis and chemotherapy-induced neutropenia. This drug has a multimodal mechanism of action. It stimulates calcium influx into T lymphocytes and increases the production of various cytokines. In addition, EC-18 enhances the cytolytic activity of natural killer (NK) cells and suppresses the expression of the transmembrane protein tumor cell toll-like receptor 4 (TLR-4) on cancer cells, thus suppresses tumor cell proliferation.

The natural tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (AcSDKP also known as Goralatide) is generated from the N-terminus of thymosin-β4 through enzymatic cleavage by prolyl oligopeptidase (POP). AcSDKP regulation of proliferation of different cells is implicated in hematopoiesis and angiogenesis. This tetrapeptide present in almost all cells was recently detected at elevated concentrations in neoplastic diseases. However, previously reported in vitro and in vivo studies indicate that AcSDKP does not contribute to the pathogenesis of cancers. AcSDKP was in the phase II clinical trial for development of a new non-radioactive test for measuring glomerular filtration rate in patient with Chronic Kidney Disease. In addition, using mice models was concluded ,that AcSDKP might be an oral antifibrotic peptide drug that would be relevant to combating fibroproliferative kidney diseases such as diabetic nephropathy.

Caracemide is a nonspecific inhibitor of macromolecules affecting the synthesis of DNA, RNA, and proteins. Caracemide is an active inhibitor of ribonucleotide reductase as evidenced in the Novikoff tumor model. These inhibitory effects are concentration-dependent with 70 percent of DNA synthesis inhibited by a drug concentration of 1 mkM with a 4 h incubation. However, RNA and protein synthesis inhibition require a concentration of 50-100 mkM. DNA strand breaks were observed only at high in vivo concentrations of 100 mkM. The antineoplastic activity of caracemide was observed in the P388 murine model and in mammary (MX-I) and colon (CX-1) human tumor xenographs implanted in the subrenal capsules of athymic mice. In the MX-1 mammary tumor, a single daily injection provided greater activity than an intermittent schedule. Caracemide was inactive against murine L1210 leukemia, B16 melanoma, Lewis lung carcinoma, CD8FI mammary carcinoma and Colon 38. The toxicity on phase I studies was frequent but generally mild. Of note, significant central nervous system dysfunction manifested by lethargy, depression, and confusion occurred in some and was not predictable. In phase I studies Caracemide failed to demonstrate efficacy in patients with advanced renal cell cancer and advanced large bowel cancer.

Triletide is a tripeptide derivative which shows cytoprotective and antiulcerogenic activity. It is a thromboxane synthase inhibitor. Analysis of both individual and pooled data indicated that triletide was well absorbed after oral administration, with a lag time of 0.3 hours and the blood peak was reached after about 1.1 to 1.3 hours. Metabolization to desmethyl, desacetyl, desmethyl-desacetyl and hydroxylated derivatives plays a major role in the biotransformation of the drug and thus in its disappearance from blood, the distribution half-life being about 1 hour. A greater proportion of patients given the combination cimetidine and triletide was found to be endoscopically healed after treatment in comparison with those who had cimetidine alone (53% vs 40%). Intensity of symptoms decreased significantly faster and to a significantly greater extent in the same patients, as did antacid intake. Triletide appears to be equally well tolerated as, but significantly more effective than, aluminium hydroxide and magnesium hydroxide in relieving symptoms and promoting healing in patients with mild to moderate duodenal ulcer. There were no complaints of possible side-effects with either triletide treatment and no evidence of any significant changes in blood pressure, heart rate or routine haematology and haematochemistry investigations.

Melogliptin (EMD 675992 or GRC 8200) is an orally bioavailable dipeptidyl peptidase IV (DPP IV) inhibitor. Melogliptin was undergoing phase II clinical trials at Glenmark Pharmaceuticals and Merck KGaA for the treatment of type 2 diabetes. The completed 12 week Phase IIb clinical trial in 494 patients with type 2 diabetes melogliptin improved glycemic control in patients with type 2 diabetes mellitus and exhibited excellent safety and tolerability profile.