Aganepag is a potent Prostanoid EP2 receptor agonist, with an EC50 of 0.19 nM, and shows no activity at EP4 receptor. Aganepag can be used in the research of wound healing, scar reduction, scar prevention and wrinkle treatment and prevention. Aganepag is an antiglaucoma agent.

Aganepag is a potent Prostanoid EP2 receptor agonist, with an EC50 of 0.19 nM, and shows no activity at EP4 receptor. Aganepag can be used in the research of wound healing, scar reduction, scar prevention and wrinkle treatment and prevention. Aganepag is an antiglaucoma agent.

Profadol is a pyrrolidine derivative patented in the 1960s by pharmaceutical company Parke-Davis as opioid analgesic. Profadol acts as a mixed agonist-antagonist of the μ-opioid receptor and in preclinical studies, Profadol precipitates abstinence in morphine-dependent monkeys and can reverse pethidine- induced narcosis in nondependent monkeys. In morphine-dependent human subjects, Profadol was also found to pre¬cipitate acute abstinence syndromes, with a potency 40 to 50 times less than that of nalorphine. Profadol, unlike other morphine-antagonists, does not produce nalorphine-like subjective effects. Over a fourfold range of doses, this drug was found to produce subjective effects indistinguishable from those of morphine. Also unlike other morphine-antagonists, profadol is quite active on the "classical" rodent tests for analgesia. It is about 1.3 times as potent as pethidine on the mouse hot-plate test, and about four times as potent on the rat tail-pressure test.

Piritrexim is a synthetic antifolate agent with antiparasitic, antipsoriatic and antitumor properties. Piritrexim inhibits the enzyme dihydrofolate reductase, thereby disrupting folate metabolism and DNA synthesis and cell division. A theoretical advantage of piritrexim over trimetrexate is a lack of any known effects on histamine metabolism, which may lower the risk of hypersensitivity reactions. Piritrexim is a nonclassical antifolate for antitumor and parasitic chemotherapy that passively diffuses into cells and hence do not have to depend on folylpoly-gamma-glutamate synthetase or the reduced folate carrier. Because piritrexim is not a substrate for polyglutamation, the drug is not selectively retained within cells for prolonged periods. Piritrexim has a reliably high oral bioavailability of about 75%, which has led to its development as an oral lipophilic antifolate. Most commonly, it has been administered in oral daily doses of 75 to 150 mg bid or tid every 5 days, with cycles repeated every 3 weeks. Oral absorption is rapid, with peak plasma levels appearing at 1.5 hours after ingestion. Elimination occurs primarily via hepatic metabolism of the drug to active metabolites, and the terminal half-life of the parent compound is about 1.5 to 4.5 hours. Single-agent oral piritrexim has clinical activity in melanoma, urothelial cancers, and head and neck cancers. Tolerable combinations of piritrexim with cisplatin, fluorouracil, and leucovorin have been tested, with promising results achieved in head and neck cancer. An interesting attempt to alternate piritrexim with methotrexate did not have any greater activity than methotrexate alone.

Moxastine is a diarylmethane derivative with an antihistamine and anticholinergic activities.

FERTIRELIN is an analog of luteinizing hormone releasing factor. The drug has been used since 1981 in Japan to treat various types of reproductive failure in cattle.

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.

ENMD-2076 is an orally-active, Aurora A/angiogenic kinase inhibitor. urora kinases are key regulators of mitosis (cell division), and are often over-expressed in human cancers. ENMD-2076 also targets the VEGFR, Flt-3 and FGFR3 kinases, which have been shown to play important roles in the pathology of several cancers. ENMD-2076 is tested in phase 2 clinical trials against ovarian cancer, breast cance, hepatocellular carcinoma and other malignancies.

Etanidazole (also known as Radinyl) is a 2-nitroimidazole with radiosensitizing properties. Etanidazole exerts its therapeutic action by depleting glutathione and inhibiting glutathione S-transferase, thus enhancing the anticancer effects of radiation therapy. Etanidazole was tested in Phase III clinical trials in patients with advanced head and neck cancer, however, its development was stopped. A fluorinated etanidazole (EF5) may also be useful as an imaging agent for identification of hypoxic, drug-resistant regions of primary tumors and metastases.