Icomucret (15(S)-HETE) is an hydroxyeicosatetraenoic acid developed by Alcon Research, Ltd for treatment Ophthalmic Disorders. In vitro Icomucret has been shown to inhibit LTB4 formation, 12-HETE formation and specifically inhibits the neutrophil chemotactic effect of LTB4. The inhibition of LTB4 formation is probably due to modulation of the 5- lipoxygenase (LO) because no changes in PGE2 formation have been determined. In vivo, Icomucret inhibits LTB4-induced erythema and edema, and reduces LTB4 in the synovial fluid of carragheenan-induced experimental arthritis in dogs. Icomucret has also some immunomodulatory effects. It inhibits the mixed lymphocyte reaction, induces generation of murine cytotoxic suppressor T cells, and it decreases interferon production by murine lymphoma cells. Furthermore, IL-4 and IL-13 have recently been shown to be potent activators of the 15-LO in mononuclear cells. Icomucret induces the secretion of membrane-bound mucins from human conjunctival and corneal epithelial cells. Icomucret was evaluated in clinical trials for Dry Eye Syndrome treatment. However from 2007 no future development reported, and Icomucret development sims to be discontinued.

Eprodisate (1,3-propanedisulfonate) is a negatively charged, sulfonated molecule of low molecular weight that has structural similarities to heparin sulfate; it is a glycosaminoglycan mimetic that binds to the glycosaminoglycan (GAG) binding site on serum A amyloid (AA) to prevent its interaction with glycosaminoglycan and arrest amyloidosis, or inhibit amyloid deposition. In nonclinical toxicity studies in two animal species (i.e., rat and dog), eprodisate was administered orally at doses of up to 2000 mg/kg/day for 39 weeks: eprodisate showed low toxicity potential at doses several fold higher than the anticipated clinical dose, was well tolerated upon chronic exposure and was found to be nonmutagenic and nonclastogenic. Furthermore, a series of safety pharmacology studies showed that eprodisate does not have any clinically significant effect on major organ function.

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.

Oxiniacic Acid is a nicotinic acid derivative, that shows potent hypolipidemic activity.

Kynurenic acid is a product of the normal metabolism of amino acid L-tryptophan which has been shown to have a neuroactive profile. It exhibits activity against NMDA receptors and Neuronal acetylcholine receptor subunit alpha-7. It has been investigated as a potential therapeutic compound and as a biomarker in a number of neurological disorders. Although Kenyruic acid exhibits a poor penetration of the blood-brain barrier, it remains to be of particular interest to those researching Schizophrenia.

Amfonelic acid (AFA) is a dopamine reuptake inhibitor. Experiments on rats have shown that AFA treatment completely prevented the effects of methamphetamine on the dopaminergic system, both morphologically and biochemically.

Hyodeoxycholic acid, also known as HDCA, is a secondary bile acid. Natural 6alpha-hydroxylated bile acids are receptor-specific activators of nuclear liver X receptor alpha (LXRalpha), a nuclear receptor regulating the expression of the cholesterol 7alpha-hydroxylase gene. AHRO-001 (Hyodeoxycholic acid) is in phase I clinical trials for the treatment of atherosclerosis. Through a complex signaling processes utilizing LXR receptors, the compound is designed to increase the efficiency of cholesterol efflux using the HDL cells, which act on all cholesterol in the arterial circulation as well as in the lipid core of plaque deposits in the artery walls. Use of AHRO-001 has shown no adverse effects on morbidity, mortality or toxicity and has been well tolerated at high doses.

Fusaric acid (J-butylpicolinic acid) is a fungal toxin with low to moderate toxicity synthesized by some Fusurium species which cause infections in cereal grains and other agricultural commodities. It may potentiate the effects of other Fusurium toxins. Fusaric acid is a potent inhibitor of DNA synthesis. Fusaric acid has potent anti-proliferative activity in vitro on various normal and cancer cell lines and suggest that it exhibits some cytotoxic specificity for growing and confluent colorectal adenocarcinoma and mammary adenocarcinoma cell lines. Fusaric acid is known as a potent dopamine-beta-hydroxylase inhibitor of high specificity. Fusaric acid calcium salt elicited the hypotensive response primarily through the reduction of total peripheral vascular resistance index.