Fenclozic acid emerged in the late 1960s as a promising carboxylic acid non-steroidal anti-inflammatory drug candidate that demonstrated potent anti-inflammatory, anti-pyretic and analgesic properties. Whole body autoradiography showed fenclozic acid distribution into all tissues except the brain, with radioactivity still detectable in blood, kidney and liver at 72 h post-dose. Fenclozic acid was compared with aspirin in a double-blind, crossover trial in patients with rheumatoid arthritis. It was concluded that fenclozic acid afforded symptomatic relief and was comparable to aspirin. Unfortunately, hepatotoxicity was observed in subsequent trials and the drug was withdrawn from the clinic.

Minodronic acid (RECALBON®, Bonoteo®), a third-generation bisphosphonate, was approved in Japan for the oral treatment of osteoporosis. This drug increases the bone mineral density and the strength by inhibiting osteoclastic bone resorption. Nitrogen-containing bisphosphonates, such as minodronic acid (RECALBON®, Bonoteo®) induce osteoclast apoptosis by inhibiting farnesyl pyrophosphate synthase (FPPS), a key enzyme in the mevalonate pathway. Inhibition of FPPS in osteoclasts prevents the biosynthesis of isoprenoid lipids that are required for the prenylation of small GTPase signaling proteins necessary for osteoclast function. Similarly, nitrogen-containing bisphosphonates have been shown to inhibit farnesyl pyrophosphate/geranyl pyrophosphate synthase activity.

Tolfenamic acid is a selective COX-2 inhibitor, which was marketed in Europe for the treatment of acute migraine disorders. Tolfenamic acid is currently unavailable for human use, however, it may be prescribed for veterinary purposes.

Taurocholic acid is a bile acid and is the product of conjugation of cholic acid with taurine. Its sodium salt is the chief ingredient of the bile of carnivorous animals. Taurocholic acid, as with all bile acids, acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as a cholagogue and cholerectic (a bile purging agent). Hydrolysis of taurocholic acid yields taurine, a nonessential amino acid. Taurocholic acid is one of the main components of urinary nonsulfated bile acids in biliary atresia. Raised levels of the bile acid taurocholate in the fetal serum in obstetric cholestasis may result in the development of a fetal dysrhythmia and in sudden intra-uterine death. In medical use, it is administered as a cholagogue and choleretic. Taurocholic acid is a potent TGR5 ligand, and in dogs, colonic perfusion with TCA induces PYY secretion. TCA enemas could stimulate GLP-1 and PYY secretion in obese patients with type 2 diabetes receiving the dipeptidyl peptidase-4 (DPP-4) inhibitor, sitagliptin. Satiogen Pharmaceuticals is developing rectally administered taurocholic acid, a bile acid, for the treatment of obesity and type 2 diabetes mellitus.

Hippuric Acid is an acyl glycine produced by the conjugation of benzoic acid and glycine, found as a normal component in urine as a metabolite of aromatic compounds from food. Increased urine hippuric acid content may have antibacterial effects. Hippuric Acid is used therapeutically in the form of its salts (hippurates of calcium and ammonium). It is an ingredient of FDA-approved drug Hiprex (methenamine hippurate tablets USP). Each yellow capsule-shaped tablet of Hiprex contains 1 g Methenamine Hippurate which is the Hippuric Acid Salt of Methenamine (hexamethylene tetramine). The tablet also contains inactive ingredients. Hiprex (methenamine hippurate tablets USP) has antibacterial activity because the methenamine component is hydrolyzed to formaldehyde in acid urine. Hippuric acid has some antibacterial activity and also acts to keep the urine acid. The drug is generally active against E. coli, enterococci and staphylococci. Enterobacter aerogenes is generally resistant. The urine must be kept sufficiently acid for urea-splitting organisms such as Proteus and Pseudomonas to be inhibited. Hiprex is indicated for prophylactic or suppressive treatment of frequently recurring urinary tract infections when long-term therapy is considered necessary.

Tetragalacturonic acid hydroxymethylester belongs to local hemostatics. It is an antihemorrhagic agent.

Potassium Trihydrogen Dioxalate is a Potassium salt used in photography, marble grinding, and in metal polishing. Potassium Trihydrogen Dioxalate is strongly irritating to eyes, mucous and gastrointestinal tract. Potassium Trihydrogen Dioxalate may cause cardiac failure and death after oral administration

Dihomo-gamma-linolenic acid (DGLA) is an n-6 polyunsaturated fatty acid that is mainly metabolized to an anti-inflammatory eicosanoid, prostaglandin (PG) E1, via the cyclooxygenase (COX) pathway. DGLA exists widely in the human body and daily animal-source foods. Concentrations of DGLA in the serum of atopic dermatitis patients are lower than those in healthy volunteers. DGLA suppressed clinical severity of skin lesions dose-dependently, with an increase in DGLA contents in phospholipids of skin, spleen, and plasma. Discontinuation of DGLA administration resulted in the onset of dermatitis and a decrease in DGLA contents in skin, spleen, and plasma. These findings indicate that oral administration of DGLA effectively prevents the development of atopic dermatitis in NC/Nga mice. DGLA may have an anti-atherosclerotic effect in apoE-deficient mice via PGE1 formation. As dihomo-γ-linolenic acid and arachidonic acid compete for processing by these oxidation enzymes, introduction of dihomo-γ-linolenic acid to platelets is correlated to suppression of arachidonic acid metabolites and promotion of dihomo-γ-linolenic acid metabolites such as PGE1, which produces an antithrombotic effect.

Beta-Hydroxyisovaleric acid (also known as 3-hydroxyisovaleric acid or 3HIA) is a normal human metabolite excreted in the urine. It is a byproduct of the leucine degradation pathway. Beta-Hydroxyisovaleric acid serves as a sensitive indicator of marginal biotin deficiency in humans. The variability of the proportion of leucine catabolites excreted as 3HIA suggests substantial population heterogeneity in the metabolic capacity of the 3HIA-carnitine detoxification pathway. In addition, was shown that in type II diabetic patients the catabolism of leucine was accelerated even in the absence of ketosis and that the urinary beta-hydroxyisovaleric acid concentration was a useful marker of short-term metabolic control in these patients.