Aldioxa is the generic name for the metal complex, dihydroxyaluminum allantoinate, which is hydrolyzed to allantoin and aluminium hydrate at the gastric mucosa. Aldioxa was approved in Japan to improve subjective symptoms or objective of gastric/duodenal ulcer and gastritis. It was discovered, that aldioxa ameliorates delayed gastric emptying through its antagonistic activity on the α-2 adrenergic receptor. The most commonly reported adverse reactions include constipation.

Anhydrous dibasic calcium phosphate is a calcium salt of phosphoric acid. It is used as a diluent in pharmaceutical industry, in some toothpastes as a polishing agent. Calcium phosphate is generally recognized as safe by FDA. Dibasic calcium phosphate is ised as a supplement to treat conditions associated with calcium deficit, such as bone loss (osteoporosis), weak bones (osteomalacia/rickets), decreased activity of the parathyroid gland (hypoparathyroidism), and a certain muscle disease (latent tetany)

Procaine is an anesthetic agent indicated for production of local or regional anesthesia, particularly for oral surgery. Procaine (like cocaine) has the advantage of constricting blood vessels which reduces bleeding, unlike other local anesthetics like lidocaine. Procaine is an ester anesthetic. It is metabolized in the plasma by the enzyme pseudocholinesterase through hydrolysis into para-aminobenzoic acid (PABA), which is then excreted by the kidneys into the urine. Procaine acts mainly by inhibiting sodium influx through voltage gated sodium channels in the neuronal cell membrane of peripheral nerves. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is thus inhibited. The receptor site is thought to be located at the cytoplasmic (inner) portion of the sodium channel. Procaine has also been shown to bind or antagonize the function of N-methyl-D-aspartate (NMDA) receptors as well as nicotinic acetylcholine receptors and the serotonin receptor-ion channel complex.

Sodium threonate (threonic acid) is a major breakdown product of ascorbic acid used as a food additive. It is formed in insignificant amounts from ascorbic acid used as a technological aid in the food industry. When administered orally to guinea-pigs (100 mg/kg body weight) for periods of 4 or 28 days, it produced a significant fall in the ascorbic acid concentration of certain organs but was without effect on other physiological and biochemical characteristics. The lifespan of scorbutic guinea-pigs was significantly reduced by dietary threonic acid (100 mg/kg body weight). The results indicate that threonic acid may modify the metabolism of ascorbic acid in guinea-pigs. Threonic acid is a normal component is aqeous humour and blood. Threonic acid is a substrate of L-threonate 3-dehydrogenase in ascorbate and aldarate metabolism pathway.

Molybdenum (Mo) is an essential trace element and is a component of vitamin and mineral supplements. Molybdenum has essential biological roles in organisms and microorganisms. Molybdenum is the only trace metal of the second row of the periodic table that exhibits biological activity when it is ligated to a cofactor. It acts as a critical cofactor in several molybdenum-dependent enzymes that are involved in important cellular reactions and pathways, including xanthine oxidoreductase. In nature two principal concepts of Mo cofactors have evolved, one is the iron Mo cofactor in bacterial nitrogenase and the other is represented by a large family of enzymes with more than 100 representatives relying on the pterin-based Mo cofactor (Moco). Moco-containing enzymes catalyze key redox reactions in the global carbon, sulfur and nitrogen cycles. Four molybdenum-dependent enzymes are known in humans, each harboring a pterin-based molybdenum cofactor (Moco) in the active site. In these enzymes, molybdenum catalyzes oxygen transfer reactions from or to substrates using water as oxygen donor or acceptor. Molybdenum shuttles between two oxidation states, Mo(IV) and Mo(VI). Following substrate reduction or oxidation, electrons are subsequently shuttled by either inter- or intra-molecular electron transfer chains involving prosthetic groups such as heme or iron-sulfur clusters. In all organisms studied so far, Moco is synthesized by a highly conserved multi-step biosynthetic pathway. A deficiency in the biosynthesis of Moco results in a pleitropic loss of all four human Mo-enzyme activities and in most cases in early childhood death. For the general population, the diet is the most important source of molybdenum and concentrations in water and air usually are negligible. The average daily dietary intake is about 0.1-0.5 mg m.o. Molybdenum is marketed both as a tablet and as a liquid supplement containing the mineral in dissolved form. Despite widespread claims, there is no evidence that one form of molybdenum is absorbed to a markedly superior extent than any other. Current marketing of molybdenum products for the treatment of medical conditions is not founded on any meaningful scientific evidence. People with serious kidney disease should avoid taking molybdenum (or any other supplement) except on the advice of a physician. People with serious kidney disease should also avoid taking molybdenum (or any other supplement) except on the advice of a physician.