Kainic acid (kainate) is a natural marine acid present in some seaweed. Kainic acid is a potent neuroexcitatory amino acid that acts by activating receptors for glutamate, the principal excitatory neurotransmitter in the central nervous system. Kainic acid is commonly injected into laboratory animal models to study the effects of experimental ablation. Kainic acid is a direct agonist of the glutamic kainate receptors and large doses of concentrated solutions produce immediate neuronal death by overstimulating neurons to death. Such damage and death of neurons is referred to as an excitotoxic lesion. Thus, in large, concentrated doses kainic acid can be considered a neurotoxin, and in small doses of dilute solution kainic acid will chemically stimulate neurons. Kainic acid is utilised in primary neuronal cell cultures and acute brain slice preparations [5] to study of the physiological effect of excitotoxicity and assess the neuroprotective capabilities of potential therapeutics. Kainic acid is a potent central nervous system excitant that is used in epilepsy research to induce seizures in experimental animals, at a typical dose of 10–30 mg/kg in mice. In addition to inducing seizures, kainic acid is excitotoxic and epileptogenic. Kainic acid induces seizures via activation of kainate receptors containing the GluK2 subunit and also through activation of AMPA receptors, for which it serves as a partial agonist.

Disodium iminodiacetate is a salt of iminodiacetic acid (IDA). The iminodiacetate anion can act as a tridentate ligand to form a metal complex with two, fused, five-membered chelate rings. Iminodiacetic acid is used to diagnose problems of the liver, gallbladder and bile ducts in an imaging procedure, called as hepatobiliary iminodiacetic acid (HIDA) scan. A nuclear medicine scanner tracks the flow of the tracer from the liver into the gallbladder and small intestine and creates computer images. In addition, iminodiacetate is a part of the iminodiacetate-modified poly-L-lysine dendrimer (IMPLD), a fluorescent bone-imaging agent. IMPLD is used in the diagnosis of bone tumors, or to be used for the delivery of chemotherapy drugs or therapeutic agents. Bones differ from other body tissues in their unique calcium mineral composition, which consists mainly of hydroxyapatite (HA). IDA functionalization could be used as a general approach to bone targeting by increasing affinity for HA, enabling the transport of other molecules or particles to bones.

Prenoxdiazine under the brand name Libexin is used as an antitussive agent. It was shown, that the use of this drug for pregnant women with an unproductive cough could be beneficial.

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.

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.

Disodium iminodiacetate is a salt of iminodiacetic acid (IDA). The iminodiacetate anion can act as a tridentate ligand to form a metal complex with two, fused, five-membered chelate rings. Iminodiacetic acid is used to diagnose problems of the liver, gallbladder and bile ducts in an imaging procedure, called as hepatobiliary iminodiacetic acid (HIDA) scan. A nuclear medicine scanner tracks the flow of the tracer from the liver into the gallbladder and small intestine and creates computer images. In addition, iminodiacetate is a part of the iminodiacetate-modified poly-L-lysine dendrimer (IMPLD), a fluorescent bone-imaging agent. IMPLD is used in the diagnosis of bone tumors, or to be used for the delivery of chemotherapy drugs or therapeutic agents. Bones differ from other body tissues in their unique calcium mineral composition, which consists mainly of hydroxyapatite (HA). IDA functionalization could be used as a general approach to bone targeting by increasing affinity for HA, enabling the transport of other molecules or particles to bones.

Ammonium hexafluorosilicate is a white crystalline solid. Corrodes aluminum. Used as a disinfectant, in etching glass, metal casting, and electroplating. Ammonium hexafluorosilicate is useful for the treatment of dentin hypersensitivity, since ammonium hexafluorosilicate induced calcium phosphate precipitation from the saliva; therefore, it has a continuous effect on dentin tubules occlusion under a simulated oral environment. Ammonium hexafluorosilicate has been applied to arrest caries without discoloration. The major use of sodium hexafluorosilicate and fluorosilicic acid is as fluoridation agents for drinking water. Sodium hexafluorosilicate has also been used for caries control as part of asilicophosphate cement, an acidic gel in combination with monocalcium phosphate monohydrate,and a two-solution fluoride mouth rinse. Both chemicals are also used as a chemical intermediate (raw material) for aluminum trifluoride, cryolite (Na3AlF6), silicon tetrafluoride,and other fluorosilicates and have found applications in commercial laundry. Other applications for sodium hexafluorosilicate include its use in enamels/enamel frits for china and porcelain, in opalescent glass, metallurgy (aluminum and beryllium), glue, ore flotation, leather and wood preservatives, and in insecticides and rodenticides. It has been used in the manufacture of pure silicon, as a gelling agent in the production of molded latex foam, and as afluorinating agent in organic synthesis to convert organodichlorophosphorus compounds to the corresponding organodifluorophosphorus compound. In veterinary practice, external applicationof sodium hexafluorosilicate combats lice and mosquitoes on cattle, sheep, swine, and poultry, and oral administration combats roundworms and possibly whipworms in swine and prevents dental caries in rats. Apparently, all pesticidal products had their registrations cancelled or they were discontinued by the early 1990s

Methylarsonic acid, monosodium salt is an organoarsenic compound formed from the methylation of inorganic arsenic by living organisms. Methylarsonate is used as a contact herbicide in either the monosodium or disodium salt form. It goes by the trade names Weed-E-Rad, Ansar 170 H.C., Ansar 529 H.C., DiTac and others. Methylarsonate is considered only slightly toxic, having an oral LD50 of 2200 mg/Kg for rats. The inhalation risk is greater with LD50 Rats >20 mg. Long term studies with people exposed to organoarsenicals has shown an increased risk of skin cancer (Spiewak, 2001), lung cancer and some liver cancers, although some recent studies have shown some arsenic containing compounds (specifically Arsine trioxide) may have anticarcinogenic properties (Wang, 2001). In mammals, Methylarsonate is also an intermediate in the detoxification of inorganic arsenic. In the arsenate detoxification I pathway, arsenite reacts with S-adenosyl-L-methionine to produce methylarsonate and S-adenosyl-L-homocysteine. Arsenite methyltransferase catalyzes this reaction. Methylarsonate then reacts with 2 glutathione molecules to produce glutathione disulfide and methylarsonite. This reaction is catalyzed by methylarsonate reductase. Methylarsonate is an organic arsenic compound with adverse effects similar to those of arsenic trioxide. Methylarsonate was formerly included in some vitamin and mineral preparations. It was once used to treat tuberculosis, chorea, and other affections in which the cacodylates were used.

Potassium canrenoate (INN, JAN) or canrenoate potassium (USAN) (brand names Venactone, Soldactone), the potassium salt of canrenoic acid, is an aldosterone antagonist of the spirolactone group. Like spironolactone, it is a prodrug, which is metabolized to canrenone in the body. Potassium canrenoate is not licensed in the UK, but may sometimes be prescribed off-licence to treat oedema. It is given intravenously. Potassium canrenoate is a mineralocorticoid receptor (MR) antagonist. The blockade with MR antagonist have beneficial effects in patients with heart failure and myocardial infarction, often attributed to blocking aldosterone action in the myocardium.

Neridronic acid (6-amino-1-idroxyesilidene-1,1-bisphosphonate) is a nitrogen-containing bisphosphonate licensed in Italy for the treatment of osteogenesis imperfecta and Paget’s disease of bone. The pharmacodynamic profile is similar to that of other nitrogen-containing bisphosphonates and is characterized by its high affinity for bone tissue particularly at sites undergoing a process of remodeling. In growing children affected by osteogenesis imperfect, neridronic acid rapidly increases bone mineral density as measured by dual X-ray absorptiometry and this is associated with a significant decrease in fracture cumulative number. Similar results have been obtained also in newborns (<12-month-old) and in adult patients. In Paget’s disease of bone, 200 mg intravenous neridronic acid is associated with a 65% rate of full remission and a biochemical response (decrease of > 75% of bone turnover markers) in 95% of the patients. Neridronic acid treatment has been reported to be effective also in other skeletal diseases such as osteoporosis, algodystrophy, hypercalcemia of malignancy and bone metastasis. Neridronic acid has been developed only for parenteral use, and it is the only one used as the intramuscular injection. This avoids all the limitations of oral bisphosphonates and may be offered for a home treatment with simple nursing assistants