Folic Acid is a B complex vitamin containing a pteridine moiety linked by a methylene bridge to para-aminobenzoic acid, which is joined by a peptide linkage to glutamic acid. Conjugates of Folic Acid are present in a wide variety of foods, particularly liver, kidneys, yeast and leafy green vegetables. Commercially available Folic Acid is prepared synthetically. Folic Acid occurs as a yellow or yellowish-orange crystalline powder and is very slightly soluble in water and insoluble in alcohol. Aqueous solutions of Folic Acid are heat sensitive and rapidly decompose in the presence of light and/or riboflavin; solutions should be stored in a cool place protected from light. Folic Acid is effective in the treatment of megaloblastic anemias due to a deficiency of Folic Acid (as may be seen in tropical or nontropical sprue) and in anemia of nutritional origin, pregnancy, infancy, or childhood. Folic Acid is relatively nontoxic in man. Rare instances of allergic responses to Folic Acid preparations have been reported and have included erythema, skin rash, itching, general malaise, and respiratory difficulty due to bronchospasm. Endocyte is developing an intravenous (IV) formulation of folic acid, called Neocepri®, which is intended for the diagnosis of positive folate receptor-positive status in patients with ovarian cancer when administered prior to the radioactive medicine, technetium Tc99m Etarfolatide. The benefits of Neocepri® are its ability to reduce the background activity observed on single photon emission computed tomography (SPECT) imaging in most normal, nontarget tissues (e.g. intestines, liver, kidney, spleen), thereby improving the image quality of the scans. The product had been granted orphan drug designation in the EU. Endocyte had filed a conditional marketing authorization application (CMA) with the European Medicines Agency (EMA) for Neocepri®.

Dimercaprol (2, 3-dimercapto-1-propanol) or British anti-Lewisite (BAL), is a colorless or almost colorless liquid chelating agent having a disagreeable, mercaptan-like odor. Dimercaprol was developed at Oxford University during World War II as a means of treating and reversing poisoning from Lewisite, an arsenical gas used in chemical warfare (and thus initially called British anti-Lewisite [BAL]). The sulfhydryl groups of dimercaprol form complexes with certain heavy metals thus preventing or reversing the metallic binding of sulfhydryl-containing enzymes. Parenterally administered dimercaprol is used to treat arsenic, gold, copper and mercury poisoning. It is indicated in acute lead poisoning when used concomitantly with edetate clcium disodium. Dimercaprol is occasionally used in the initial treatment of severe, symptomatic Wilson disease, but generally for a short time only.

Chloroquine (brand name Aralen) is indicated for the suppressive treatment and for acute attacks of malaria due to P. vivax, P.malariae, P. ovale, and susceptible strains of P. falciparum. The drug is also indicated for the treatment of extraintestinal amebiasis. In addition, chloroquine is in clinical trials as an investigational antiretroviral in humans with HIV-1/AIDS and as a potential antiviral agent against chikungunya fever. The mechanism of plasmodicidal action of chloroquine is not completely certain. However, is existed theory, that like other quinoline derivatives, it is thought to inhibit heme polymerase activity. The heme moiety consists of a porphyrin ring called Fe(II)-protoporphyrin IX (FP). To avoid destruction by this molecule, the parasite biocrystallizes heme to form hemozoin, a non-toxic molecule. Chloroquine enters the red blood cell, inhabiting parasite cell, and digestive vacuole by simple diffusion. Chloroquine then becomes protonated (to CQ2+), as the digestive vacuole is known to be acidic (pH 4.7); chloroquine then cannot leave by diffusion. Chloroquine caps hemozoin molecules to prevent further biocrystallization of heme, thus leading to heme buildup. Chloroquine binds to heme (or FP) to form what is known as the FP-Chloroquine complex; this complex is highly toxic to the cell and disrupts membrane function.

Benzhydrocodone is a prodrug of hydrocodone. Benzhydrocodone is formed by covalently bonding hydrocodone to benzoic acid. Benzhydrocodone itself is not pharmacologically active, but must be metabolized to hydrocodone by enzymes in the intestinal tract to optimally deliver its pharmacologic effects. Hydrocodone is a full agonist of the opioid receptors with a higher affinity for the mu-opioid receptor. Upon binding, hydrocodone produces an analgesic effect with no ceiling. APADAZ a combination of benzhydrocodone and acetaminophen is FDA approved and indicated for the short-term (no more than 14 days) management of acute pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. APADAZ, even when taken as recommended, can result in addiction, abuse, and misuse, which can lead to overdose and death.

Cyanocobalamin (commonly known as Vitamin B12) is the most chemically complex of all the vitamins. Cyanocobalamin's structure is based on a corrin ring, which, although similar to the porphyrin ring found in heme, chlorophyll, and cytochrome, has two of the pyrrole rings directly bonded. The central metal ion is Co (cobalt). Cyanocobalamin is naturally found in foods including meat (especially liver and shellfish), eggs, and milk products.Vitamin B12 is essential to growth, cell reproduction, hematopoiesis, and nucleoprotein and myelin synthesis. Cells characterized by rapid division (e.g., epithelial cells, bone marrow, myeloid cells) appear to have the greatest requirement for vitamin B12. Vitamin B12 can be converted to coenzyme B12 in tissues, and as such is essential for conversion of methylmalonate to succinate and synthesis of methionine from homocysteine, a reaction which also requires folate. In the absence of coenzyme B12, tetrahydrofolate cannot be regenerated from its inactive storage form, 5- methyltetrahydrofolate, and a functional folate deficiency occurs. Vitamin B12 also may be involved in maintaining sulfhydryl (SH) groups in the reduced form required by many SH-activated enzyme systems. Through these reactions, vitamin B12 is associated with fat and carbohydrate metabolism and protein synthesis. Vitamin B12 deficiency results in megaloblastic anemia, GI lesions, and neurologic damage that begins with an inability to produce myelin and is followed by gradual degeneration of the axon and nerve head. Cyanocobalamin is the most stable and widely used form of vitamin B12, and has hematopoietic activity apparently identical to that of the antianemia factor in purified liver extract. Parenteral (intramuscular) administration of vitamin B12 completely reverses the megaloblastic anemia and GI symptoms of vitamin B12 deficiency.

Ergoalcifediol (Vitamin D2) is a fat soluble steroid hormone precursor of vitamin D. The principal biologic function of vitamin D is the maintenance of normal levels of serum calcium and phosphorus in the bloodstream by enhancing the efficacy of the small intestine to absorb these minerals from the diet. Cholecalciferol is synthesized within our bodies naturally, but if UV exposure is inadequate or the metabolism of cholecalciferol is abnormal, then an exogenous source is required. Vitamin D2 is converted to 25-hydroxyvitamin D (25OHD) in the liver, and then to the active form, 1,25-dihydroxyvitamin D (1,25(OH)2D), in the kidney. Once transformed, it binds to the vitamin D receptor, which leads to a variety of regulatory roles. Vitamin D plays an important role in maintaining calcium balance and in the regulation of parathyroid hormone (PTH). It promotes renal reabsorption of calcium, increases intestinal absorption of calcium and phosphorus, and increases calcium and phosphorus mobilization from bone to plasma. Very few foods naturally contain vitamin D. Sources that contain the vitamin include fatty fish, the liver and fat of aquatic mammals (e.g., seals, polar bears), and eggs from chickens fed vitamin D-fortified feed. As such, many countries have instituted policies to fortify certain foods with vitamin D to compensate for the potentially low exposures of skin to sunlight. Vitamin D deficiency results in inadequate mineralization of bone or compensatory skeletal demineralization and causes decreased ionized calcium concentrations in blood and a resultant increase in the production and secretion of PTH. Increase in PTH stimulates the mobilization of skeletal calcium, inhibits renal excretion of calcium, and stimulates renal excretion of phosphorus. This results in normal fasting serum calcium concentrations and low or near-normal serum phosphorus. The enhanced mobilization of skeletal calcium induced by this secondary hyperparathyroidism leads porotic bone. Ergoalcifediol is used for use in the management of hypocalcemia and its clinical manifestations in patients with hypoparathyroidism, as well as for the treatment of familial hypophosphatemia (vitamin D resistant rickets). This drug has also been used in the treatment of nutritional rickets or osteomalacia, vitamin D dependent rickets, rickets or osteomalacia secondary to long-term high dose anticonvulsant therapy, early renal osteodystrophy, osteoporosis (in conjunction with calcium), and hypophosphatemia associated with Fanconi syndrome (with treatment of acidosis). Ergocalciferol is manufactured and marketed under various names, including Deltalin (Eli Lilly and Company), Drisdol (Sanofi-Synthelabo) and Calcidol (Patrin Pharma).

Sulfacetamide is a synthetic sulfonamide antibiotic, which exerts its effect through inhibition of bacterial dihydrofolate synthetase, an enzyme responsible for the conversion of p-aminobenzoic acid into folic acid in bacterias. The topical formulation of the drug is prescribed for the treatment of acne vulgaris and the ophtalmic formulation is used in patients with eye infections.

Sulfadiazine is a sulfonamide antibiotic. The sulfonamides are synthetic bacteriostatic antibiotics with a wide spectrum against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfonamides inhibit multiplication of bacteria by acting as competitive inhibitors of p-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Most sulfonamides are readily absorbed orally. However, parenteral administration is difficult, since the soluble sulfonamide salts are highly alkaline and irritating to the tissues. The sulfonamides are widely distributed throughout all tissues. High levels are achieved in pleural, peritoneal, synovial, and ocular fluids. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Their antibacterial action is inhibited by pus. Sulfadiazine is a competitive inhibitor of the bacterial enzyme dihydropteroate synthetase. This enzyme is needed for the proper processing of para-aminobenzoic acid (PABA) which is essential for folic acid synthesis. The inhibited reaction is necessary in these organisms for the synthesis of folic acid. Used for the treatment of rheumatic fever and meningococcal meningitis.

Estradiol benzoate is the synthetic benzoate ester of estradiol, a steroid sex hormone vital to the maintenance of fertility and secondary sexual characteristics in females. As the primary, most potent estrogen hormone produced by the ovaries, estradiol binds to and activates specific nuclear receptors. This agent exhibits mild anabolic and metabolic properties, and increases blood coagulability. Although estradiol benzoate is not approved by the FDA for use in humans in the United States, it is approved for veterinary use as a subdermal implant both alone (CELERIN®) and in combination with the anabolic steroid trenbolone acetate (SYNOVEX® Plus).

Histamine is a depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and a centrally acting neurotransmitter. Phosphate salt of jistamine was used as a diagnostic aid for evaluation of gastric acid secretory function. In addition, this compound is used as a positive control in evaluation of allergenic (immediate hypersensitivity or "Type I") skin testing. In addition, histamine is being studied for treatment of multiple sclerosis. It was approved, that histamine physiological functions are mediated by four 7-transmembrane G protein-coupled receptors (H1R, H2R, H3R, H4R) that are all targets of pharmacological intervention. The receptors display molecular heterogeneity and constitutive activity. H1R antagonists are long known antiallergic and sedating drugs, whereas the H2R led to the development of H2R-antagonists that revolutionized stomach ulcer treatment. The H3R is an auto receptor and heteroreceptor providing negative feedback on histaminergic and inhibition on other neurons. The H4R occurs on immuncompetent cells and the development of anti-inflammatory drugs is anticipated.