Estrone, one of the major mammalian estrogens, is an aromatized C18 steroid with a 3-hydroxyl group and a 17-ketone. It is produced in vivo from androstenedione or from testosterone via estradiol. It is produced primarily in the ovaries, placenta, and in peripheral tissues (especially adipose tissue) through conversion of adrostenedione. Estrone may be further metabolized to 16-alpha-hydroxyestrone, which may be reduced to estriol by estradiol dehydrogenase. Estrogens enter the cells of responsive tissues (e.g. female organs, breasts, hypothalamus, pituitary) where they interact with estrogen receptors. Hormone-bound estrogen receptors dimerize, translocate to the nucleus of cells and bind to estrogen response elements (ERE) of genes. Binding to ERE alters the transcription rate of affected genes. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) release from the anterior pituitary. Estrone dl-Form is a derivative of estrone. As early as 1935 extensive research programs directed toward the total synthesis of the female sex hormone estrone were well under way. These studies have since been continued with increasing interest in laboratories all over the world. In 1942 Bachmann, Kushner and Stevenson succeeded in synthesizing a stereoisomer of the hormone,''estrone a." Using essentially the same synthetic scheme as Bachmann, et al., Anner and Miescher were able to isolate additional stereoisomers including dl-estrone (Estrone, (+-)-Isomer) . Six of the eight possible racemic forms, estrone, a-f, have now been reported. Dl-Estrone (Estrone, (+-)-Isomer) is less active than Estrone.

Pentaerythritol tetranitrate is an organic nitrate that has been used for the treatment of angina pectoris. Upon administration, the drug undergoes exstensive metabolism to NO which causes vasodilation and the relaxation of smooth muscle cells. The compound belongs to a familiy of explosive substances and may be used accordingly.

Acetic acid (a component of vinagre) is used in medicine for the treatment of otitis externa caused by bacterial infections. The solution containing acetic acid was approved by FDA.

Phenobarbital is a barbiturate derivative used to treat insomnia and anxiety, seizures, hyperbilirubinemia in neonates and cholestasis. Phenobarbital promotes binding to inhibitory gamma-aminobutyric acid subtype receptors, and modulates chloride currents through receptor channels.

Ticalopride is an isomer of the active metabolite of cisapride, which is marketed by Janssen for the treatment of nocturnal heartburn due to gastroesophageal reflux disease. Ticalopride acts through the stimulation of the serotonin 5-HT4 receptors which increases acetylcholine release in the enteric nervous system (specifically the myenteric plexus). This results in increased tone and amplitude of gastric contractions, relaxation of the pyloric sphincter and the duodenal bulb, and increased peristalsis of the duodenum and jejunum resulting in accelerated gastric emptying and intestinal transit. Phase II clinical trials of the Ticalopride are being suspended while investigators study reports of adverse events in patients with gastroesophageal reflux disease and diabetes.

Urocanic acid is a breakdown (deamination) product of histidine. In the liver, urocanic acid is an intermediate in the conversion of histidine to glutamic acid, whereas in the epidermis, it accumulates and may be both a UV protectant and an immunoregulator. Urocanic acid (UA) exists as a trans isomer (t-UA, approximately 30 mg/cm2) in the uppermost layer of the skin (stratum corneum). t-UA is formed as the cells of the second layer of skin become metabolically inactive. During this process, proteins and membranes degrade, histidine is released, and histidase (histidine ammonia lyase) catalyzes the deamination of histidine to form t-UA. t-UA accumulates in the epidermis until removal by either the monthly skin renewal cycle or sweat. Upon absorption of UV light, the naturally occurring t-UA isomerizes to its cis form, c-UA. Because DNA lesions (e. g. , pyrimidine dimers) in the lower epidermis can result from UV-B absorption, initial research proposed that t-UA acted as a natural sunscreen absorbing UV-B in the stratum corneum before the damaging rays could penetrate into lower epidermal zones. c-UA also suppresses contact hypersensitivity and delayed hypersensitivity, reduces the Langerhans cell count in the epidermis, prolongs skin-graft survival time, and affects natural killer cell activity. It has also been proposed that c-UA may mediate the transient alteration in immune surveillance resulting in immunosuppression induced after UV-irradiation, by interacting with immune cells locally and/or systemically to generate T cells with suppressor function.

Antineoplaston (Phenylacetylglutamine) is the amino acid acetylation product of phenylacetate (or phenylbutyrate after beta-oxidation). The chemical structure of Antineoplaston AS2-5 corresponds to phenylacetylglutamine. Two synthetic derivatives of Antineoplaston A10 were named Antineoplaston AS2-1 and AS2-5. All antineoplaston formulations were submitted for Phase I clinical studies in advanced cancer patients. The treatment was free from significant side-effects and resulted in objective response in a number of advanced cancer cases. Antineoplastons are an experimental cancer therapy developed by S.R. Burzynski, MD, PhD. Chemically, antineoplastons are a mixture of amino acid derivatives, peptides, and amino acids found in human blood and urine. The developer originally isolated antineoplastons from human blood and later found the same peptides in urine. Urine was subsequently used because it was less expensive and easier to obtain. Since 1980, antineoplastons have been synthesized from commercially available chemicals at the Burzynski Research Institute. According to the developer, antineoplastons are part of a biochemical surveillance system in the body and work as "molecular switches." For the developer, cell differentiation is the key to cancer therapy. At the molecular level, abnormal cells that are potential cancer cells need to be "switched" to normal mode. Antineoplastons are the surveillance system that directs cancer cells into normal channels of differentiation. According to statements published by the developer, people with cancer lack this surveillance system because they do not have an adequate supply of antineoplastons.