Levothyroxine (T4) is a synthetically prepared levo isomer of thyroxine, the major hormone secreted from the thyroid gland. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Thyroxine is peripherally deiodinated to form triiodothyronine (T3) which exerts a broad spectrum of stimulatory effects on cell metabolism. Thyroid hormone increases the metabolic rate of cells of all tissues in the body. In the fetus and newborn, thyroid hormone is important for the growth and development of all tissues including bones and the brain. In adults, thyroid hormone helps to maintain brain function, food metabolism, and body temperature, among other effects. The symptoms of thyroid deficiency relieved by levothyroxine include slow speech, lack of energy, weight gain, hair loss, dry thick skin and unusual sensitivity to cold. Levothyroxine acts like the endogenous thyroid hormone thyroxine (T4, a tetra-iodinated tyrosine derivative). In the liver and kidney, T4 is converted to T3, the active metabolite. In order to increase solubility, the thyroid hormones attach to thyroid hormone binding proteins, thyroxin-binding globulin, and thyroxin-binding prealbumin (transthyretin). Transport and binding to thyroid hormone receptors in the cytoplasm and nucleus then takes place. Thus by acting as a replacement for natural thyroxine, symptoms of thyroxine deficiency are relieved. Levothyroxine is used for use alone or in combination with antithyroid agents to treat hypothyroidism, goiter, chronic lymphocytic thyroiditis, myxedema coma, and stupor.

Thiamine, also known as vitamin B1, plays a key role in the human metabolism. It is present in many dietary sources such as meats, eggs, fish, beans and peas, nuts, and whole grains. Upon administration thiamine is converted by thiamine pyrophosphokinase-1 (TPK1) to the active form, thiamine pyrophosphate, which serves as a cofactor for enzymes involved in the TCA cycle and the non-oxidative part of the pentose phosphate pathway. The lack of thiamine may cause the thiamine deficiency. The classical syndrome caused primarily by thiamine deficiency in humans is beriberi, however, symptoms of thiamine deficiency also include congestive heart failure, metabolic acidosis, confusion, ataxia and seizures. Thiamine is a component of many vitamin complexes, which are approved for the treatmen and prevention of general vitamin deficiency, including the thiamine deficiency.

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.

Guaifenesin is an expectorant the action of which promotes or facilitates the removal of secretions from the respiratory tract. The precise mechanism of action of guaifenesin is not known; however, it is thought to act as an expectorant by increasing the volume and reducing the viscosity of secretions in the trachea and bronchi. In turn, this may increase the efficiency of the cough reflex and facilitate removal of the secretions. Guaifenesin is over-the-counter drug for the treatment of cough and common cold.

Undecylenic acid is unsaturated fatty acid, which naturally occurs in sweat, and is commercially produced by the vacuum distillation of castor bean oil. It is recognized as GRASE by FDA, and is marketed over the counter to treat skin infections and to relieve itching. Undecylenic acid acts by inhibition of morphogenesis from yeast to hyphae forms.

Glycerin (glycerol) is 3-carbon alcohol naturally occurring in the human body. It is the structural backbone triacylglycerol molecules, and can also be converted to a glycolytic substrate for subsequent metabolism. Glycerin is a colorless, odorless, viscous, sweet-tasting liquid. The FDA classifies glycerol as "generally recognized as safe". Glycerin is used in the pharmaceutical industry as a sweetener in syrups, lozenges, and as an excipient in eyewash solutions. As an individual prescription product, glycerin has uses as a hyperosmotic, osmotic diuretic, and ophthalmic agent. It may be used as an eye drop in the treatment of glaucoma to reduce intraocular pressure, as a solution or suppository for short-term treatment of constipation, to evacuate the bowel prior to a colonoscopy, and in some ocular surgeries. It may be given intravenously to reduce pressure inside the brain and used externally on the skin as a moisturizer. Glycerin has many other uses in the agricultural, food and pharmaceutical industry.

Morphine-6-glucuronide is a pharmacologically active metabolite of morphine that is being developed by CeNeS Pharmaceuticals as an alternative to morphine for the management of postoperative pain. Compared to morphine, Morphine-6-glucuronide has been reported to have6 and 86 times lower affinity for the human mu and kappa opioid receptors, respectively, and similar affinity for the delta opioid receptor. Morphine-6-glucuronide is was studied in phase III clinical trials for postoperative pain management. Unfortunately, Morphine-6-glucuronide failed to demonstrate superior safety compared to Morphine and further development was discontinued. Morphine-6-glucuronide accumulates after administration of morphine to patients with renal insufficiency, and analgesia can be obtained with lower doses of morphine compared to patients with normal renal function. More importantly, the dose should be reduced to avoid serious side-effects, although the simulations in this review did not account for side-effects.

Tozasertib, originally developed as VX-680 by Vertex (Cambridge, MA) and later renamed MK-0457 by Merck (Whitehouse Station, NY), was the first aurora kinase inhibitor to be tested in clinical trials. The drug, a pyrimidine derivative, has affinity for all aurora family members at nanomolar concentrations with inhibitory constant values (Ki(app)) of 0.6, 18, and 4.6 nM for aurora A, aurora B, and aurora C, respectively. Preclinical studies confirmed that tozasertib inhibited both aurora A and aurora B kinase activity, and activity has been reported against prostate, thyroid, ovarian, and oral squamous cancer cell lines. Upon treatment with tozasertib, cells accumulate with a 4N DNA content due to a failure of cytokinesis. This ultimately leads to apoptosis, preferentially in cells with a compromised p53 function. Tozasertib is an anticancer chemotherapeutic pan-aurora kinase (AurK) inhibitor that also inhibits FMS-like tyrosine kinase 3 (FLT3) and Abl. Tozasertib is currently in clinical trials as a potential treatment for acute lymphoblastic leukemia (ALL). In cellular models of cancer, tozasertib activates caspase-3 and PARP and decreases expression of HDAC, increasing apoptosis and inhibiting cell growth. In other cellular models, tozasertib inhibits cell proliferation and metastasis by blocking downstream ERK signaling and downregulating cdc25c and cyclin B. This compound also decreases tumor growth in an in vivo model of prostate cancer.