Desoxycorticosterone pivalate (DOCP) is a mineralocorticoid hormone and an analog of desoxycorticosterone. DOCP is a long-acting ester of desoxycorticosterone acetate (DOCA) which is recognized as having the same qualitative effects as the natural mineralocorticoid hormone aldosterone. It’s used as Percorten-V for replacement therapy for the mineralocorticoid deficit in dogs with primary adrenocortical insufficiency. Percorten-V is only available in the U.S., Canada, Australia and recently, Denmark. Percorten was originally developed for the treatment of Addison's disease in humans but the demand for it decreased significantly once Florinef was available. Unaware that their product was being prescribed “off-label” for the treatment of canine Addison’s Disease and faced with a decreased demand for Percorten, the manufacturer *almost* discontinued production until the veterinary community rose up and voiced their distress. Field trials were run and the FDA approved the use of Percorten-V (the "v" is for veterinary). DOCP like other adrenocorticoid hormones is thought to act by controlling the rate of synthesis of proteins. It reacts with receptor proteins in the cytoplasm to form a steroid-receptor complex. This complex moves into the nucleus, where it binds to chromatin that result in genetic transcription of cellular DNA to messenger RNA. The steroid hormones appear to induce transcription and synthesis of specific proteins, which produce the physiologic effects seen after administration. The most important effect of DOCP is to increase the rate of renal tubular absorption of sodium. This effect is seen most intensely in the thick portion of the ascending limb of the loop of Henle. It also increases sodium absorption in the proximal convoluted tubule but this effect is less important in sodium retention. Chloride follows the sodium out of the renal tubule. Another important effect of DOCP is enhanced renal excretion of potassium. This effect is driven by the resorption of sodium that pulls potassium from the extracellular fluid into the renal tubules, thus promoting potassium excretion.

Ethylparaben is produced naturally and found in several fruits and insects, where it acts as an antimicrobial agent. Ethylparaben is mainly used as antiseptics in cosmetics, food and medicine (E number E214). It is also can be used as feed preservatives and antiseptic for bacteria. Ethylparaben is readily absorbed from the gastrointestinal tract or through the skin. It is hydrolyzed to p-hydroxybenzoic acid and rapidly excreted in urine without accumulating in the body. Under the Federal Food, Drug, and Cosmetic Act (FD&C Act), cosmetic products and ingredients, other than color additives, do not need FDA approval before they go on the market. Broad concentration ranges reported in each product category in 1981 were < 0.1% and > 0.1% to 1%. Studies show the in vivo estrogenicity of MP and EP at human exposure levels, and indicate that populations exposed to large amounts of MP and EP may have a high burden of estrogenicity-related diseases.

Cefteram is a semisynthetic cephalosporin formulated for oral administration as the prodrug ester, cefteram pivoxil. The mechanism of action of cefteram is inhibition of bacterial cell wall synthesis. Cefteram exerts its bactericidal activity by strongly binding to penicillin-binding protein (PBP) 3, 1A, and 1Bs. The drug is available in Japan and is used for the treatment of bacterial infections.

Fluocortolone is a topical corticosteroid (class of steroid hormones formed in the adrenal gland). Is primary indicated in condition like, Ana fissure, Dermatosis haemorrhoids, proctitis. The signs and symptoms that are produced after the acute overdosage include convulsions, respiratory arrest, allergic skin reactions. Glucocorticoids, such as fluocortolone, act through nuclear hormone receptors Schaaf and Cidlowski (2002). The two members of this family are glucocorticoid receptor (GR) type I and GR type I I. Activation of these sites alters gene expression of endogenous agents that influence immune and inflammatory responses.

The potential antiviral effect of adefovir, an acyclic nucleoside phosphonate analog of 2′-deoxyadenosine monophosphate, was first studied by Holý and De Clercq in 1980s. Adefovir is an acyclic nucleotide analog of adenosine monophosphate which is phosphorylated to the active metabolite adefovir diphosphate by cellular kinases. Adefovir diphosphate inhibits HBV DNA polymerase (reverse transcriptase) by competing with the natural substrate deoxyadenosine triphosphate and by causing DNA chain termination after its incorporation into viral DNA. Oral adefovir dipivoxil is effective and generally well tolerated in HBeAg-positive and -negative patients chronically infected with wild-type or lamivudine-resistant HBV.

Lorazepam (brand name Ativan) is indicated for the management of anxiety disorders or for the short-term relief of the symptoms of anxiety or anxiety associated with depressive symptoms. Anxiety or tension associated with the stress of everyday life usually does not require treatment with an anxiolytic. Lorazepam binds to an allosteric site on GABA-A receptors, which are pentameric ionotropic receptors in the CNS. Binding potentiates the effects of the inhibitory neurotransmitter GABA, which upon binding opens the chloride channel in the receptor, allowing chloride influx and causing hyperpolarization of the neuron. Studies in healthy volunteers show that in single high doses Ativan (lorazepam) has a tranquilizing action on the central nervous system with no appreciable effect on the respiratory or cardiovascular systems. Ativan (lorazepam) is readily absorbed with an absolute bioavailability of 90 percent. The mean half-life of unconjugated lorazepam in human plasma is about 12 hours and for its major metabolite, lorazepam glucuronide, about 18 hours. At clinically relevant concentrations, lorazepam is approximately 85% bound to plasma proteins. Lorazepam is rapidly conjugated at its 3-hydroxy group into lorazepam glucuronide which is then excreted in the urine. Lorazepam glucuronide has no demonstrable CNS activity in animal. Most adverse reactions to benzodiazepines, including CNS effects and respiratory depression, are dose dependent, with more severe effects occurring with high doses. Paradoxical reactions, including anxiety, excitation, agitation, hostility, aggression, rage, sleep disturbances/insomnia, sexual arousal, and hallucinations may occur. Small decreases in blood pressure and hypotension may occur but are usually not clinically significant, probably being related to the relief of anxiety produced by lorazepam.