Gemcitabine is a nucleoside analog used as chemotherapy. It is marketed as Gemzar® by Eli Lilly and Company. Gemcitabine inhibits thymidylate synthetase, leading to inhibition of DNA synthesis and cell death. Gemcitabine is a prodrug so activity occurs as a result of intracellular conversion to two active metabolites, gemcitabine diphosphate and gemcitabine triphosphate by deoxycitidine kinase. Gemcitabine diphosphate also inhibits ribonucleotide reductase, the enzyme responsible for catalyzing synthesis of deoxynucleoside triphosphates required for DNA synthesis. Finally, Gemcitabine triphosphate (diflurorodeoxycytidine triphosphate) competes with endogenous deoxynucleoside triphosphates for incorporation into DNA. Gemcitabine is indicated for the treatment of advanced ovarian cancer that has relapsed at least 6 months after completion of platinum-based therapy; metastatic ovarian cancer; inoperable, locally advanced (Stage IIIA or IIIB), or metastatic (Stage IV) non-small cell lung cancer; and locally advanced (nonresectable Stage II or Stage III) or metastatic (Stage IV) adenocarcinoma of the pancreas.

Sodium phenylbutyrate is a salt of an aromatic fatty acid. The compound is used to treat urea cycle disorders, because its metabolites offer an alternative pathway to the urea cycle to allow excretion of excess nitrogen. Sodium phenylbutyrate is also a histone deacetylase inhibitor and chemical chaperone, leading respectively to research into its use as an anti-cancer agent and in protein misfolding diseases such as cystic fibrosis. It is used as adjunctive therapy for the management of chronic urea cycle disorders due to deficiencies in carbamylphosphate (CPS), ornithine transcarbamylase (OTC), or argininosuccinic acid synthetase. It is indicated in all neonatal- onset efficiency presenting within the first 28 days of life. Also indicated in patients with late-onset, presenting after the first month of life with a history of hyperammonemic encephalopathy. Sodium phenylbutyrate is a pro-drug and is rapidly metabolized to phenylacetate. Phenylacetate is a metabolically active compound that conjugates with glutamine via acetylation to form phenylacetylglutamine. The kidneys then excrete Phenylacetylglutamine. PBA (phenylbutyric acid) is absorbed from the intestine and converted by way of β-oxidation to the active moiety, phenylacetic acid (PAA). PAA is conjugated with glutamine in the liver and kidney by way of N-acyl coenzyme A-l-glutamine N-acyltransferase to form phenylacetylglutamine (PAGN). Like urea, PAGN incorporates two waste nitrogens and is excreted in the urine. On a molar basis, it is comparable to urea (each containing two moles of nitrogen). Therefore, phenylacetylglutamine provides an alternate vehicle for waste nitrogen excretion.

Levofloxacin is the L-isomer of the racemate, ofloxacin, a quinolone antimicrobial agent. Levofloxacin is used for oral and intravenous administration. Levofloxacin is sold under brand name levaquin and is used to treat infections in adults (≥18 years of age) caused by designated, susceptible bacteria such as, pneumonia: nosocomial and community acquired; skin and skin structure infections: complicated and uncomplicated; chronic bacterial prostatitis; inhalational anthrax. In addition this drug is used to treat plague; urinary tract infections: complicated and uncomplicated; acute pyelonephritis; acute bacterial exacerbation of chronic bronchitis and acute bacterial sinusitis. Levofloxacin, like other fluoroquinolones, inhibits the bacterial DNA gyrase, halting DNA replication. This results in strand breakage on a bacterial chromosome, supercoiling, and resealing. In addition, levofloxacin inhibits a bacterial type II topoisomerase.

Levolansoprazole is the levorotary (L-enantiomer) form of proton-pump inhibitor (PPI) Lansoprazole. Lansoprazole is a racemic 1:1 mixture of the enantiomers dexlansoprazole (Dexilant, formerly named Kapidex) and Levolansoprazole. Lansoprazole has used to the treatment of acid-reflux disorders (GERD), peptic ulcer disease, H. pylori eradication, and prevention of gastrointestinal bleeds with NSAID use. Levolansoprazole is extensively metabolized in the liver. Two metabolites have been identified in measurable quantities in plasma (the hydroxylated sulfinyl and sulfone derivatives of Levolansoprazole).

Penciclovir (DENAVIR®) is a synthetic acyclic guanine derivative with antiviral activity, mainly used to treat infections from herpes simplex virus (HSV) types 1 and 2. In cells infected with HSV-1 or HSV-2, the viral thymidine kinase phosphorylates penciclovir to a monophosphate form that, in turn, is converted by cellular kinases to the active form penciclovir triphosphate. Biochemical studies demonstrate that penciclovir triphosphate inhibits HSV polymerase competitively with deoxyguanosine triphosphate. Consequently, herpes viral DNA synthesis and, therefore, replication are selectively inhibited. Famciclovir (FAMVIR®) is a prodrug form of penciclovir with improved oral bioavailability.

Perindoprilat is a metabolite of perindopril. Perindopril is a long-acting angiotensin converting enzyme (ACE) inhibitor and it is used to treat high blood pressure, heart failure or stable coronary artery disease. Perindopril is designed to allow oral administration as perindoprilat is poorly absorbed from the gastrointestinal tract.

Tenivastatin (well known as simvastatin acid or simvastatin hydroxy acid) is a pharmacologically active metabolite, which is formed in the mammalian organism from lactone prodrug, simvastatin. Tenivastatin is a potent reversible inhibitor of HMGCR (HMG-CoA reductase), reduces cholesterol synthesis and increases low-density lipoprotein (LDL) receptors on cell membranes of liver and extrahepatic tissues. It is also a substrate of organic anion transporting polypeptide 1B1 (OATP1B1/Oatp2), an influx transporter expressed on the sinusoidal membrane of hepatocytes. Recent studies have shown that OATP1B1 plays a clinically important role in the hepatic elimination of several drugs including statins, via mediating the hepatic uptake. In addition, was discovered, that the tenivastatin was a substrate of another transporter protein, human organic anion transporting polypeptide 3A1 (OATP3A1), which is predominately expressed in the heart. Presence of OATP3A1 in cardiomyocytes suggested that transporter could modulate the exposure of cardiac tissue to simvastatin acid due to its enrichment in cardiomyocytes. Increases in the uptake of simvastatin acid by OATP3A1 when combined with OATP substrates suggest the potential for drug-drug interactions that could influence clinical outcomes.

Ramipril (sold under the brand name Altace ) is a prodrug belonging to the angiotensin-converting enzyme (ACE) inhibitors. It is metabolized to ramiprilat in the liver and, to a lesser extent, kidneys. Ramiprilat is a potent, competitive inhibitor of ACE, the enzyme responsible for the conversion of angiotensin I (ATI) to angiotensin II (ATII). ATII regulates blood pressure and is a key component of the renin-angiotensin-aldosterone system (RAAS). Ramipril is indicated for the treatment of hypertension, to lower blood pressure; also used to reduce the risk of myocardial infarction, stroke, or death from cardiovascular causes; in addition, this drug is used to reduce the rate of death, myocardial infarction and stroke in individuals at high risk of cardiovascular events.

Esomeprazole strontium is a proton pump inhibitor. It suppresses gastric acid secretion by specific inhibition H+/K+ ATPase in the gastric parietal cell. The S- and R-isomers of omeprazole are protonated and converted in the acidic compartment of the parietal cell forming the active inhibitor, the achiral sulphenamide. By acting specifically on the proton pump, esomeprazole blocks the final step in acid production, thus reducing gastric acidity. The drug is indicated for the treatment of gastroesophageal reflux disease, reduction the risk of NSAID-associated gastric ulcer, eradication of H.pylori, and pathological hypersecretory conditions.

Omeprazole belongs to a class of antisecretory compounds, which suppress gastric acid secretion by specific inhibition of the H+ /K+ ATPase enzyme system at the secretory surface of the gastric parietal cell. Because this enzyme system is regarded as the acid (proton) pump within the gastric mucosa, omeprazole has been characterized as a gastric acid-pump inhibitor, in that it blocks the final step of acid production. This effect is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus. Omeprazole is used under brand names Prilosec and Losec for treatment of duodenal ulcer in adults, gastric ulcer in adults, Gastroesophageal Reflux Disease. In addition it used for maintenance of healing of erosive esophagitis in pediatric patients and adults and for treatment of pathological hypersecretory conditions in adults (eg, Zollinger-Ellison syndrome, multiple endocrine adenomas and systemic mastocytosis). The most frequent significant adverse effects occurring in at least of patients include headache; upper respiratory tract infection, abdominal pain, diarrhea, back pain, weakness and rash.