Paritaprevir is a potent inhibitor of the NS3/4A protease that rapidly and consistently suppresses HCV. Paritaprevir is metabolized by the Cytochrome P450 isoform 3A (CYP3A); therefore, ritonavir was used concurrently to increase plasma concentrations and to prolong the half-life of this agent allowing for once-daily dosing. Several antiviral regimens combining paritaprevir with other agents have shown impressive results, tolerable side effects, and importantly, provided support of ‘all-oral’ interferon-free regimens against HCV. Paritaprevir monotherapy is discontinued now but paritaprevir is used as a component of Viekira Pak and Technivie for the treatment of patients with genotype 1 chronic hepatitis C virus (HCV) infection.

Simeprevir is a hepatitis C virus (HCV) NS3/4A protease inhibitor approved for the treatment of Chronic Hepatitis C (genotype 1 and 4). Inhibiting NS3/4A, simeprevir blocks viral replication. In in vitro assays simeprevir was potent against HCV genotype 1a and 1b. Simeprevir must not be administered as monotherapy and should only be prescribed with both peginterferon alfa and ribavirin.

Telaprevir (marketed under the brand names Incivek and Incivo) is a direct-acting antiviralagent against the hepatitis C virus (HCV). It is a hepatitis C virus NS3/4A protease inhibitor indicated for the treatment of genotype 1 chronic hepatitis C (CHC) in adult patients with compensated liver disease, including cirrhosis, who are treatment-naïve or who have been previously treated with interferon-based treatment, including prior null responders, partial responders, and relapsers in combination with peginterferon alfa and ribavirin. Telaprevir is not used as a monotherapy. It is necessary for the proteolytic cleavage of the HCV encoded polyprotein into mature forms of the NS4A, NS4B, NS5A and NS5B proteins and essential for viral replication. It belongs to the chemical class of alpha-ketoamids and binds to NS3/4A in a covalent but reversible manner.

Cerivastatin (BAYCOL®) is a competitive inhibitor of HMG-CoA reductase, which is responsible for the conversion of 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) to mevalonate, a precursor of sterols, including cholesterol. The inhibition of cholesterol biosynthesis by cerivastatin reduces the level of cholesterol in hepatic cells, which stimulates the synthesis of low-density lipoprotein (LDL) receptors, thereby increasing the uptake of cellular LDL particles. The end result of these biochemical processes is a reduction of the plasma cholesterol concentration. On August 8, 2001 the U.S. Food and Drug Administration (FDA) announced that Bayer Pharmaceutical Division voluntarily withdrew BAYCOL® from the U.S. market, due to reports of fatal rhabdomyolysis, a severe adverse reaction from this cholesterol-lowering (lipid-lowering) product. It has also been withdrawn from the Canadian market.

Tacrine is a parasympathomimetic- a reversible cholinesterase inhibitor that is indicated for the treatment of mild to moderate dementia of the Alzheimer's type. An early pathophysiological feature of Alzheimer's disease that is associated with memory loss and cognitive deficits is a deficiency of acetylcholine as a result of selective loss of cholinergic neurons in the cerebral cortex, nucleus basalis, and hippocampus. Tacrine is postulated to exert its therapeutic effect by enhancing cholinergic function. This is accomplished by increasing the concentration of acetylcholine at cholinergic synapses through reversible inhibition of its hydrolysis by acetylcholinesterase. If this proposed mechanism of action is correct, tacrine's effect may lessen as the disease progresses and fewer cholinergic neurons remain functionally intact. There is no evidence that tacrine alters the course of the underlying dementing process. The mechanism of tacrine is not fully known, but it is suggested that the drug is an anticholinesterase agent which reversibly binds with and inactivates cholinesterases. This inhibits the hydrolysis of acetylcholine released from functioning cholinergic neurons, thus leading to an accumulation of acetylcholine at cholinergic synapses. The result is a prolonged effect of acetylcholine. is used for the palliative treatment of mild to moderate dementia of the Alzheimer's type. Tacrine was marketed under the trade name Cognex. Because of its liver toxicity and attendant requirement for monitoring liver function, tacrine prescriptions dropped after other acetylcholinesterase inhibitors were introduced, and its use has been largely discontinued.

Trimetrexate, a second-generation folate antagonist which was used under brand name NEUTREXIN with concurrent leucovorin administration (leucovorin protection) was indicated as an alternative therapy for the treatment of moderate-to-severe Pneumocystis carinii pneumonia (PCP) in immunocompromised patients, including patients with the acquired immunodeficiency syndrome (AIDS). Nevertheless, this product was discontinued. In present time, trimetrexate with a different combinations is in the phase II of clinical trial for the treatment the following cancer diseases: pancreatic cancer and colorectal cancer (in combination with fluorouracil and leucovorin) and to treat a refractory acute leukemia in combination with leucovorin. Trimetrexate is a competitive inhibitor of dihydrofolate reductase (DHFR) from bacterial, protozoan, and mammalian sources. DHFR catalyzes the reduction of intracellular dihydrofolate to the active coenzyme tetrahydrofolate. Inhibition of DHFR results in the depletion of this coenzyme, leading directly to interference with thymidylate biosynthesis, as well as inhibition of folate-dependent formyltransferases, and indirectly to inhibition of purine biosynthesis. The result is disruption of DNA, RNA, and protein synthesis, with consequent cell death.

Misoprostol is an antineoplastic drug used to treat skin growths caused by sun exposure. Masoprocol is a novel antineoplastic agent was used for the treatment of actinic keratoses (precancerous skin growths that can become malignant if left untreated). Masoprocol was withdrawn from the U.S. market in June 1996. It is not known exactly how Masoprocol works. Studies have shown that masoprocol is a potent 5-lipoxygenase inhibitor and has antiproliferative activity against keratinocytes in tissue culture, but the relationship between this activity and its effectiveness in actinic keratoses is unknown. Masoprocol also inhibits prostaglandins but the significance of this action is not yet known. Symptoms of overdose or allergic reaction include bluish coloration of skin, dizziness, severe, or feeling faint, wheezing or trouble in breathing.

Trilostane is a synthetic steroid, which interferes with the formation of both cortisol and aldosterone. It is an inhibitor of 3 beta-hydroxysteroid dehydrogenase. This drug under trade name MODRASTANE was withdrawn from human use in the United States market. But marketed under the trade names Modrenal and is already approved in the United Kingdom for the treatment of advanced post-menopausal breast cancer and Cushing 's disease. In addition, this drug has been successfully developed and marketed for veterinary use in the United Kingdom under the trade name Vetoryl.

Azaribine (2′, 3′, 5′-triacetyl-6-azauridine) is the orally absorbable triacetylated derivative of the pyrimidine analog 6-azauridine. Ribonucleoside of 6-azauracil, which can be derived in the tissues by the deacetylation of azaribine, has been shown, after its intracellular conversion to 6-azauridine-5'-monophosphate, to serve as an inhibitor of the activity of a key enzyme, orotidine-5'-monophosphate (OMP) decarboxylase, critically concerned with the biosynthesis de novo of pyrimidines essential for the formation of nucleic acids. Azaribine exerts antineoplastic action. In 1975 azaribine was approved for the treatment of psoriasis. The drug was withdrawn because it may cause life-threatening or fatal blood clots in the veins and arteries.

Thioguanine is an antineoplastic anti-metabolite used in the treatment of several forms of leukemia including acute nonlymphocytic leukemia. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA. They prevent these substances becoming incorporated in to DNA during the "S" phase (of the cell cycle), stopping normal development and division. Thioguanine was first synthesized and entered into clinical trial more than 30 years ago. It is a 6-thiopurine analogue of the naturally occurring purine bases hypoxanthine and guanine. Intracellular activation results in incorporation into DNA as a false purine base. An additional cytotoxic effect is related to its incorporation into RNA. Thioguanine is cross-resistant with mercaptopurine. Cytotoxicity is cell cycle phase-specific (S-phase). Thioguanine competes with hypoxanthine and guanine for the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRTase) and is itself converted to 6-thioguanilyic acid (TGMP), which reaches high intracellular concentrations at therapeutic doses. TGMP interferes with the synthesis of guanine nucleotides by its inhibition of purine biosynthesis by pseudofeedback inhibition of glutamine-5-phosphoribosylpyrophosphate amidotransferase, the first enzyme unique to the de novo pathway of purine ribonucleotide synthesis. TGMP also inhibits the conversion of inosinic acid (IMP) to xanthylic acid (XMP) by competition for the enzyme IMP dehydrogenase. Thioguanine nucleotides are incorporated into both the DNA and the RNA by phosphodiester linkages, and some studies have shown that incorporation of such false bases contributes to the cytotoxicity of thioguanine. Its tumor inhibitory properties may be due to one or more of its effects on feedback inhibition of de novo purine synthesis; inhibition of purine nucleotide interconversions; or incorporation into the DNA and RNA. The overall result of its action is a sequential blockade of the utilization and synthesis of the purine nucleotides. Thioguanine is used for remission induction and remission consolidation treatment of acute nonlymphocytic leukemias. It is marketed under the trade name Lanvis and Tabloid among others.