Vinpocetine is a synthetic derivative of the vinca alkaloid vincamine. Vinpocetine was first isolated from the plant in 1975 by the Hungarian chemist Csaba Szántay. The mass production of the synthetic compound was started in 1978 by the Hungarian pharmaceutical company Richter Gedeon. Vinpocetine has been reported to have cerebral blood-flow enhancing and neuroprotective effects, and has been used as a drug in Eastern Europe for the treatment of cerebrovascular disorders and age-related memory impairment. Vinpocetine acts as a phosphodiesterase (PDE) type-1 inhibitor in isolated rabbit aorta, Independent of vinpocetine's action on PDE, vinpocetine inhibits IKK preventing IκB degradation and the following translocation of NF-κB to the cell nucleus. Increases in neuronal levels of DOPAC, a metabolic breakdown product of dopamine, have been shown to occur in striatal isolated nerve endings as a result of exposure to vinpocetine. Such an effect is consistent with the biogenic pharmacology of reserpine, a structural relative of vinpocetine. However, this effect tends to be reversible upon cessation of vinpocetine administration, with full remission typically occurring within 3–4 weeks. Vinpocetine is generally well-tolerated in humans. No serious side effects have thus far been noted in clinical trials although none of these trials were long-term. Some users have reported headaches, especially at doses above 15 milligrams per day, as well as occasional upset stomach. The safety of vinpocetine in pregnant women has not been evaluated. Vinpocetine is not FDA approved in the United States for therapeutic use. The U.S. Food & Drug Administration (FDA) has ruled that vinpocetine, due to its synthetic nature and proposed therapeutic uses, was ineligible to be marketed as dietary supplement under the Federal Food, Drug, and Cosmetic Act (FDCA).

Bezafibrate is a lipid-lowering fibric acid derivative. Bezafibrate directly bound to and activated all three peroxisome proliferator-activated receptor (PPAR) subtypes respectively in PPAR binding and transactivation assays. However, from a biochemical point of view, bezafibrate is a PPAR ligand with a relatively low potency. Bezafibrate leads to considerable raising of HDL cholesterol and reduces triglycerides, improves insulin sensitivity and reduces blood glucose level, significantly lowering the incidence of cardiovascular events and new diabetes in patients with features of metabolic syndrome. It is the only pan-PPAR activator with more than a quarter of a century of therapeutic experience with a good safety profile.

Cefsulodin is a third-generation of cephalosporin antibiotic with a narrow spectrum of activity. It has a specific activity against Pseudomonas aeruginosa. Cefsulodin’s targets are bacterial penicillin binding proteins. Drug is indicated for the treatment of infections of lower respiratory tract, skin and skin structures, urinary tract, bone and joint; treatment of gynecological infections; treatment of intra-abdominal infections; treatment of septicemia and CNS infections including meningitis caused by susceptible strains of specific microorganisms. Cefsulodin appears to be well tolerated and relatively free of any significant toxicity except for nausea and vomiting.

Rizatriptan (trade name Maxalt) is a 5-HT1 receptor agonist of the triptan class of drugs developed by Merck & Co. for the treatment of migraine headaches. Rizatriptan (trade name Maxalt) is a 5-HT1 receptor agonist of the triptan class of drugs developed by Merck & Co. for the treatment of migraine headaches. Rizatriptan acts as an agonist at serotonin 5-HT1B and 5-HT1D receptors. Rizatriptan binds with high affinity to human cloned 5-HT1B/1D receptors. Rizatriptan benzoate presumably exerts its therapeutic effects in the treatment of a migraine headache by binding to 5-HT1B/1D receptors located on intracranial blood vessels and sensory nerves of the trigeminal system. Rizatriptan is completely absorbed following oral administration. The mean oral absolute bioavailability of the rizatriptan benzoate tablet is about 45%, and mean peak plasma concentrations are reached in approximately 1-1.5 hours. The presence of a migraine headache did not appear to affect the absorption or pharmacokinetics of rizatriptan. Food has no significant effect on the bioavailability of rizatriptan but delays the time to reach peak concentration by an hour. The primary route of rizatriptan metabolism is via oxidative deamination by monoamine oxidase-A (MAO-A) to the indole acetic acid metabolite, which is not active at the 5-HT1B/1D receptor. N-mono-desmethyl-rizatriptan, a metabolite with activity similar to that of parent compound at the 5-HT1B/1D receptor, is formed to a minor degree. Plasma concentrations of N-mono-desmethyl-rizatriptan are approximately 14% of those of parent compound, and it is eliminated at a similar rate. Other minor metabolites, the N-oxide, the 6-hydroxy compound, and the sulfate conjugate of the 6-hydroxy metabolite are not active at the 5-HT1B/1D receptor.

Rizatriptan (trade name Maxalt) is a 5-HT1 receptor agonist of the triptan class of drugs developed by Merck & Co. for the treatment of migraine headaches. Rizatriptan (trade name Maxalt) is a 5-HT1 receptor agonist of the triptan class of drugs developed by Merck & Co. for the treatment of migraine headaches. Rizatriptan acts as an agonist at serotonin 5-HT1B and 5-HT1D receptors. Rizatriptan binds with high affinity to human cloned 5-HT1B/1D receptors. Rizatriptan benzoate presumably exerts its therapeutic effects in the treatment of a migraine headache by binding to 5-HT1B/1D receptors located on intracranial blood vessels and sensory nerves of the trigeminal system. Rizatriptan is completely absorbed following oral administration. The mean oral absolute bioavailability of the rizatriptan benzoate tablet is about 45%, and mean peak plasma concentrations are reached in approximately 1-1.5 hours. The presence of a migraine headache did not appear to affect the absorption or pharmacokinetics of rizatriptan. Food has no significant effect on the bioavailability of rizatriptan but delays the time to reach peak concentration by an hour. The primary route of rizatriptan metabolism is via oxidative deamination by monoamine oxidase-A (MAO-A) to the indole acetic acid metabolite, which is not active at the 5-HT1B/1D receptor. N-mono-desmethyl-rizatriptan, a metabolite with activity similar to that of parent compound at the 5-HT1B/1D receptor, is formed to a minor degree. Plasma concentrations of N-mono-desmethyl-rizatriptan are approximately 14% of those of parent compound, and it is eliminated at a similar rate. Other minor metabolites, the N-oxide, the 6-hydroxy compound, and the sulfate conjugate of the 6-hydroxy metabolite are not active at the 5-HT1B/1D receptor.

Rizatriptan (trade name Maxalt) is a 5-HT1 receptor agonist of the triptan class of drugs developed by Merck & Co. for the treatment of migraine headaches. Rizatriptan (trade name Maxalt) is a 5-HT1 receptor agonist of the triptan class of drugs developed by Merck & Co. for the treatment of migraine headaches. Rizatriptan acts as an agonist at serotonin 5-HT1B and 5-HT1D receptors. Rizatriptan binds with high affinity to human cloned 5-HT1B/1D receptors. Rizatriptan benzoate presumably exerts its therapeutic effects in the treatment of a migraine headache by binding to 5-HT1B/1D receptors located on intracranial blood vessels and sensory nerves of the trigeminal system. Rizatriptan is completely absorbed following oral administration. The mean oral absolute bioavailability of the rizatriptan benzoate tablet is about 45%, and mean peak plasma concentrations are reached in approximately 1-1.5 hours. The presence of a migraine headache did not appear to affect the absorption or pharmacokinetics of rizatriptan. Food has no significant effect on the bioavailability of rizatriptan but delays the time to reach peak concentration by an hour. The primary route of rizatriptan metabolism is via oxidative deamination by monoamine oxidase-A (MAO-A) to the indole acetic acid metabolite, which is not active at the 5-HT1B/1D receptor. N-mono-desmethyl-rizatriptan, a metabolite with activity similar to that of parent compound at the 5-HT1B/1D receptor, is formed to a minor degree. Plasma concentrations of N-mono-desmethyl-rizatriptan are approximately 14% of those of parent compound, and it is eliminated at a similar rate. Other minor metabolites, the N-oxide, the 6-hydroxy compound, and the sulfate conjugate of the 6-hydroxy metabolite are not active at the 5-HT1B/1D receptor.

Trandolapril is a non-sulhydryl prodrug that belongs to the angiotensin-converting enzyme (ACE) inhibitor class of medications. It is metabolized to its biologically active diacid form, trandolaprilat, in the liver. Trandolaprilat inhibits 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). Trandolapril may be used to treat mild to moderate hypertension, to improve survival following myocardial infarction in clinically stable patients with left ventricular dysfunction, as an adjunct treatment for congestive heart failure, and to slow the rate of progression of renal disease in hypertensive individuals with diabetes mellitus and microalbuminuria or overt nephropathy. Trandolapril is marketed by Abbott Laboratories under the brand name Mavik.

Trandolapril is a non-sulhydryl prodrug that belongs to the angiotensin-converting enzyme (ACE) inhibitor class of medications. It is metabolized to its biologically active diacid form, trandolaprilat, in the liver. Trandolaprilat inhibits 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). Trandolapril may be used to treat mild to moderate hypertension, to improve survival following myocardial infarction in clinically stable patients with left ventricular dysfunction, as an adjunct treatment for congestive heart failure, and to slow the rate of progression of renal disease in hypertensive individuals with diabetes mellitus and microalbuminuria or overt nephropathy. Trandolapril is marketed by Abbott Laboratories under the brand name Mavik.

Dexlansoprazole (trade names Kapidex, Dexilant) is a proton pump inhibitor (PPI) that is marketed by Takeda Pharmaceuticals for the treatment of erosive esophagitis and gastro-oesophageal reflux disease. Dexlansoprazole is used to heal and maintain healing of erosive esophagitis and to treat heartburn associated with gastroesophageal reflux disease (GERD). It lasts longer than lansoprazole, to which it is chemically related, and needs to be taken less often. Dexlansoprazole is supplied for oral administration as a dual delayed-release formulation in capsules and orally disintegrating tablets. The capsules and tablets contain dexlansoprazole in a mixture of two types of enteric-coated granules with different pH-dependent dissolution profiles. The most significant adverse reactions (≥2%) reported in clinical trials were diarrhea, abdominal pain, nausea, upper respiratory tract infection, vomiting, and flatulence.

Dexlansoprazole (trade names Kapidex, Dexilant) is a proton pump inhibitor (PPI) that is marketed by Takeda Pharmaceuticals for the treatment of erosive esophagitis and gastro-oesophageal reflux disease. Dexlansoprazole is used to heal and maintain healing of erosive esophagitis and to treat heartburn associated with gastroesophageal reflux disease (GERD). It lasts longer than lansoprazole, to which it is chemically related, and needs to be taken less often. Dexlansoprazole is supplied for oral administration as a dual delayed-release formulation in capsules and orally disintegrating tablets. The capsules and tablets contain dexlansoprazole in a mixture of two types of enteric-coated granules with different pH-dependent dissolution profiles. The most significant adverse reactions (≥2%) reported in clinical trials were diarrhea, abdominal pain, nausea, upper respiratory tract infection, vomiting, and flatulence.