Moxonidine is a second-generation, centrally acting antihypertensive drug with a distinctive mode of action. Moxonidine activates I1-imidazoline receptors (I1-receptors). Imidazoline I1-receptor agonism represents a new mode of antihypertensive action to inhibit peripheral alpha-adrenergic tone by a central mechanism. Adrenaline, noradrenaline and renin levels are reduced, a finding consistent with central inhibition of sympathetic tone. Moxonidine acts centrally to reduce peripheral sympathetic activity, thus decreasing peripheral vascular resistance. In patients with mild to moderate hypertension, moxonidine reduces blood pressure (BP) as effectively as most first-line antihypertensives when used as monotherapy and is also an effective adjunctive therapy in combination with other antihypertensive agents. It improves the metabolic profile in patients with hypertension and diabetes mellitus or impaired glucose tolerance, is well tolerated, has a low potential for drug interactions and may be administered once daily in most patients. Moxonidine is a good option in the treatment of patients with mild to moderate hypertension, particularly as adjunctive therapy in patients with the metabolic syndrome.

Levosimendan (Simdax) is a novel intravenous agent that exerts inotropic effects through sensitization of myofilaments to calcium and vasodilator effects by binding to cardiac troponin C in a calcium-dependent manner. It also has a vasodilatory effect, by opening adenosine triphosphate (ATP)-sensitive potassium channels in vascular smooth muscle to cause smooth muscle relaxation. Unlike other calcium sensitizing compounds, the binding of levosimendan is highly dependent on the intracellular concentration of calcium, such that calcium sensitivity is enhanced only when the calcium level is elevated. Levosimendan is licensed for the treatment of decompensated heart failure in many countries but not in North America. This drug also passed phase III clinical trials for the prevention of low cardiac output syndrome in pediatric patients after open heart surgery.

Biapenem (INN) is a carbapenem antibiotic. It has in vitro activity against anaerobes. Approved in Japan in 2001. Biapenem is a carbopenems antibiotic which suppresses bacterial growth by inhibiting the enzymes responsible for bacterial cell wall synthesis, and shows broad-spectrum antibacterial activity both against gram-positive bacteria and gram-negative bacteria. Biapenem is stable to dehaloperoxidase-I (DHP-I) and can not be administered together with DHP-I inhibitor. This product is applicable to the treatment of a variety of infections caused by sensitive bacteria: septicemia, pneumonia, lung abscess, secondary infections resulting from chronic respiratory disease, cystitis, pyelonephritis, peritonitis, appendagitis, etc. Biapenem is generally well tolerated. The most common adverse events in clinical trials were skin eruptions/rashes, nausea and diarrhoea.

ISOPENTYL NITRITE (Amyl nitrite) is a chemical compound with an amyl group attached to the nitrite functional group. Amyl nitrite, in common with other alkyl nitrites, is a potent vasodilator; it expands blood vessels, resulting in lowering of the blood pressure. Alkyl nitrites are a source of nitric oxide, which signals for relaxation of the involuntary muscles. Physical effects include the decrease in blood pressure, headache, flushing of the face, increased heart rate, dizziness, and relaxation of involuntary muscles, especially the blood vessel walls and the internal and external anal sphincter. There are no withdrawal symptoms. Overdose symptoms include nausea, vomiting, hypotension, hypoventilation, shortness of breath, and fainting. The effects set in very quickly, typically within a few seconds and disappear within a few minutes. Amyl nitrite may also intensify the experience of synesthesia. Amyl nitrite is employed medically to treat heart diseases as well as angina. Amyl nitrite is sometimes used as an antidote for cyanide poisoning. It can act as an oxidant, to induce the formation of methemoglobin. Methemoglobin, in turn, can sequester cyanide as cyanomethemoglobin.

Triflusal (trade names Disgren, Grendis, Aflen, Triflux, ets) is a member of the salicylate family with a well-established platelet aggregation inhibitory profile that differs from that of acetylsalicylic acid (ASA) in its pharmacokinetic and pharmacodynamic properties. Triflusal irreversibly inhibits cyclooxygenase-1 through its potency is lower than that of acetylsalicylic acid (ASA). Triflusal shows potent inhibition of vascular prostacyclin synthesis, and weak inhibition of platelet phosphodiesterase. Triflusal also favors the production of NO and increases the concentration of cyclic nucleotides. A number of experimental and clinical studies have shown that triflusal is a potentially useful choice in the treatment and prophylaxis of brain ischemia because of its antithrombogenic as well as neuroprotective effects. Triflusal anti-thrombogenic properties have been demonstrated clinically and experimentally, while its neuroprotective effects have been shown only in animal models. Triflusal is administered orally. It Is absorbed primarily in the small intestines and its bioavailability in humans ranges from 83% to 100%. Once absorbed, 99% of triflusal binds to plasma proteins in experimental animals as well as in humans. Triflusal readily crosses organic barriers, but its blood levels are always higher than tissue levels. Upon passage through the liver, triflusal is deacetylated, forming 2-hydroxy-4-trifluoro-methyl-benzoicacid (HTB) as the main active metabolite. Triflusal inhibits platelet aggregation and interaction of platelets with subendothelium. The antiplatelet effect of triflusal has been documented in experimental animals and in humans, in in vitro and ex vivo studies, and in in vivo models of thrombogenesis in animals. Triflusal inhibited collagen- or arachidonic acid-induced platelet aggregation in platelet-rich plasma more effectively than ADP-induced platelet aggregation. Independently of its antithrombotic effect, triflusal acts directly on the nervous tissue to reduce the damage caused by ischemic or cytotoxic insults. The daily oral intake of 600 mg triflusal led to HTB levels in the cerebrospinal fluid that had neuroprotective effects in experimental animals. Traditionally, antiplatelet drugs have been associated with an increased risk of bleeding complications.

Acipimox (5-methylpyrazinecarboxylic acid 4-oxide) is a new lipolysis inhibitor that has a distant chemical relationship with nicotinic acid (NA). The anti-lipolytic action of acipimox is mediated through suppression of intracellular cyclic AMP levels, with the subsequent decrease in cyclic AMP-dependent protein kinase activity, leading to the reduced association of hormone-sensitive lipase with triacylglycerol substrate in the lipid droplet of adipocytes. Acipimox has been identified as an agonist at G-protein coupled nicotinic acid HM74A and HM74B receptors. Acipimox (Olbetam) is indicated for the treatment as alternative or adjunct treatment to reduce triglyceride levels in patients who have not responded adequately to other treatments such as statin or fibrate treatment for hypertriglyceridaemia (Fredrickson type IV hyperlipoproteinaemia) and hypercholesterolaemia and hypertriglyceridaemia (Fredrickson type IIb hyperlipoproteinaemia).

Ornidazole is nitroimidazole derivative. It is an antiprotozoal drug that has proven to be effective against Trichomonas vaginalis, Entoamoeba histolytica, Giardia lamblia and Helicobacter pylori. The reduction of the nitro group and the generation of short-lived reactive intermediates are the basis of its parasiticidal activity. Ornidazole is a DNA-tropic drug with selective activity against microorganisms with enzyme systems capable of reducing the nitrogroup and catalyze the interaction between ferrodoxin proteins and nitrocompounds. After the drug penetrates the microbial cell, the mechanism of its action is based reducing the nitrogroup under the influence of the microorganism’s nitroreductases and the activity of the reduced nitroimidazole. The reduction products create compounds with DNA causing it to degrade, and disrupt the DNA replication and transcription processes. Furthermore, the drug’s metabolism products have cytotoxic properties and disrupt cellular respiration processes. It is indicated for the treatment of anaerobic systemic infections caused by ornidazole-sensitive microflora, prevention of infections caused by anaerobic bacteria, during operative treatment (especially middle and straight intestine surgeries), gynecological surgeries, severe intestinal ameobiasis, all extra-intestinal ameobiasis forms, giardiasis. Ornidazole was shown to be effective for the prevention of recurrence of Crohn's disease after ileocolonic resection.

Rafoxanide is a halogenated salicylanilide used as a fasciolicide in cattle, sheep, goats, and horses. It is also active against nematodes, and the sheep nasal bot fly. Rafoxanide acts as by uncoupling oxidative phosphorylation of flukes, including reduced ATP levels, decreased glycogen content and accumulation of succinate.

Hymecromone (4-methylumbelliferone) is already approved drug in Europe and Asia where it is used to treat biliary spasm. It is used as choleretic and antispasmodic drugs and as a standard for the fluorometric determination of enzyme activity. The concomitant administration of Hymecromone with products, containing metoclopramide, leads to mutual decrease of their action. Due to a danger of diarrhea with subsequent hypokalemia, Hymecromone should be applied with caution to patients on cardiac glycosides therapy (in these cases the sensitivity to them is increased). Hymecromone can be administered simultaneously with otherspasmolytics and analgesics. Very rare allergic reactions, itching, erythema, rashes; diarrhea which normally disappears by reduction of dose or discontinuance of therapy.

Tenonitrozole is an antiprotozoal given in the treatment of trichomoniasis. It is given orally in a dose of 250 mg twice daily with meals, for 4 days.