Acadesine, also known as 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside, AICA-riboside, and AICAR, is an AMP-activated protein kinase activator which is used for the treatment of acute lymphoblastic leukemia (ALL) and may have applications in treating other disorders such as mantle cell lymphoma (MCL). The mechanism by which acadesine selectively kills B-cells is not yet fully elucidated. The action of acadesine does not require the tumour suppressor protein p53 like other treatments. This is important, as p53 is often missing or defective in cancerous B-cells. Studies have shown acadesine activates AMPK and induces apoptosis in B-cell chronic lymphocytic leukemia cells but not in T lymphocytes. Antiapoptotic proteins of the Bcl-2 family regulate MCL cell sensitivity to acadesine and combination of this agent with Bcl-2 inhibitors might be an interesting therapeutic option to treat MCL patients. Acadesine has anti-ischemic properties that is currently being studied (Phase 3) for the prevention of adverse cardiovascular outcomes in patients undergoing coronary artery bypass graft (CABG) surgery. Adenosine itself has many beneficial cardioprotective properties that may therefore be harnessed by this new class of drugs. Unlike adenosine, acadesine acts specifically at sites of ischemia and is therefore void of the systemic hemodynamic effects that may complicate adenosine therapy. Animal and in vitro studies have established acadesine as a promising new agent for attenuating ischemic and reperfusion damage to the myocardium. Acadesine also possesses the theoretical (but unproven) benefit of attenuating reperfusion injury after acute myocardial infarction (MI). Further research is needed to define the full potential of this unique agent in various clinical situations involving myocardial ischemia.

Phosmet is a non-systemic, organophosphate insecticide used on both plants and animals. Phosmet is mainly used on apple trees for control of coddling moth, though it is used on a wide range of fruit crops, ornamentals and vines for the control of aphids, suckers, mites and fruit flies. Phosmet is a moderately potent cholinesterase inhibitor.

Trapidil, a platelet-derived growth factor antagonist, was originally developed as a vasodilator and anti-platelet agent and has been used to treat patients with ischemic coronary heart, liver, and kidney disease. Used to treat patients with ischemic coronary heart, liver, and kidney disease.

Aceclofenac is a non-steroidal anti-inflammatory drug (NSAID) analog of Diclofenac. It is used for the relief of pain and inflammation in rheumatoid arthritis, osteoarthritis and ankylosing spondylitis. The dose is 100 mg twice daily, and should not be given to people with porphyria or breastfeeding mothers and is not recommended for children. Aceclofenac is a cytokine inhibitor. Aceclofenac works by blocking the action of a substance in the body called cyclo-oxygenase. Cyclo-oxygenase is involved in the production of prostaglandins (chemicals in the body which cause pain, swelling and inflammation). Aceclofenac is the glycolic acid ester of diclofenac. The incidence of gastric ulcerogenicity of aceclofenac has been reported to be significantly lower than that of other frequently prescribed NSAIDs: for instance, 2-fold less than naproxen, 4-fold less than diclofenac, and 7-fold less than indomethacin. Aceclofenac is metabolized in human hepatocytes and human microsomes to form [2-(2',6'-dichloro-4'-hydroxy- phenylamino)phenyl] acetoxyacetic acid as the major metabolite, which is then further conjugated.

Lonazolac is a nonsteroidal anti-inflammatory drug. The mononuclear cell response to a synovial stimulus can be abolished by very low concentrations of lonazolac. This blockade can be completely released by the addition of prostaglandin E2. Lonazolac appears therefore as an agent able in addition to modulate the immune response. The release of histamine from human basophils was significantly decreased after preincubation of the cells with lonazolac Ca. Preincubation of human polymorphonuclear leukocytes with lonazolac Ca led to an inhibition of leukotriene generation induced by either the Ca ionophore or opsonized zymosan. Lonazolac Ca affected different enzymes of the platelet activating factor metabolism. After pre- and post-treatment with lonazolac-Ca, the numbers of animals with lung metastases and the score of metastases significantly decreased. Lonazolac-Ca is indicated for the treatment of painful inflammatory rheumatic diseases of the joints and the spine. Acute irritation in osteoarthritis and spondylosis. Soft tissue rheumatism. Post-traumatic and postoperative pain and swelling states.

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.