APAFANT is a platelet activating factor receptor (PAF-R) antagonist shown to have anticancer and cell differentiation effects. APAFANT has been found to be a specific PAF-R antagonist in pulmonary vasculature and when administered intratracheally in rats. APAFANT was observed to decrease lung nuclear factor-κB (NF-κB) activation, myeloperoxidase activity, and lavage neutrophil numbers. It has been shown to be a cytodifferentiating agent in murine erythroleukemia cells in vitro.

Meticrane is a diuretic. Meticrane is used to treat essential hypertension.

Atrinositol antagonizes the effect of neuropeptide Y (NPY) in guinea pig basilar arteries. Atrinositol molecule derived from phytic acid. It seems to exert potent protective effects on some of the manifestations associated with diabetes in rats. Atrinositol inhibits glucose-stimulated insulin secretion by a direct effect on the pancreatic islets. Atrinositol appears to modulate fatty acid desaturases and aldose reductase in platelets and delay by a few weeks the development of cataract in this acute model of diabetes. It normalizes platelet aggregation in diabetic animals after long-term administration in vivo.

Velaresol, also known as BW12C or BW12C79, is an oxyhemoglobin stabilizer that has the potential to induce normal tissue and tumor hypoxia preferential binding to the oxy conformation of hemoglobin, increasing its affinity for oxygen and thereby reducing oxygen availability to tissues. Velaresol stabilizes oxyhemoglobin also protect sickle cells against calcium-mediated dehydration. The activity of a number of bioreductive anticancer drugs, such as mitomycin C, maybe enhanced under hypoxic conditions. Velaresol administration caused significant radioprotection of normal tissues and induced tumor necrosis.

Ibudilast (KETAS®) is a non-selective cyclic nucleotide phosphodiesterase (PDE) inhibitor. It is an antithrombotic, antiasthmatic drug that is used for improving prognosis and relieving symptoms in patients suffering from ischemic stroke and for the treatment of bronchial asthma. A definitive mechanism of its action is yet to be established. However, inhibition of the release of inflammatory cytokines, inhibition of leukocyte activation, and inhibition of the expression of cell adhesion molecules have been proposed as likely mechanisms of action of ibudilast (KETAS®). It is currently in development in the US (for instance as a potential therapy for multiple sclerosis), but is approved for use in Japan.

Ethiazide is a diuretic.

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.

Xipamide is a diuretic of thiazide class. It is used for the treatment of hypertension and edema. The diuretic effect of the drug is due to reduction of sodium reabsorption and increase in potassium excretion.

Azosemide is a monosulfamyl belonging to the class of loop diuretics, used to treat hypertension, edema, and ascites. Azosemide inhibits sodium and chloride reabsorption throughout the thick ascending limb of the loop of Henle. The exact mechanism of action is not fully understood, but it mainly acts on both the medullary and cortical segments of the thick ascending limb of the loop of Henle. Delayed tolerance was demonstrated in humans by homeostatic mechanisms (principally an increase in aldosterone secretion and perhaps also an increase in the reabsorption of solute in the proximal tubule). After oral administration to healthy humans in the fasting state, the plasma concentration of azosemide reached its peak at 3–4 h with an absorption lag time of approximately 1 h and a terminal half-life of 2–3 h. The estimated extent of absolute oral bioavailability in humans was approximately 20.4%. After oral administration of the same dose of azosemide and furosemide, the diuretic effect was similar between the two drugs, but after intravenous administration, the effect of azosemide was 5.5–8 times greater than that in furosemide. This could be due to the considerable first-pass effect of azosemide. Azosemide is actively secreted in the renal proximal tubule possibly via nonspecific organic acid secretory pathway in humans. Thus, the amount of azosemide that reaches its site of action could be significantly modified by changes in the capacity of this transport system. This capacity, in turn, could be predictably changed in disease states, resulting in decreased delivery of the diuretic to the transport site, as well as in the presence of other organic acids such as nonsteroidal anti-inflammatory drugs which could compete for active transport of azosemide.

AZOLIMINE, an imidazolidinone, is a diuretic drug. It can antagonize the effects of mineralocorticoids on electrolyte excretion in the kidneys.