Prorenoate Potassium is a water-soluble synthetic aldosterone antagonist patented by Merck and Co., Inc. as an antihypertensive agent. In preclinical studies a significant natriuretic response was obtained at dosages of 1 mg/kg and approximately 1.8 mg/kg in the dog and rat, respectively. Prorenoate is relatively inactive at the renal level in adrenalectomized rats without mineralocorticoid replacement. Prorenoate possesses no more than 2% of the natriuretic activity of hydrochlorothiazide in the intact animal. Clearance studies in dogs indicate a direct renal tubular site of interaction between prorenoate and aldosterone independent of changes in renal hemodynamics. The natriuretic response occurred within 100 minutes after a single oral dose and was sustained for at least 7 hours. In clinical trials Prorenoate reversing the renal effects of the synthetic mineralocorticoid fludrocortisone in healthy individuals. Prorenoate was significantly more potent in retaining K+ than in increasing Na+ excretion.

Nafcaproic acid (DA-808) is a synthetic choleretic agent.

Camonagrel is a novel selective thromboxane synthetase inhibitor patented by Ferrer Internacional S. A. Camonagrel reduced platelet-subendothelium interaction under flow conditions, showing this effect in a range of concentrations lower than in inhibition of platelet aggregation.

Oxeglitazar (also known as EMD 336340 or LM 4156), an orally administered poorly water-soluble dual peroxisome proliferator-activated receptor α/γ agonist. This drug was used in the treatment of type II diabetes mellitus and metabolic syndrome. In addition, oxeglitazar participated in phase I trials for the gout treatment; however, this study was halted. Information about the further development of this drug is not available.

Linotroban is a potent and selective thromboxane (TXA2) receptor antagonist. It is known as a novel antithrombotic agent. Linotroban ingestion reduced significantly the thrombus volume. The coagulation, as measured by fibrin deposition and FPA plasma levels, was not significantly affected by Linotroban. It appears that the thromboxane A2 receptor antagonist linotroban reduces the thrombotic response by primarily impairing the platelet function at arterial blood flow conditions, and particularly at high wall shear rates. Linotroban had been in phase II clinical trial for the treatment of thrombosis. But this research was discontinued.