Cinnamic acid is a polyphenol found in cinnamon oil and used in commercial flavorings. Recent studies have shown the pharmacological properties of cinnamic acid and its derivatives, including hepatoprotective, anti-oxidant, and anti-diabetic activities. In preclinical studies cinnamic acid demonstrated to be a promising candidate for the treatment ob obesity and diabetes. The mechanism of action of cinnamic acid in obesity is explained by its ability to inhibit lipases and ACE (angiotensin-converting enzyme). However, there are several hypotesis regarding the effect of cinnamic acid in diabetes: cinnamic acid enhances glucose-induced insulin secretion, prevents palmitic acid-induced lipotoxicity, inhibits palmitic acid-induced alteration of lipogenic gene and protein expression (AMPK, SREBP-1c, FAS, ACC), inhibits DPP IV, exhibits an additive effect on the uptake of glucose, stimulates adiponectin secretion, etc.

Diisopropylamine (DIPA) is a secondary amine, which is used as a chemical intermediate, and catalyst for the synthesis of pesticides and pharmaceuticals. DIPA is primarily used as a precursor for the herbicides dilate and triallate, as well as certain sulfenamides used in the vulcanization of rubber. It is used for adjusting pH in cosmetic formulations, in colognes, and toilet cleaners. It is associated with tobacco either as a natural component of tobacco, pyrolysis product (in tobacco smoke), or additive for one or more types of tobacco products. When given intravenously to hypertensive patients, DIPA is known as an antihypertensive agent. DIPA exerts its action by lowering arterial blood pressure, reduction of stroke volume and cardiac output. DIPA reduced blood glucose concentrations in fasted mice and in fasted, glucose-loaded, or streptozotocin-diabetic rats. DADA (diisopropylamine dichloroacetate) was identified as an active domain of pangamic acid. DADA is a vasodilator of peripheral and cerebral arterioles. DADA also considered to aid in the detoxification of chemical and metallic metabolites, possibly by the formation of chelate-like compounds whose excretion by the kidneys is facilitated and increased. DADA increases oxygen utilization and cortical glucose uptake.

Cyclopenthiazide is a thiazide diuretic. It inhibits the Na+-Cl− symporter in the distal convoluted tubule of the kidney. Cyclopenthiazide is used for the treatment of edema, including that associated with heart failure, and for the treatment of hypertension.

Benidipine is an orally triple L-, T-, and N-type calcium channel blocker for the treatment of hypertension and angina pectoris synthesized and developed by Kyowa Hakko Kogyo Co., Ltd. Benidipine, approved in Japan in November 1991, has become one of the three best selling CCBs and is highly useful as a potent, long-lasting antihypertensive and antianginal agent.

Benidipine is an orally triple L-, T-, and N-type calcium channel blocker for the treatment of hypertension and angina pectoris synthesized and developed by Kyowa Hakko Kogyo Co., Ltd. Benidipine, approved in Japan in November 1991, has become one of the three best selling CCBs and is highly useful as a potent, long-lasting antihypertensive and antianginal agent.

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.

Zofenopril is an inhibitor of Angiotensin Converting Enzyme (ACE), which is approved in Europe for the treatment of hypertension and acute myocardial infarction.

Cilazapril (Vascace and Dynorm are brand names in a number of European countries) is an angiotensin converting enzyme (ACE; kininase II) inhibitor. It competes with angiotensin I for binding at the angiotensin-converting enzyme, blocking the conversion of angiotensin I to angiotensin II. Cilazapril is a prodrug that is hydrolyzed after absorption to its main metabolite cilazaprilat. The half-life (30–50 hours) of cilazapril allows for once daily dosing unless the hypertension is severe. Cilazapril is used for the treatment of hypertension, congestive heart failure, post-myocardial infarction, and some other indications. Adverse events were mostly observed within the first 8-16 weeks of treatment, with headache, dizziness, fatigue, nausea, cough and chest pain being the most frequent.

Indoramin is an alpha-1 selective antagonist of adrenergic receptor, sold under trade names Baratol and Doralese, and now available as a generic. It has no reflex tachycardia and direct myocardial depression action and is used to treat benign prostate hyperplasia (as 20 mg tablets) or reduce blood pressure (as 25 mg strength tablets). It was also investigated as a treatment of a migraine and congestive heart failure.

Cilnidipine (FRC-8653) is a dihydropyridine (DHP) type of calcium channel antagonist. The L-type Ca2+ channel blockade by cilnidipine affects predominantly vascular smooth muscle, thereby producing vasodilation of peripheral resistance vessels and coronary arteries. The blockade of N-type Ca2+ channels affects predominantly peripheral nerve endings of sympathetic neurons, thereby dilating blood vessels by lowering plasma catecholamine levels. Furthermore, renoprotective and neuroprotective effects as well as cardioprotective action of cilnidipine have been demonstrated in clinical practice or animal examinations. Cilnidipine was originated by Fuji & Rebio Pharmaceutical Co., Ltd. and developed jointly with Ajinomoto for the treatment of hypertension. Cilnidipine has been launched in Japan.