Timonacic or thioproline (4-Thiazolidinecarboxylic acid) is the product of condensation between cysteine and formaldehyde. Dietary timonacic slows the aging process in mammals and prolongs their life span. It exerts antioxidant and antineoplastic actions however its mechanism of action is elusive. Timonacic (brand names Heparegen or Arbitol) is used for the treatment of liver diseases.

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.

Timonacic or thioproline (4-Thiazolidinecarboxylic acid) is the product of condensation between cysteine and formaldehyde. Dietary timonacic slows the aging process in mammals and prolongs their life span. It exerts antioxidant and antineoplastic actions however its mechanism of action is elusive. Timonacic (brand names Heparegen or Arbitol) is used for the treatment of liver diseases.

Ethamsylate (2,5-dihydroxy-benzene-sulfonate diethylammonium salt) is a synthetic hemostatic drug indicated in cases of capillary bleeding. Ethamsylate acts on the first step of hemostasis by improving platelet adhesiveness and restoring capillary resistance. In addition it inhibits prostaglandin biosynthesis. Well-controlled clinical trials clearly showed the therapeutic efficacy of ethamsylate in dysfunctional uterine bleeding, with the magnitude of blood-loss reduction being directly proportional to the severity of the menorrhagia. Other well-controlled clinical trials showed therapeutic efficacy of ethamsylate in periventricular hemorrhage in very low birth weight babies and surgical or postsurgical capillary bleeding.

Pemafibrate (Parmodia®) is a novel, highly selective peroxisome proliferator-activated receptor (PPAR)-α modulator (SPPARM). It acts by binding to PPAR-α and regulating the expression of target genes that modulate lipid metabolism, thereby decreasing plasma triglyceride levels and increasing high-density lipoprotein cholesterol levels. Developed by Kowa Company, Ltd., oral pemafibrate has been approved in Japan for the treatment of hyperlipidaemia (including familial hyperlipidaemia). Pemafibrate is undergoing phase III development in a number of countries for the treatment of dyslipidaemias and is also in phase III development for the treatment of hypertriglyceridaemia.

(S)-Lercanidipine is enantiomer of antihypertensive drugs Lercanidipine, that acts by blocking L-type calcium channels, allowing relaxation and opening of blood vessels. The dihydropyridine calcium antagonists promote systemic vasodilatation by a reversible blockade of voltage-dependent Ca2+ influx through L-type channels in the cell membrane. (S)-Lercanidipine has 100- to 200-fold greater affinity than the (R)-enantiomer for the L-type calcium channel. The pharmacokinetics of (S)- Lercanidipine has been evaluated in healthy volunteers, in elderly and non-elderly patients with hypertension, and in patients with renal or hepatic impairment. Patients from these studies were investigated after receiving a single 10 or 20 mg dose of [14C]-labeled rac-Lercanidipine as a solution. The maximum plasma concentrations of (S)-Lercanidipine were reached within 2–3 h and the area under the plasma concentration-time curves were not linearly related to the dose, indicating a saturable first-pass metabolism. The absorption of (S)-LER increases after the ingestion of a high-fat meal. Lercanidipine is highly bound to plasma protein (>98%) in humans. Its volume of distribution of 2–2.5 L/kg was determined in healthy volunteers after intravenous infusion of 2 mg. Lercanidipine is extensively metabolized by CYP 3A4 to inactive pyridine derivatives. A crossover study involving a single administration of either 10 mg of (R)- or (S)-LER or 20 mg of rac-LER as a solution demonstrated no in vivo enantiomer interconversion

Bietamiverine is an antispasmodic agent.

Olanexidine [1-(3,4-dichlorobenzyl)-5-octylbiguanide] (formerly OPB-2045), an antimicrobial agent exhibited antimicrobial activity against a wide range of bacteria, especially Gram-positive bacteria, was synthesized in 1997. To optimize its use as a topical antiseptic, olanexidine was converted to the gluconate salt. The resulting formulation (OPB) had more potent bactericidal activity against methicillin-resistant S. aureus and vancomycin-resistant enterococci in both in vitro and in vivo animal models than chlorhexidine and PVP-I. The mechanism of action was considered to be follows: olanexidine binds to the cell membrane, disrupts membrane integrity, and exerts its bacteriostatic and bactericidal activities by causing the irreversible leakage of intracellular components. At relatively high concentrations, olanexidine aggregates the cells through a protein-denaturing effect.

(R)-Lercanidipine is enantiomer of antihypertensive drugs Lercanidipine, that acts by blocking L-type calcium channels, allowing relaxation and opening of blood vessels. The dihydropyridine calcium antagonists promote systemic vasodilatation by a reversible blockade of voltagedependent Ca2+ influx through L-type channels in the cell membrane. (S)-Lercanidipine has 100- to 200-fold greater affinity than the (R)-enantiomer for the L-type calcium channel. The pharmacokinectics of (S)- Lercanidipine has been evaluated in healthy volunteers, in elderly and non-elderly patients with hypertension, and in patients with renal or hepatic impairment. Patients from these studies were investigated after receiving a single 10 or 20 mgdose of [14C]-labeled rac-Lercanidipine as a solution. The maximum plasma concentrations of (S)-Lercanidipine were reached within 2–3 h and the area under the plasma concentration–time curves were not linearly related to the dose, indicating a saturable first-pass metabolism. The absorption of (S)-LER increases after the ingestion of a highfat meal. Lercanidipine is highly bound to plasma protein (>98%) in humans. Its volume of distribution of 2–2.5 L/kg was determined in healthy volunteers after intravenous infusion of 2 mg. Lercanidipine is extensively metabolized by CYP 3A4 to inactive pyridine derivatives. A crossover study involving a single administration of either 10 mg of (R)- or (S)-LER or 20 mg of rac-LER as a solution demonstrated no in vivo enantiomer interconversion

Aminopropyl racementhyl phosphate is a prodrug of menthol patented by Pacific Corporation (Korea). Upon administration, it is enzymatically decomposed into menthol and 3-aminopropylphosphoric acid, a component used for anti-aging cosmetic composition. Aminopropyl racementhyl phosphate was found to reduce the irritation of menthol while maintaining its useful effects.