Hydroxyresveratrol (Oxyresveratrol) is a major active compound in the heartwood of Artocarpus lacucha. It was first isolated from the heartwood of Artocarpus lakoocha, and has also been found in various plants, including Smilax China, Morus alba, Varatrum nigrum, Scirpus maritinus, and Maclura pomifera. Oxyresveratrol, an aglycone of mulberroside A, has been produced by microbial biotransformation or enzymatic hydrolysis of a glycosylated stilbene mulberroside A, which is one of the major compounds of the roots of M. alba. Oxyresveratrol plays an important role in anti-tyrosinase, antioxidant, anti-inflammatory, antiviral and neuroprotective properties. There are many A. lacucha commercial products available on the market for skin whitening and anti-aging effects. OxyResvenox™ is the registered trademark of Oxyresveratrol from Sabinsa. Oxyresveratrol is an analog of Resveratrol and is of synthetic origin. The hydroxystilbene compounds including oxyresveratrol and resveratrol showed the potent inhibitory effect on tyrosinase activity. Oxyresveratrol is also naturally present in Morus alba L., Morus bombycis. Oxyresveratrol exhibits a potent inhibitory effect on dopa oxidase activity of tyrosinase which catalyzes rate-limiting steps of melanin biosynthesis. Oxyresveratrol showed superoxide scavenging effects with the IC50 values 3.81 ± 0.5 uM, Oxyresveratrol exhibited a DPPH free radical scavenging effect (IC50 = 23.4 ± 1.5 uM). Oxyresveratrol also showed hepatoprotective effects with EC50 values 32.3 ± 2.62 uM, on tacrine-induced cytotoxicity in human liver-derived Hep G2 cells. Oxyresveratrol significantly inhibited LPS-evoked nuclear translocation of NF-kappaB and cyclooxygenase-2 (COX-2) activity in RAW 264.7 cells. The results suggest that the anti-inflammatory properties of oxyresveratrol might be correlated with inhibition of the iNOS expression through down-regulation of NF-kappaB binding activity and significant inhibition of COX-2 activity. Oxyresveratrol revealed a dose-dependent neuroprotective effect in an in vivo stroke model. This may prove to be beneficial for a therapeutic strategy to limit brain injury in acute brain ischemia.

Ipragliflozin L-proline is a sodium-glucose cotransporter 2 (SGLT2) inhibitor. It was developed and marketed as Suglat® by Astellas cooperating with Kotobuki Pharmaceutical and Merck Sharp & Dohme, and approved by Pharmaceuticals and Medical Devices Agency of Japan (PMDA) on Jan 17, 2014. It is indicated for the treatment of type 2 diabetes.

Voglibose is an alpha glucosidase inhibitor, which was initially marketed in Japan as an improving agent for postprandial hyperglycemia in diabetes mellitus. Later on the drug was approved for the prevention of type 2 diabetes. The drug is available in Asia under the name Basen.

Glyclopyramide (N-p-chlorobenzene sul-fonyl, N'-pyrrolidinourea) marketed under the tradename Deamelin-S is a sulfonylurea drug used in the treatment of diabetes mellitus. It has been marketed in Japan.

Carbutamide (or BZ-55) under the brand name Glucidoral was used as the anti-diabetic drug to treat diabetes in France. Carbutamide belongs to the family of sulphonylureas and reduces the excess sugar in the blood by promoting the secretion of insulin.

Glycyclamide (Tolcyclamide) isn a cyclohexyl-containing sulfonylurea compound with antihyperglycemic activity. Tolcyclamide is closely related to tolbutamide, with a cyclohexyl ring in place of the butyl group. It is much less potent than glipizide, being active at a daily dose of 1000 mg.

Taurocholic acid is a bile acid and is the product of conjugation of cholic acid with taurine. Its sodium salt is the chief ingredient of the bile of carnivorous animals. Taurocholic acid, as with all bile acids, acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as a cholagogue and cholerectic (a bile purging agent). Hydrolysis of taurocholic acid yields taurine, a nonessential amino acid. Taurocholic acid is one of the main components of urinary nonsulfated bile acids in biliary atresia. Raised levels of the bile acid taurocholate in the fetal serum in obstetric cholestasis may result in the development of a fetal dysrhythmia and in sudden intra-uterine death. In medical use, it is administered as a cholagogue and choleretic. Taurocholic acid is a potent TGR5 ligand, and in dogs, colonic perfusion with TCA induces PYY secretion. TCA enemas could stimulate GLP-1 and PYY secretion in obese patients with type 2 diabetes receiving the dipeptidyl peptidase-4 (DPP-4) inhibitor, sitagliptin. Satiogen Pharmaceuticals is developing rectally administered taurocholic acid, a bile acid, for the treatment of obesity and type 2 diabetes mellitus.

Ginsenoside C is a triterpene saponin originally found in species of Panax (ginseng) that exhibits anti-osteoporotic, antioxidative, antiviral, anti-hyperlipidemic, anti-metastatic, anti-angiogenic, and anticancer chemotherapeutic activities. In vivo, ginsenoside C decreases levels of malondialdehyde and increases levels of glutathione, improving bone microarchitecture and bone mineral density. In other animal models, this compound decreases virus titers and protects against infection of hemagglutinating virus of Japan. In adipocytes, ginsenoside C decreases levels of cholesterol and triglycerides and increases expression of SREBP. In uterine endometrial cancer cells, ginsenoside C decrease expression of matrix metalloproteinase 2 (MMP2), suppressive cellular invasion; this compound also inhibits neovascularization and tumor growth in animal models of melanoma. Ginsenoside C is a component of Korean Red Ginseng, marketed in Korea. Korean ginseng (Panax ginseng Meyer, Araliaceae) is traditionally used as an important herbal medicine in Far East Asia. Korean Red Ginseng is possibly effective for: • Alzheimer's disease. Evidence shows that taking Panax ginseng root daily for 12 weeks can improve mental performance in people with Alzheimer's disease. • Lung disease called chronic obstructive pulmonary disease (COPD). Taking Panax ginseng by mouth seems to improve lung function and some symptoms of COPD. • Mental function. Taking Panax ginseng by mouth might improve abstract thinking, mental arithmetic skills, and reaction times in healthy, middle-aged people but not in young adults. Panax ginseng alone does not seem to improve memory. But there is some evidence that a combination of Panax ginseng and ginkgo leaf extract can improve memory in otherwise healthy people between the ages of 38 and 66. • Erectile dysfunction (ED). Taking Panax ginseng by mouth seems to improve sexual function in men with erectile dysfunction. • Flu. Taking a specific Panax ginseng by mouth appears to reduce the risk of getting a cold or the flu. But, taking Panax ginseng does not seem to reduce flu symptoms or the length of the illness. • Multiple sclerosis-related fatigue. Taking Panax ginseng daily for 3 months reduces feelings of tiredness and improves quality of life in females with MS. • Premature ejaculation. Applying a cream containing Panax ginseng, angelica root, Cistanches deserticola, Zanthoxyl species, torlidis seed, clover flower, asiasari root, cinnamon bark, and toad venom (SS Cream) to the penis one hour before intercourse and washing off immediately before intercourse seems to help prevent premature ejaculation.

Omarigliptin is a new once-weekly dipeptidyl peptidase-4 (DPP-4) inhibitor developed for the treatment of type 2 diabetes. It potently but reversibly inhibits DPP-4 enzyme, which prolongs the circulating half-life of glucagon-like peptide-1 that increases insulin secretion in a glucose-dependent manner. Benefiting from glucose-dependent insulin secretion, omarigliptin is associated with low risk of hypoglycemia. Marizev (omarigliptin) 25 mg and 12.5 mg tablets were approved by Japan's Pharmaceuticals and Medical Devices Agency (PMDA) on 28th Sept 2015. Japan was the first country to have approved omarigliptin.

Trelagliptin (SYR-472), a novel dipeptidyl peptidase-4 inhibitor used for the treatment of type 2 diabetes mellitus. Trelagliptin (as the salt Trelagliptin succinate) was approved for use in Japan in March 2015. Takeda, the company that developed Trelagliptin, chose to not get approval for the drug in the USA and EU.