Rofecoxib is a nonsteroidal anti-inflammatory drug which selectively inhibits COX-2 and subsequent prostaglandin synthesis. The drug was developed by Merk and approved by FDA in 1999 for relief of signs and symptoms of arthritis, acute pain in adults, and painful menstrual cycles under the name Vioxx. Later on Merck voluntarily withdrawn Vioxx from the market due to safety concerns (high risk of heart attack and stroke).

Chloramphenicol is a broad-spectrum antibiotic that was first isolated from Streptomyces venezuelae in 1947. The drug was subsequently chemically synthesized. It has both a bacteriostatic and bactericidal effect; in the usual therapeutic concentrations it is bacteriostatic. Chloramphenicol is used for the treatment of serious gram-negative, gram-positive, and anaerobic infections. It is especially useful in the treatment of meningitis, typhoid fever, and cystic fibrosis. It should be reserved for infections for which other drugs are ineffective or contraindicated. Chloramphenicol, a small inhibitor of bacterial protein synthesis, is active against a variety of bacteria and readily enters the CSF. It has been used extensively in the last decades for the treatment of bacterial meningitis. In industrialized countries, chloramphenicol is restricted mostly to topical uses because of the risk of induction of aplastic anemia. However, it remains a valuable reserve antibiotic for patients with allergy to β-lactam antibiotics or with CNS infections caused by multiresistant pathogens.

Sesamin is the most prominent lignan compound found in sesame seeds, one of the two highest sources of lignans in the human diet (the other being flax). Sesamin is catered to be a nutritional supplement that confers antioxidant and antiinflammatory effects (if touting its health properties) or possibly being an estrogen receptor modulator and fat burner (if targeting atheltes or persons wishing to lose weight). Sesamin has a few mechanisms, and when looking at it holistically it can be summed up as a fatty acid metabolism modifier. It appears to inhibit an enzyme known as delta-5-desaturase (Δ5-desaturase) which is a rate-limiting enzyme in fatty acid metabolism; inhibiting this enzyme results in lower levels of both eicosapentaenoic acid (EPA, one of the two fish oil fatty acids) as well as arachidonic acid, and this mechanism appears to be relevant following oral ingestion. The other main mechanism is inhibiting a process known as Tocopherol-ω-hydroxylation, which is the rate limiting step in the metabolism of Vitamin E; by inhibiting this enzyme, sesamin causes a relative increase of vitamin E in the body but particularly those of the gamma subset (γ-tocopherol and γ-tocotrienol) and this mechanism has also been confirmed to be active following oral ingestion. Sesamin is a potent and specific inhibitor of delta 5 desaturase in polyunsaturated fatty acid biosynthesis. Sesamin inhibits a particular CYP3A enzymes that is involved in vitamin E metabolism, where the enzyme initially ω-hydroxylates vitamin E (required step) and then the rest of vitamin E is subject to fat oxidation. By inhibiting this step, sesamin causes an increase in circulating and organ concentrations of vitamin E. Sesamin is thought to have PPARα activating potential in the liver, but it is uncertain how much practical relevance this has in humans due to this being a mechanism that differs between species.

Epacadostat (INCB024360) is an orally available hydroxyamidine and inhibitor of indoleamine 2,3- dioxygenase (IDO1). It shows little activity against other related enzymes such as IDO2 or tryptophan 2,3-dioxygenase (TDO). Epacadostat displays potential immune modulating and antineoplastic activities. Epacadostat has been tested in phase II and III studies for the treatment of malignant melanoma, fallopian tube cancer, non-small cell lung cancer, ovarian cancer, peritoneal cancer, solid tumors, pancreatic cancer. The most common detected adverse events were fatigue, nausea, decreased appetite, vomiting, constipation, abdominal pain, diarrhea, dyspnea, back pain, and cough.

Falecalcitriol is an analog of calcitriol. Falecalcitriol was first approved by Pharmaceuticals and Medicals Devices Agency of Japan (PMDA) on Apr 4, 2001. It was co-developed by Taisho, Dainippon Sumitomo and Kissei, then marketed as Hornel by Taisho and Taisho Toyama or as Fulstan by Dainippon Sumitomo Pharma and Kissei in JP. It has a higher potency both in vivo and in vitro systems, and longer duration of action in vivo. This medicine improves bone disease and symptoms caused by shortage of vitamin D, etc. It also prompts calcium absorption to supply lacked calcium and prevents bone-thinning. It is usually used to treat secondary hyperparathyroidism under maintenance dialysis, hypoparathyroidism, rickets or osteomalacia. Falecalcitriol regulates the proliferation of parathyroid cells and parathyroid hormone synthesis possibly via binding to a nuclear receptor for vitamin D (VDR). It is often not possible to administer doses high enough to sufficiently inhibit parathyroid hormones because of the risk of hypercalcemia and hyperphosphatemia.

Vildagliptin, previously identified as LAF237, is a new oral anti-hyperglycemic agent (anti-diabetic drug) of the new dipeptidyl peptidase-4 (DPP-4) inhibitor class of drugs. Vildagliptin inhibits the inactivation of GLP-1 and GIP by DPP-4, allowing GLP-1 and GIP to potentiate the secretion of insulin in the beta cells and suppress glucaon release by the alpha cells of the islets of Langerhans in the pancreas. It is currently in clinical trials in the U.S. and has been shown to reduce hyperglycemia in type 2 diabetes mellitus. While the drug is still not approved for use in the US, it was approved in Feb 2008 by European Medicines Agency for use within the EU and is listed on the Australian PBS with certain restrictions. Vildagliptin is marketed under the trade names Galvus, Zomelis.