Azelaic acid, a naturally occurring saturated dicarboxylic acid found in wheat, rye, and barley, possesses antimicrobial activity, affects keratin production, and reduces inflammation. One of the brand name for azelaic acid is FINACEA,Gel, 15% is indicated for topical treatment of the inflammatory papules and pustules of mild to moderate rosacea. Although some reduction of erythema, which was present in patients with papules, and pustules of rosacea occurred in clinical studies, efficacy for treatment of erythema in rosacea in the absence of papules and pustules has not been evaluated. Rosacea is a common skin condition thought to be primarily an inflammatory disorder. Neutrophils, in particular, have been implicated in the inflammation associated with rosacea and mediate many of their effects through the release of reactive oxygen species. Many effective agents for rosacea, including topical azelaic acid have anti-inflammatory properties. Azelaic acid per se has multiple modes of action in rosacea, but an anti-inflammatory effect achieved by reducing reactive oxygen species appears to be the main pharmacological action. A possible mechanism of action for azelaic acid in the human epidermis includes its possibility to inhibit tyrosinase and of membrane-associated thioredoxin reductase enzymes, this enzyme is shown to regulate tyrosinase through a feedback mechanism involving electron transfer to intracellular thioredoxin, followed by a specific interaction between reduced thioredoxin and tyrosinase.

Mesalamine, also known as Mesalazine or 5-aminosalicylic acid (5-ASA), is an anti-inflammatory drug used to treat inflammation of the digestive tract (Crohn's disease) and mild to moderate ulcerative colitis. Mesalazine is a bowel-specific aminosalicylate drug that is metabolized in the gut and has its predominant actions there, thereby having fewer systemic side effects. As a derivative of salicylic acid, 5-ASA is also an antioxidant that traps free radicals, which are potentially damaging by-products of metabolism. Although the mechanism of action of mesalazine is not fully understood, it appears to be topical rather than systemic. Mucosal production of arachidonic acid metabolites, both through the cyclooxygenase pathways, i.e., prostanoids, and through the lipoxygenase pathways, i.e., leukotrienes and hydroxyeicosatetraenoic acids, is increased in patients with chronic inflammatory bowel disease, and it is possible that mesalazine diminishes inflammation by blocking cyclooxygenase and inhibiting prostaglandin production in the colon. Mesalazine is used for the treatment of active ulcerative proctitis.

Prilocaine is a local anesthetic that is similar pharmacologically to lidocaine. Prilocaine binds to the intracellular surface of sodium channels which blocks the subsequent influx of sodium into the cell. Action potential propagation and never function is, therefore, prevented. This block is reversible and when the drug diffuses away from the cell, sodium channel function is restored and nerve propagation returns. Prilocaine acts on sodium channels on the neuronal cell membrane, limiting the spread of seizure activity and reducing seizure propagation. The antiarrhythmic actions are mediated through effects on sodium channels in Purkinje fibers. Currently, Prilocaine is used most often for infiltration anesthesia in dentistry.

Acetylcysteine (also known as N-acetylcysteine or N-acetyl-L-cysteine or NAC) is primarily used as a mucolytic agent and in the management of acetaminophen poisoning. Acetylcysteine likely protects the liver by maintaining or restoring the glutathione levels, or by acting as an alternate substrate for conjugation with, and thus detoxification of, the reactive metabolite. Nacystelyn (NAL), a recently-developed lysine salt of N-acetylcysteine (NAC) is known to have excellent mucolytic capabilities and is used to treat cystic fibrosis (CF) lung disease. NAC as a precursor to the antioxidant glutathione modulates glutamatergic, neurotrophic, and inflammatory pathways. The potential applications of NAC to facilitate recovery after traumatic brain injury, cerebral ischemia, and in treatment of cerebrovascular vasospasm after subarachnoid hemorrhage. Acetylcysteine serves as a prodrug to L-cysteine, which is a precursor to the biologic antioxidant, glutathione, and hence administration of acetylcysteine replenishes glutathione stores. L-cysteine also serves as a precursor to cystine, which in turn serves as a substrate for the cystine-glutamate antiporter on astrocytes hence increasing glutamate release into the extracellular space. Acetylcysteine also possesses some anti-inflammatory effects possibly via inhibiting NF-κB through redox activation of the nuclear factor kappa kinases thereby modulating cytokine synthesis. NAC is associated with reduced levels of inflammatory cytokines and acts as a substrate for glutathione synthesis. These actions are believed to converge upon mechanisms promoting cell survival and growth factor synthesis, leading to increased neurite sprouting.

Luminol (5-amino-2,3-dihydro-1,4-phthalazinedione) is a yellow-colored crystalline solid powder and soluble in most polar organic solvents, but insoluble in water. An alkaline solution of luminol oxidized by oxidizing agents exhibits chemiluminescence. Luminol was first synthesized by Schmitz in 1902, the chemiluminescence property of luminol was first discovered by Albrecht in 1928. Luminol is one of the most widely used chemiluminescent compounds because of its availability and low cost. Luminol-based methods are used in environmental monitoring as biosensors, in the pharmaceutical industry for cellular localization and as biological tracers, and in reporter gene-based assays and several other immunoassays.

Schisandrin is a bioactive compound found in Schisandra chinensis. Schisandrin exhibits antioxidant properties and ameliorates ovariectomy-induced memory impairment in rats, and Aβ1-42-induced memory impairment in mice. Schisandrin has an anti-asthmatic effect on OVA-induced airway inflammation in a murine asthma model. The compound inhibits proliferation of breast cancer cell lines at concentrations of 20-100 uM.

Piericidin A (also named piericidin A1 in some references) was reported as a new insecticidal metabolite, produced by cultures of the soil-derived actinomycete Streptomyces mobaraensis. Piericidin A resembles coenzyme Q in its overall structure containing a pyridine ring with two adjacent methoxy groups. The most widely recognized biological target of Piericidin A is the mitochondrial electron transport chain protein NADH-ubiquinone reductase (Complex I). Respiratory inhibition by piericidin A can be reversed by the addition of vitamin-K3 (menadione) to the inhibited respiratory chain in mammalian mitochondria. Piericidin A increases ROS production. Piericidin A showed significant cytotoxic activities against several tumor cells, such as mouse leukemia cell line, human colon carcinoma cells and was selectively cytotoxic toward human multiple myeloma cells. Moreover, it was identified as a highly selective antitumor agent with greater selectivity and potency than the comparison standard mitomycin C. Piericidin A aggravates the course of genetically determined tau pathology.