Alpha (α)-tomatine (simply tomatine) is the major saponin and occurs naturally in tomatoes, possesses a variety of biological properties including antioxidant, and anti-inflammatory. In additıon, tomatine is also known that it breaks down the cell membrane induces growth inhibition and apoptosis in different cancer cells: myeloid leukemia cells; prostate cancer cells; lung adenocarcinoma cells. However, the mechanisms of α-tomatine actions were not well understood. Nevertheless, was shown, that tomatine inhibited the NF-κB and phosphatidyl-inositol-3-kinase/Akt signaling pathways activation. However, the primary cellular target(s) for α-tomatine and its mechanisms for modulating apoptosis-associated pathways remain to be elucidated. The interaction of α-tomatine with cholesterol and the disruptive effect on the cell membrane may be one of the mechanisms by which α-tomatine induces apoptosis. The formation of complexes of α-tomatine and cholesterol may modulate the responsiveness of cell membrane receptors to growth stimuli and thus decrease the growth of cancer cells. Moreover, the anti-inflammatory mechanisms of α-tomatine, which may be a valuable therapeutic agent in the treatment of inflammation-related diseases was due to the ability of tomatine accelerated the phosphorylation of Akt in macrophages.

Gamma-cyclodextrin is cycloamylose composed of eight alpha-(1-4) linked D-glucopyranose units and is formed by bacterial digestion of starch. Gamma-cyclodextrin is a hydrophilic molecule that does not readily permeate biological membranes and is rapidly digested by bacteria in the gastrointestinal tract. In humans, it is metabolized by α-amylase that is found in, for example, saliva, bile fluid, and tears. Gamma-cyclodextrin is generally recognized as safe by the FDA. It is used in bread spreads, frozen dairy desserts, ready-to-eat dairy desserts, desserts prepared from dry mixes, fruit fillings, cheese, and cream fillings, and chewing gum as a stabilizer, emulsifier, carrier and formulation aid at varying levels.

Norvancomycin is an analog of glycopeptide antibiotic vancomycin. It was first found to be produced by a soil microorganisms such Nocardia orientalis and Amycolatopsis orientalis and recently was found in actinomycete Amycolatopsis orientalis CPCC200066. Norvancomycin can be derived by demethylation at N-terminus of vancomycin. It has significant inhibitory activity against Gram-positive cocci and bacilli. The mode of action of norvancomycin is based on its ability to bind to the cell-wall peptidoglycan of Gram-positive bacteria terminating tripeptide -L-Lys-D-Ala-D-Ala. Similar to vancomycin in terms of antibacterial activity, spectrum and clinical efficacy norvancomycin has more potent antibiotic activity against Staphylococcus aureus and higher affinity for bacteria cell wall analogue DALAA than vancomycin. Norvancomycin has been widely used in China to treat endocarditis, osteomyelitis and other severe infections caused by Staphylococcus aureus (including methicillin-resistant strains). The adverse drug reactions of norvancomycin are like vancomycin, such as nephrotoxicity, ototoxicity, rash and itching. Norvancomycin is not available therapeutically outside of China.

Solasonine, a known glycoalkaloid, is a potential anti-cancer agent. Solasonine is a component of Curaderm BEC5 indicated for the topical treatment of actinic keratosis, keratoacanthoma, basal cell carcinoma and cutaneous superficial squamous cell carcinoma. BEC is a standardized mixture of Solamargine (33%), Solasonine (33%) and di-and monoglycosides of solasodine (34%) extracted from S. sodomaeum, now reclassified as S. linnaeanum. Solasonine could inhibit cell proliferation, migration and colony formation of glioma cells. Treatment of solasonine induced apoptosis via modulating cytochrome c and caspase signaling. Besides, solasonine decreased the expression of proinflammatory mediators and nuclear translocalization of NF-κB p50/p65. Mechanistic investigation further revealed that solasonine may target anti-inflammatory signaling pathway, and more specifically p-p38 and p-JNK MAPKs.