Emodin-8-O-beta-D-glucoside extracted from the traditional Chinese medicinal herb Polygonum cuspidatum Sieb. et Zucc, which is used to treat fractures, rheumatoid arthritis, muscle injury and pain possible by antioxidative mechanism. Emodin-8-O-beta-D-glucoside can be a promising antitumor agent for cancer treatment, because experiments with cervical cancer SKOV3 cells have shown, that it can inhibit the proliferation of cells and promote apoptosis by down regulation of Bcl-2 expression and up regulation of Bax expression, as well as the increase of relative activity of caspase 3 and caspase 9. In addition, emodin-8-O-beta-D-glucoside is able to provide neuroprotection against cerebral ischemia-reperfused injury and glutamate induced neuronal damage through exerting antioxidative effects and inhibiting glutamate neurotoxicity.

S-Allylcysteine (SAC), the most abundant organosulfur compound in aged garlic extract, has multifunctional activity via different mechanisms and neuroprotective effects that are exerted probably via its antioxidant or free radical scavenger action. Anticancer effects of SAC were reported in prostate cancer, breast cancer, oral cavity cancer, non-small cell lung cancer, neuroblastoma, and hepatocellular carcinoma through the restoration of E-cadherin, the reduction of Slug and matrix metalloproteinase (MMP) protein expression, and stimulating apoptotic pathways. In addition, recently was revealed, that SAC might have imperative implications for the deterrence and early treatment of type 2 diabetes by reducing the influx of glucose in the polyol pathway, thereby elevating the GSH level and reducing the activities of aldose reductase (AR) and sorbitol dehydrogenase (SDH).

5-Fluoroorotic acid is a fluorinated derivative of the pyrimidine precursor orotic acid. 5-Fluoroorotic acid exert considerable antitumor activity against transplanted tumors in rats and mice. 5-Fluoroorotate shows increased cytotoxicity on ovarian carcinoma cell lines following encapsulation in liposomes. 5-Fluoroorotic acid is used in vitro in the positive selection of genetically transformed yeast cells.

Aloesin is a chromone derivative isolated from aloe vera. It has many biological effects, such as wound and burn healing properties, and antioxidant, free radical scavenging, anti-inflammatory, and immunomodulatory effects. Aloesin has been shown to be a potent and selective inhibitor of tyrosinase. It exhibited direct inhibitory effects on melanogenesis. Aloesin treatment showed pigmentation suppression in a dose-dependent manner. Thus, aloesin may be used as an agent that inhibits melanin formation induced by UV radiation. Aloesin is thought to be one of the active ingredients in regards to the anti-diabetic activity of Aloe. Aloesin exerts its anticancer effect through the MAPK signaling pathway. It is a novel therapeutic drug for ovarian cancer treatment.

Phenformin is a biguanide hypoglycemic agent with actions and uses similar to those of metformin. It activates AMP-activated protein kinase (AMPK) and inhibits mTORC1 signaling. Phenformin used for the treatment of diabetes. Phenformin was removed from the U.S. market 20 years ago because of a high incidence of lactic acidosis. Risk factors for the development of lactic acidosis include renal deficiency, hepatic disease, cardiac disease, and drug interaction such as cimetidine. Phenformin exerts potential anti-neoplastic action.

Potassium Glycyrrhetinate (CAS no. 85985-61-1) is the potassium salt of Glycyrrhetinic Acid. Potassium Glycyrrhetinate is also known as Olean-12-En-29-Oic Acid, 3-Hydroxy-1, 1-Oxo-, Monopotassium Salt. Potassium Glycyrrhetinate functions as a flavoring agent and skin-conditioning agent—miscellaneous in cosmetic products.

Niraparib (MK-4827) displays excellent PARP 1 and 2 inhibition. Inhibition of PARP in the context of defects in other DNA repair mechanisms provide a tumor specific way to kill cancer cells. Niraparib is in development with TESARO, under licence from Merck & Co, for the treatment of cancers (ovarian, fallopian tube and peritoneal cancer, breast cancer, prostate cancer and Ewing's sarcoma). Niraparib was characterized in a number of preclinical models before moving to phase I clinical trials, where it showed excellent human pharmacokinetics suitable for once a day oral dosing, achieved its pharmacodynamic target for PARP inhibition, and had promising activity in cancer patients. It is currently being tested in phase 3 clinical trials as maintenance therapy in ovarian cancer and as a treatment for breast cancer.

Lysophosphatidic acid (LPA) is a multifunctional intercellular phospholipid messenger. LPA stimulates the growth of a variety of cells including fibroblasts, vascular smooth muscle cells, endothelial cells, and keratinocytes. It is produced in relatively high levels from activated platelets and can be detected in bodily fluids including serum, saliva, follicular fluid, and malignant effusions. LPA acts as a proliferative and anti-apoptotic factor and is a ligand for LPA1 (EDG-2), LPA2 (EDG-4) and LPA3 (EDG-7) receptors. The plasma LPA level can be a useful marker for ovarian cancer, particularly in the early stages of the disease. It is known, that the therapeutic administration of LPA also blocked APAP-induced liver damage, leading to an increased survival rate by increasing the glutathione level but decreasing inflammatory cytokines in an LPA1,3,5-independent manner. Thus, LPA might be an important therapeutic agent for drug-induced liver injury. In addition, was shown, that LPA levels in plasma and ascites may be useful diagnostic biomarkers for peritoneal carcinomatosis of gastric cancer.

Baicalin is a flavonoid compound with anti-inflammatory and anti-oxidant activity extracted from Scutellarua rivularis. Limited distribution data suggest that baicalin reached several sites such as the brain, eye lens, thymus, etc. Metabolism data suggest the rapid conversion of baicalin to baicalein. Baicalin has the potential to be used in novel anti-cancer therapeutic formulations for treatment of ovarian cancer and other cancers. Baicalin markedly inhibits replication of human immunodeficiency virus type 1 (HIV-1) in a concentration-dependent manner in normal peripheral blood mononuclear cells (PBMC) stimulated with phytohemagglutinin (PHA) in vitro. The preventive medication of baicalin shows a protective effect on C57 BL mouse with Parkinson's disease induced by 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP).

Lonidamine is a derivative of the indazole-3-carboxylic acid, with limited antineoplastic activity as a single agent but with exceptional potential in modulating the activities of conventional chemotherapeutic agents such as N-mustard alkylating agents and anthracyclines as well as hyperthermia, radiation therapy and photodynamic therapy. The most critical property of Lonidamine is its selective activity against a broad range of tumors with little to no effect on normal tissues provided that doses are below a threshold level of ~400 mg/m^2 (oral or i.v. doses). Selective effects of Lonidamine on tumors compared to other potential targets probably result from the dependence of most tumors on glycolytic metabolism, but the exact mechanism of specificity is still not fully known. Current evidence indicates that Lonidamine inhibits lactate export by the proton-linked monocarboxylate transporter(s) (MCT) and pyruvate uptake into mitochondria via the mitochondrial pyruvate carrier (MPC), whereas inhibition of respiration involves both diminished mitochondrial uptake of pyruvate via the MPC as well as inhibition of the mitochondrial electron-transport chain at Complex II and perhaps also Complex I, in both instances at the ubiquinone reduction step. There is also evidence that the drug may indirectly inhibit hexokinase as well as possibly other glycolytic and pentose shunt enzymes as a result of cytosolic acidification. Key problems that remain to be addressed are the production of Lonidamine under GMP conditions since Angelini Pharmaceuticals in Rome, Italy, the sole commercial source of this drug, stopped producing it in 2006. In addition, utilization of Lonidamine in the US requires IND approval by the FDA, which has previously been granted for a number of clinical trials. Finally, even though LND is a potent enhancer of the activity of a number of potent anti-cancer agents, potentially less toxic (and patentable) “targeted-tumor agents” are replacing traditional chemotherapy. Another problem remaining to be addressed is the limited solubility of Lonidamine at neutral pH. Oral delivery has led to variable results; more soluble derivatives that can be administered by the intravenous administration are needed to accurately control the dosing schedules.