Robinetin is a bioactive plant flavonol. Robinetin inhibited the mutagenic activity resulting from the metabolic activation of benzo[a]-pyrene and (+/-)-trans-7,8-dihydroxy-7,8-dihydrobenzo[a]-pyrene by rat liver microsomes.

Methyl jasmonate (MJ) is a natural cyclopentanone lipid belonging to the jasmonates (JAs) family of plant oxylipin stress hormones (oxygenated fatty acids). Methyl jasmonate is found universally in the plant kingdom and functions to regulate plant growth and development, as well as in stress responses through signal transduction pathways. Methyl jasmonate has recently been found to have anti-cancer activity. MJ (1) arrests cell cycle, inhibiting cell growth and proliferation, (2) causes cell death through the intrinsic/extrinsic proapoptotic, p53-independent apoptotic, and nonapoptotic (necrosis) pathways, (3) detaches hexokinase from the voltage-dependent anion channel, dissociating glycolytic and mitochondrial functions, decreasing the mitochondrial membrane potential, favoring cytochrome c release and ATP depletion, activating pro-apoptotic, and inactivating antiapoptotic proteins, (4) induces reactive oxygen species mediated responses, (5) stimulates MAPK-stress signaling and redifferentiation in leukemia cells, (6) inhibits overexpressed proinflammatory enzymes in cancer cells such as aldo-keto reductase 1 and 5-lipoxygenase, and (7) inhibits cell migration and shows antiangiogenic and antimetastatic activities. Finally, MJ may act as a chemosensitizer to some chemotherapics helping to overcome drug resistant. The complete lack of toxicity to normal cells and the rapidity by which MJ causes damage to cancer cells turn MJ into a promising anticancer agent that can be used alone or in combination with other agents. Methyl jasmonate detached hexokinase 2 from a voltage-dependent anion channel causing a reduction in mitochondrial transmembrane potential that led to the release of cytochrome C and apoptosis inducing factor resulting in intrinsic apoptosis. Blocked adenosine triphosphate synthesis caused by mitochondrial injury hampered oxidative phosphorylation and led to cell necrosis. Methyl jasmonate may be an adjuvant therapy for liver tumors due to its mechanism in cancer cells compared to that in normal cells: The major function is to inhibit glycolysis instead of changing aerobic metabolism.

Auraptene (7-Geranyloxycoumarin) is the best known and most abundant prenyloxycoumarin present in nature. It is synthesized by various plant species, mainly those of the Rutaceae and Umbelliferae (Apiaceae) families, comprising many edible fruits and vegetables such as lemons, grapefruit, and orange. Auraptene has shown a remarkable effect in the prevention of degenerative diseases, in particular, it has been reported to be one the most promising known natural chemopreventive agents against several types of cancer. The effect in humans is not yet known.

Indolebutyric acid (IBA) is a plant hormone in the auxin family. IBA promoted plant rooting and used commercially world wide to root many plant species. IBA considered to be toxic to animals and human. IBA demonstrated antineoplastic action in animal model. According to in silico and in vitro study IBA can act as competitive inhibitor to the phospholipase A₂ and may be used as anti inflammatory agent.

7-hydroxyflavone belongs to the flavone subgroup of flavonoids. It is a potent inhibitor of 20alpha-hydroxysteroid dehydrogenase (AKR1C1), aromatase (cytochrome P450 19; CYP19), aldo-keto reductases AKR1B10 and AKR1B1. It can inhibit LPS-induced inflammation via attenuating the production of NO, PGE2, TNF-alpha and IL-6, indicating that it may be lead compound for developing anti-inflammatory agent. 7-hydroxyflavone may serve as potential protective agents in the treatment of patients with chronic EV71 infection.

Saikosaponin D is a triterpene saponin found in Bupleurum that exhibits antioxidative, immunomodulatory, anti-fibrotic, anti-angiogenic, anticancer, and chemopreventive activities. Saikosaponin D increases activity of superoxide dismutase, catalase, and glutathione peroxidase and decreases activity of malondialdehyde in cellular models of oxidative damage. In other in vitro models, saikosaponin D increases secretion of IL-12, maturation of dendritic cells, and proliferation of lymphocytes. Saikosaponin D inhibits SERCA, increasing intracellular Ca2+ and inducing autophagy. In vivo, this compound decreases severity of fibrosis. In embryos, saikosaponin D decreases microvessel formation. Additionally, this compound decreases tumor formation in DEN-treated animal models and suppresses expression of CEBP-β and COX-2. Saikosaponin D also induces apoptosis and activation of caspases 3 and 7 in hepatocellular carcinoma cells. Saikosaponin D is a Glucocorticoid receptor agonist. It is a COX-2 and iNOS inhibitor.

Apigetrin, a flavonoid glycoside, is present in a variety of medicinal plants with anti-inflammatory and ant-oxidant properties. It is isolated from various herbal medicines, including Matricaria chamomilla, Scutellaria baicalensis Georgi, Teucrium gnaphalodes and Stachys tibetica Vatke. Apigetrin may induce cancer cell differentiation – it could be one of the possible explanations of its antitumor effects. Inhibition of bright light-induced retinal oxidative stress and retinal inflammatory responses was associated with the retinal protection conferred by Apigetrin.

Lycorine is a natural pyrrolo[de]phenanthridine ring-type alkaloid extracted from Amaryllidaceae. It has been reported to exhibit a wide range of physiological effects, including anti-viral, anti-malarial, anti-cancer and anti-inflammatory. Although a defined target or mechanism of action of lycorine is still unknown, it is a candidate anti-inflammatory and anti-cancer drug.

Nomilin is a limonoid/triterpenoid found in citrus fruits that exhibits anti-parasitic, antiviral, anticancer, anti-metastatic, anti-angiogenic, anti-inflammatory, immunomodulatory, anti-obesity, anti-diabetic, and antiviral activities. Nomilin prevents growth of Aedes and suppresses replication of HIV-1 by inhibiting HIV-1 protease. In animal models, nomilin induces phase II enzymes by increasing expression of glutathione-S-transferase and NADPH:Quinone reductase. In animals fed high fat diets, nomilin activates GR5, increases glucose tolerance, and decreases body weight, glucose levels, and insulin levels. In vivo, nomilin increases white blood cell counts and antibody titers but suppresses delayed-type hypersensitivity reactions. In vitro, this compound inhibits cell proliferation, migration, invasion, and capillary tube formation and decreases levels of IL-1β, IL-6, TNF-α, VEGF, NO, and GM-CSF. Additionally, nomilin also inhibits aromatase and cellular proliferation in breast cancer cells. Nomilin also inhibits osteoclastogenesis in vitro by suppression of NFATc1 and MAPK signaling pathways. Nomilin inhibits tumor-specific angiogenesis by downregulating VEGF, NO and proinflammatory cytokine profile and also by inhibiting the activation of MMP-2 and MMP-9.

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.