Datiscetin is a yellow plant dye from the flavonol group. It exhibited inhibitory activity against methicillin-resistant Staphylococcus aureus (MRSA). Datiscetin demonstrated antioxidant activity – it inhibits CCl4-induced microsomal lipid peroxidation and behaved as potent scavenger of the superoxide anion radicals. Datiscetin activated the human constitutive androstane receptor. It inhibited amyloid beta-42 protein aggregation. Datiscetin interacts with amyloid beta-42 protein directly, with monomers and small aggregates.

Oroxylin A is a flavonoid compound, one of the main components extracted from Scutellariae radix. It possess a broad spectrum of pharmacological effects, especially anti-cancer, anti-inflammatory and neuroprotective activity. Oroxylin A inactivated HIF1α and reprogrammed fatty acid metabolism of HCT116 cells, decreasing intracellular fatty acid level and enhancing fatty acid oxidation. Oroxylin A improves attention-deficit hyperactivity disorder-like behaviors in spontaneously hypertensive rats via enhancement of dopamine neurotransmission and not modulation of GABA pathway as previously reported. Importantly, the present study indicates the potential therapeutic value of oroxylin A in the treatment of attention-deficit hyperactivity disorder. Both in vitro and in vivo study showed that oroxylin A possesses low toxicity, but the field was just limited in cancer research.

9,10-PHENANTHRENEDIONE (9,10-Phenanthrenequinone) is a quinone and a useful fluorescent compound. It is a TRPA1 activator. Inhalation of 9,10-phenanthrenequinone (9,10-PQ), a major quinone in diesel exhaust, exerts fatal damage against a variety of cells involved in respiratory function. Exposure to 9,10-phenanthrenequinone accelerates malignant progression of lung cancer cells through up-regulation of aldo-keto reductase 1B10.

Ashwagandha (root of Withania somnifera) has been used for many purposes, it is mainly considered a tonic in traditional Ayurvedic medicine. Withanoside VI is an active constituent of Ashwagandha. In vivo, oral withanoside VI (10 umol/kg/day for 12 days) improved Abeta(25-35)-induced memory impairment, neurite atrophy, and synaptic loss in the cerebral cortex and hippocampus in mice. Withanoside VI facilitates the regeneration of axons and dendrites by reconstructing preand post-synapses in neurodegenerative diseases and preventing pathogenesis and neuronal death. Withanoside VI is important candidate for the therapeutic treatment of neurodegenerative diseases.

Aflatoxin G1 ((7aR,10aS)-3,4,7a,10a-tetrahydro-5-methoxy-1H,12H-furo[3',2':4,5]furo[2,3-h]pyrano[3,4-c][1]benzopyran-1,12-dione) is a food contaminant produced by various species of the common soil fungus, Aspergillus and is associated with toxicity and hepatocarcinogenicity in human and animal populations. Epidemiological studies have shown that Aflatoxin G1 is one of the most frequently detected contaminating mycotoxins in grains and foodstuffs in areas with high-incidence of lung and esophageal cancer

Aflatoxin B2 is the dihydro derivative of aflatoxin B1, a naturally occurring mycotoxin and food contaminant that is a likely pathogen that causes hepatocellular carcinoma. Aflatoxin B2 induces mitochondria-mediated apoptosis via the production of reactive oxygen species (ROS) and promotion of the translocation of Bax and cytochrome c between mitochondria and the cytosol, triggering the formation of apoptosomes. Aflatoxin B2 also inhibited the phosphoinositide 3-kinase/Akt/ mammalian target of rapamycin (PI3K/Akt/mTOR) pathway by activating PI3K, Akt, and mTOR and inhibiting their phosphorylation, contributing to the pro-autophagic activity of Aflatoxin B2.

Grayanotoxin I is found in the leaves of plants belonging to the family Ericaceae (Leucothoe, Rhododendron, Andromeda, Kalmia). It binds to the sodium channel in its open state and upon binding the sodium channel gating is altered. A shift occurs in the activation of the sodium channel to the hyperpolarizing direction, leading to its persistent opening even at resting potentials (ranging from −70 to −100mV). In addition, the inactivation process of these modified sodium channels is suppressed. The resulting massive influx of Na+ ions will cause excitation followed by complete inexcitability of nerve cells. These lipid-soluble neurotoxins may modify sodium channels gating by causing immobilization of S6 segments during gating transitions and thereby during depolarization the channels ‘are freezed’ in the open state. In the guineapig atria, Grayanotoxin I produces a membrane depolarization, positive inotropic effects and arrhythmias.