Evodiamine, a naturally occurring indole alkaloid, is one of the main bioactive ingredients of Evodia Rutaecara, the dried unripe fruit of which is also known as Wu zhu yu (Wu Zhu Yu, interchangeably) or Evodia Fruit. Evodia Fruit used in Traditional Chinese Medicine for the purposes of warmth, intestinal comfort (specifically; to alleviate abdominal pain, acid regurgitation, nausea and diarrhea), dysmenorrheal, and fighting inflammation and infections. With respect to the pharmacological actions of evodiamine, more attention has been paid to beneficial effects in insults involving cancer, obesity, nociception, inflammation, cardiovascular diseases, Alzheimer's disease, infectious diseases and thermo-regulative effects. Evodiamine has evolved a superior ability to bind various proteins including TRPV1, the aryl hydrocarbon receptor (AhR), and topoisomerases I and II. There are currently no human studies on evodia rutaecarpa berries or evodiamine.

Ethionine is a non-proteinogenic amino acid structurally related to methionine, with an ethyl group in place of the methyl group. Ethionine is an antimetabolite and methionine antagonist. It prevents amino acid incorporation into proteins and interferes with cellular use of adenosine triphosphate (ATP). Ethionine is a far more potent inhibitor of RNA synthesis than of protein synthesis. While both stereoisomers were active, the L isomer was a more potent inhibitor of RNA synthesis than was the D isomer. In male mice, 3 hr after 20 mg/kg L-ethionine, RNA synthesis was inhibited 80%, while after D-ethionine it was inhibited only 51%. Ethionine was a potent inhibitor of wool growth in sheep; the L- and D-isomers appeared equally effective. Because of these pharmacological effects, ethionine is highly toxic and is a potent carcinogen. L and D-ethionine have being shown to be equally effective in producing tissue damage in rats and mice. The L- and ID-isomers of ethionine are equally effective in producing pancreatic and renal changes in the rat as well as fatty infiltration of the liver and pancreatic damage in the albino mouse.

Ethionine is a non-proteinogenic amino acid structurally related to methionine, with an ethyl group in place of the methyl group. Ethionine is an antimetabolite and methionine antagonist. It prevents amino acid incorporation into proteins and interferes with cellular use of adenosine triphosphate (ATP). DL-Ethionine is a racemic mixture of the anti-methylation agent L-Ethionine and its enantiomer D-Ethionine. DL-Ethionine is used as a dietary supplement to accelerate cholangiocarcinogenesis in vivo. D-Ethionine and D,L-ethionine strongly enhanced the activity of prolidase II compared with L-ethionine. DL-Ethionine is used to induce oxidative stress in liver to study the levels and activities of anti-oxidative enzymes and compounds such as glutathione. As a therapeutic agent in the treatment of malignant tumors of man, ethionine had no demonstrable efficacy. No changes in the appearance of tumor cells were noted after its administration, even when marked effects on other tissues were evident. The distressing toxicity of ethionine prevented further extension of the investigation.

Guanosine 3′,5′-cyclic monophosphate (cGMP) is a cyclic nucleotide derived from guanosine triphosphate (GTP). Cyclic GMP is a cellular regulatory agent that acts as a second messenger. Its levels increase in response to a variety of signals (acetylcholine, insulin, oxytocin). cGMP is involved in the regulation of kinases G. cGMP binds to sites on the regulatory units of protein kinase G (PKG) and activates the catalytic units, enabling them to phosphorylate their substrates. cGMP is a common regulator of ion channel conductance, glycogenolysis, and cellular apoptosis. It also relaxes smooth muscle tissues. In blood vessels, relaxation of vascular smooth muscles lead to vasodilation and increased blood flow. cGMP is a secondary messenger in phototransduction in the eye. In the photoreceptors of the mammalian eye, the presence of light activates cGMP phosphodiesterase 5 (PDE5), which degrades cGMP. The sodium ion channels in photoreceptors are cGMP-gated, so degradation of cGMP causes sodium channels to close, which leads to the hyperpolarization of the photoreceptor's plasma membrane and ultimately to visual information being sent to the brain. Mutations in the cGMP phosphodiesterase cause defects in cGMP metabolism leading to retinal disease. Inhibition of cGMP degrading PDE5 by its selective inhibitor sildenafil induced migraine without aura in 10 of 12 migraine patients and in healthy subjects.

Phillyrin, an active ingredient found in many medicinal plants and certain functional foods, elicits anti-obesity and anti-inflammatory properties in vivo. Phillyrin is one of the main chemical constituents of Forsythia suspensa (Thunb.), which has shown to be an important traditional Chinese medicine. Phillyrin, has being shown to possess various bioactivities, including anti-inflammatory, anti-oxidant, and antiviral activities. It has being reported that Phillyrin attenuates high glucose-induced lipid accumulation in human HepG2 hepatocytes through the activation of LKB1/AMP-activated protein kinase-dependent signalling.

1,9-Dideoxyforskolin (DFK) is an inhibitor of glucose transporter, has been synthesized in 8 steps and 37% overall yield. 1,9-Dideoxyforskolin is a biologically inactive forskolin analog and does not stimulate adenylyl cyclase. DFK mimics some activity of forskolin, demonstrating alteration of K+ channel activity, reversal of doxorubicin resistance in multidrug resistant sarcoma cells, protection against TNF-α-mediated cytotoxicity, and desensitization at GABAA receptors. The inhibitory effect of DFK on high K (+)-induced contraction was antagonized by an increase in extracellular Ca2+ concentration. DFK inhibited the increase in cytosolic Ca2+ level and contraction in parallel whereas forskolin inhibited the contraction more strongly than the cytosolic Ca2+ level. These results suggest that DFK, but not forskolin, inhibits vascular smooth muscle contraction by a Ca2+ channel blocker-like action.