Musk ketone can induce the growth repression and the apoptosis of cancer cells. Musk ketone increases activity of glutathione S-transferase and thus may prove to be useful cancer chemoprotectant.

Cimicifugoside H1 shows the protective function to cerebral neuron during cerebral ischemia.

Butylphthalide (3-Butylphthalide) is an anti-cerebral-ischemia drug; first isolated from the seeds of Apium graveolens Linn.

Verbenalin (Verbenaloside) induces angiogenesis via a programmed PI3K/Akt/eNOS/VEGF signaling axis.

Emodin-8-glucoside (Anthraglycoside B) functions to protect from focal cerebral injury induced by ischemia and reperfusion. Emodin-8-beta-D-glucoside directly stimulates cell proliferation and differentiation of osteoblasts.

Gardenin has regulatory effect on the gene expression in rats with focal cerebral ischemia.

Dihydrocapsaicin (CCRIS1589) is isolated from Capsicum fruit. Capsaicin is the primary active component of the heat and pain-eliciting lipid soluble fraction of the Capsicum pepper. Like capsaicin, dihydrocapsaicin is an irritant. Capsaicin is found in natural hot pepper extracts along with a number of impurities, including dihydrocapsaicin and several lesser impurities. Separation by HPLC is required in order to obtain pure dihydrocapsaicin. Dihydrocapsaicin represents about 10% of the compound present in commercial preparations purporting to be pure capsaicin, but it has about the same pungency as capsaicin. VR1 (vanilloid receptor 1) is a heat activated calcium ion channel which functions as a part of the normal nociceptive pain pathway. Capsaicin elicits a sensation of burning pain by activation of VR1 on small, non-myelinated polymodal C-type nociceptive nerve fibers. The potency of dihydrocapsaicin at VR1 appears equivalent to capsaicin. Antioxidant. Reduces oxidation of serum lipids. Mutagenic. Dihydrocapsaicin is an activator of VR1.

Barlerin (8-O-Acetylshanzhiside methyl ester) has potential against cerebral ischemic injury, and its protective effect on oxygen-glucose deprivation-induced injury might be due to the suppression of intracellular Ca2+ elevation and caspase-3 activity, and improvement of mitochondrial energy metabolism.8-O-Acetylshanzhiside methylester can increase angiogenesis and improve functional recovery after stroke.8-O-Acetylshanzhiside methylester has protective effects on experimental myocardial ischemia injury, the effects might be due to block of myocardial inflammatory cascades through an HMGB1-dependent NF-κB signaling pathway.8-O-Acetylshanzhiside methylester protects diabetic brain against I/R injury by alleviating diabetic cerebral I/R injury and attenuating blood–brain barrier (BBB) breakdown, and its protective effects may involve HMGB-1 and NF-κB signalling pathway.

Erigeroside has the protective effects on cerebral ischemia-reperfusion injury in rat, its ability of anti-oxidation and scavenging oxidation free radical may be one of its protective mechanisms.

Sesamin is a selective delta 5 desaturase inhibitor in the biosynthesis of polyunsaturated fatty acids and is a lignan abundantly present in sesame oil. It has potent neuroprotective effects against cerebral ischemia.

Forsythoside B binds to LPS and reduces the biological activity of serum LPS, and inhibits NF-κB activation. Forsythoside B inhibits the inflammatory response and has antioxidant properties. Potent neuroprotective effects with a favorable therapeutic time

Citicoline sodium (CDP-choline) is an endogenous intermediate in the synthesis of phosphatidylcholine. It also serves as a choline donor in the biosynthesis of the neurotransmitter acetylcholine. Citicoline sodium demonstrates protective effects in cerebral ischemia, traumatic brain injury, and memory disorders. Exogenous administration of citicoline to rodents (500 mg/kg i.p. immediately after ischemia and at 3-h reperfusion) has been shown to stimulate the synthesis of phosphatidylcholine, sphingomyelin, and cardiolipin and to attenuate the release of arachidonic acid and the accumulation of ceramide.

Morroniside would act as a regulator of hepatic inflammatory reactions and lipid metabolism in db/db mice. It exhibits protective effects against diabetic renal damage and human umbilical vein endothelial cells, by inhibiting hyperglycemia and oxidative s

Oxysophoridine (Sophoridine N-oxide) has a protective effect on focal cerebral ischemic injury through antioxidant and anti-apoptotic mechanisms; it may be a potential neuroprotective agent for cerebral ischemia injury, that the effect may be due to its ability to inhibit oxidative stress and expression of the N-methyl-D-aspartate receptor subunit NR1.Oxysophoridine ameliorates cardiac damage in a rat model of AMI and that this cardioprotection may be linked with its anti-oxidative, anti-apoptotic and anti-inflammatory properties.