Ginsenoside Rg3 is the main component of Red ginseng, it inhibits Na+ and hKv1.4 channel with IC50s of 32.2±4.5 and 32.6±2.2 μM, respectively, it also inhibits Aβ levels, NF-κB activity, and COX-2 expression. Ginsenoside-Rg3 possesses an ability to inhibit the lung metastasis of tumor cells, and the mechanism of its antimetastatic effect is related to inhibition of the adhesion and invasion of tumor cells, and also to anti-angiogenesis activity. It is a novel drug, capable of inhibiting the early of scarring (HS) and later HS. (20S)-ginsenoside Rg3 is a ginsenoside found in Panax ginseng and Panax japonicus var. major that is dammarane which is substituted by hydroxy groups at the 3beta, 12beta and 20 pro-S positions, in which the hydroxy group at position 3 has been converted to the corresponding beta-D-glucopyranosyl-beta-D-glucopyranoside, and in which a double bond has been introduced at the 24-25 position.

Aconine is a diterpene alkaloid with formula C25H41NO9 that is isolated from several Aconitum species. It has a role as a xenobiotic, a NF-kappaB inhibitor, a plant metabolite and a human urinary metabolite. It is a diterpene alkaloid, a tertiary alcohol, a secondary alcohol, a bridged compound, a pentol, an organic heteropolycyclic compound, a polyether and a tertiary amino compound. It derives from a hydride of an aconitane. Aconine can inhibit RANKL-induced osteoclast differentiation in RAW264.7 cells by suppressing NF-κB and NFATc1 activation and DC-STAMP expression. Aconine can attenuate hepatic fat degeneration of rats with fatty liver induced by high-fat diet through decreasing TG,TC deposit in liver. Aconine inhibits NF - κ B activation induced by ligands of nuclear factor kappa B receptor activators.

20(R)-Ginsenoside Rh1 is a triterpenoid saponin.

Bacopaside II is a potential anti-angiogenic agent, it can reduce endothelial cell migration and tubulogenesis and induce apoptosis. Bacopaside II shows antioxidant and antidepressant activities, it can inhibit both basal activity as well as verapamil-stimulated ATPase activity, suggesting its affinity towards P-gp.

Anemoside B4(AB4) and tetrandrine(Tet) have some reversal effect on resistant to L-OHP in Lo Vo/L-OHP cells, the molecular mechanism of the resistance reverse effect was related to down-regulation of P-gp for AB4 and down-regulation of z DHHC9 for Tet. Anemoside B4 can inhibit the production of IL-6,secretion of IL-8, downregulate E-selectin expression, and decrease the content of TXB(2), it reduces inflammatory response, thus relieving intestinal dysfunction via multiple pathways. Anemoside B4 may potentially have a capacity to regulate immune responses in vivo via changes in production of these select cytokines by infected endothelial cells.

Atractyloside is a toxic compound from wedelia glauca. It acts as inhibitor of oxidative phosphorylation by a specific interference with energy-transfer reactions, the effect is due to inhibition of the ADP utilizing process in the coupling system. Atractyloside, has been proposed for the antibiotic oligomycin, is an inhibitor of the energy-transfer reactions in animal mitochondria; it inhibits the phosphate uptake and the respiratory stimulation induced by P1-acceptor, but it does not interfere with the so-called resting respiration.

Delsoline has hypotensive effects.Delsoline is not only effective in preventing ventricular fibrillation and arrythmia, but can raise the intebsity of the threthold of electrical shocks to cause ventricular fibrillation in rabbits, the antiarrythmic effect of it may be mainly attributed to itsganglionic blocking and negative cardiac inotropic effect.

Ginsenoside Rg2 has therapeutic potential for type 2 diabetic patients, it also may represent a potential neurorestorative treatment strategy for vascular dementia or other ischemic insults, has protective effects against H2O2-induced injury and apoptosis in H9c2 cells. Ginsenoside Rg2 suppresses the hepatic glucose production via AMPK-induced phosphorylation of GSK3β and induction of SHP gene expression, regulates the 5-HT3A receptors that are expressed in Xenopus oocytes, inhibits nicotinic acetylcholine receptor-mediated Na+ influx and channel activity. Ginsenoside Rg2 is a ginsenoside found in Panax species that is dammarane which is substituted by hydroxy groups at the 3beta, 6alpha, 12beta and 20 pro-S positions, in which the hydroxy group at position 6 has been converted to the corresponding alpha-L-rhamnopyranosyl-(12)-beta-D-glucopyranoside, and in which a double bond has been introduced at the 24-25 position. It has a role as an anticoagulant, a plant metabolite and a cardioprotective agent.

Ginsenoside Ro has antioxidative properties against UV-B-induced oxidative stress in human dermal fibroblasts, it possesses a potential skin anti-photoaging property against UV-B radiation in fibroblasts. It also exerts anti-apoptosis and anti-inflammation in IL-1β-induced rat chondrocytes, which might be related to NF-κB signal pathway, it might be a potential novel drug for the treatment of osteoarthritis. Ginsenoside Ro enhances in vivo hair re-growth based on their inhibitory activity against 5αR in the androgenetic alopecia model, it shows immunomodulatory effects by regulating the production and expression of Th1/Th2 cytokines in murine splenocytes. Chikusetsusaponin-V is a triterpenoid saponin. It has a role as a metabolite.

Arenobufagin is a steroid lactone. It is functionally related to a bufanolide. Arenobufagin is a potent Na + /K + pump inhibitor, and is also a specific inhibitor of VEGF-mediated angiogenesis. Arenobufagin has antineoplastic effect that involves cross talk between apoptosis and autophagy via inhibition of the PI3K/Akt/mTOR pathway. Arenobufagin is a natural bufadienolide that can be extracted from toad venom. Arenobufagin can induce apoptosis and autophagy in human liver cancer cells by inhibiting the PI3K/Akt/mTOR pathway. Arenobufagin exhibits potent anti-tumor activity against hepatocellular carcinoma HepG2 cells and corresponding multidrug-resistant HepG2/ADM cells. Arenobufagin can inhibit VEGF mediated angiogenesis by suppressing the VEGFR-2 signaling pathway.