Ginsenoside Rc, one of major Ginsenosides from Panax ginseng, enhances GABA receptorA (GABAA)-mediated ion channel currents (IGABA). Ginsenoside Rc inhibits the expression of TNF-α and IL-1β.

Ginsenoside Rd inhibits TNFα-induced NF-κB transcriptional activity in HepG2 cells, inhibits expression of COX-2 and iNOS mRNA, also inhibits Ca2+ influx. Ginsenoside Rd inhibits CYP2D6, CYP1A2, CYP3A4, and CYP2C9.

Ginsenoside Re is an extract from Panax notoginseng. Ginsenoside Re decreases the β-amyloid protein (Aβ).

Ginsenoside Rf is a trace component of ginseng root. Ginsenoside Rf inhibits N-type Ca2+ channel.

Ginsenoside Rg1 is one of the major active components of Panax ginseng. Ginsenoside Rg1 displays promising effects by reducing cerebral Aβ levels. Ginsenoside Rg1 also reduces NF-κB nuclear translocation.

Ginsenoside Rg2 is one of the major active components of ginseng. Ginsenoside Rg2 inhibits VCAM-1 and ICAM-1expressions stimulated with lipopolysaccharide (LPS). Ginsenoside Rg2 also reduces Aβ1-42 accumulation.

Ginsenoside Rg3 is one of the major active components of ginseng.

Ginsenoside Rh1 inhibits the expression of PPAR-γ, TNF-α, IL-6, and IL-1β.

Ginsenoside Rg3(S-Form) is the main component of Panax ginseng C. A. Meyer. It inhibits Na+ and hKv1.4channel, and also inhibits Aβ levels, NF-κB activity, and COX-2 expression.

Ginsenoside Rg3(R-Form), one of the active compounds present in ginseng root, inhibits angiogenesis.

Ginsenoside Rh2 induces the activation of caspase-8 and caspase-9. Ginsenoside Rh2 induces cancer cell apoptosis in a multi-path manner.

20(R)-Ginsenoside Rh2 is a protopanaxadiol-type saponin with multiple biological activities.

Harpagoside can be obtained by Harpagophytum procumbens. Harpagoside has an inhibitory effect on COX-1 and COX-2 active, and suppresses NO production.

Harringtonine is a natural Cephalotaxus alkaloid that inhibits protein synthesis.

Homoharringtonine is a cytotoxic alkaloid.

Hydroxysafflor yellow A is a natural product of flavonoids isolated from safflower.