Asiatic acid is a triterpene aglycone originally found in Centella; it exhibits cardioprotective, hepatoprotective, anti-inflammatory, antioxidative, antihypertensive, anticancer, anti-fibrotic, and anti-osteoporotic activities. In vitro and in vivo, asiatic acid inhibits TGF-β1-induced and overload-induced cardiac hypertrophy, decreasing production of TGF-β1 and activation of NF-κB, ERK1/2, and p38 MAPK. In high fat diet-fed rats, asiatic acid decreases expression of NF-κB, p38 MAPK, IL-1β, ROS, IL-6, and TNF-α and increases activity of glutathione peroxidase and catalase, preventing hepatic steatosis. Additionally, asiatic acid inhibits L-NAME-induced hypertension, increasing levels of NO and improving vascular function. In multiple myeloma cells, this compound induces G2/M phase cell cycle arrest, decreases expression of FAK, and inhibits cell proliferation. Asiatic acid inhibits adipogenesis, suppresses activation of G3PDH, and modulates differentiation in bone marrow stromal cells. In animal models of fibrosis, this compound decreases tubular injury and fibroblast activation by suppressing activation of Smad2/3, regulating PPARγ activation, and decreasing levels of α-SMA and TGF-β1. Asiatic acid stimulates wound healing by increasing collagen production. Asiatic acid is considered to be the most therapeutically active ingredient of Madecassol, marketed in Korea as wound healing agent for traumatic or surgical wounds, burns, skin grafts, fistulas, abnormal retractile or decubitus scars, cutaneomucous lesions in ENT, gynaecology, ulcerous lesions in leprosy, striae distensae, cellulitis, varicose leg ulcers, haemorrhoid.

Madecassic acid is a naturally produced terpene from Centella asiatica. It has demonstrated anti-inflammatory and anti-diabetic effects by blocking NF-kB activation and altering lipid metabolism in mice. Madecassic acid has also shown anti-tumor effects in a mouse model of colon cancer; and, was demonstrated in vitro to stimulate the growth of neurofilaments from rat PC1 cells.

Glucuronic acid is a sugar acid that was first identified in urine. It is an intermediate metabolite of the uronic acid pathway. Moreover, glucuronic acid is involved in detoxification of certain drugs and toxins by conjugating with them and forming glucuronides. Glucuronic acid has been found to cause an increase in TLR4-dependent reporter protein expression in a cell line transfected with TLR4 and associated co-signaling molecules, and can cause TLR4-dependent pain in humans.