Ganoderic acid S
A novel combination of triterpenoids includes at least ganoderic acid S (GAS), ganoderic acid T (GAT), ganoderic acid Me (GAMe), ganoderic acid R (GAR), and ganodermic acid S (GMAS), the composition is suitable for the treatment or prophylaxis of colon cancer, hepatic cancer, breast cancer, lung cancer or leukemia. Ganoderic acid S and Mf induce mitochondria mediated apoptosis in human cervical carcinoma HeLa cells.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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US20140294753[P]. 2014.
Therapeutic Composition for Treating Cancers.[Reference:
WebLink]
Disclosed herein is a composition that includes a novel combination of triterpenoids for the treatment or prophylaxis of a cancer. The triterpenoids includes at least Ganoderic acid S (GAS), ganoderic acid T (GAT), ganoderic acid Me (GAMe), ganoderic acid R (GAR), and ganodermic acid S (GMAS). The composition is suitable for the treatment or prophylaxis of colon cancer, hepatic cancer, breast cancer, lung cancer or leukemia.
Phytomedicine. 2011 Mar 15;18(5):349-55.
Ganoderic acid Mf and S induce mitochondria mediated apoptosis in human cervical carcinoma HeLa cells.[Pubmed:
21036023 ]
METHODS AND RESULTS:
In this work, the effects of a pair of positional isomer of ganoderic acids (GAs), namely ganoderic acid Mf (GA-Mf) and Ganoderic acid S (GA-S) purified from the fermented mycelia of Ganoderma lucidum, on induction of cell apoptosis and the apoptotic pathway in HeLa cells were investigated. The results demonstrate that both isomers decreased cell population growth on various human carcinoma cell lines by MTT assay, while GA-Mf had better selectivity between normal and cancer cells. The flow cytometry analysis indicated that treatment of HeLa cells with GA-S caused cell cycle arrest in the S phase, while GA-Mf caused cell cycle arrest in the G1 phase. Compared with GA-S, GA-Mf had more potent increase in the number of early and late apoptotic cells. Treatment of HeLa cells with each isomer decreased the mitochondria membrane potential and caused the release of cytochrome c from mitochondria into the cytosol. In addition, stimulation of caspase-3 and caspase-9 activity was observed. The Bax/Bcl-2 ratio was also increased in GA-treated HeLa cells. The results demonstrated that both isomers GA-Mf and GA-S induced apoptosis of human HeLa cells through a mitochondria mediated pathway, but they had the different cell cycle arrest specificity.
CONCLUSIONS:
The findings will be helpful to the development of useful cancer chemopreventive compounds from G. lucidum.
