Product Name Actein
CAS No.: 18642-44-9
Catalog No.: CFN99864
Molecular Formula: C37H56O11
Molecular Weight: 676.9 g/mol
Purity: >=98%
Type of Compound: Triterpenoids
Physical Desc.: Powder
Targets: cAMP | TNF-α | NF-kB | Sodium Channel | ATPase | Potassium Channel | MEK | p53 | Akt | P450 (e.g. CYP17)
Source: The roots of Cimicifuga racemosa
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Actein has a stimulatory effect on osteoblastic bone formation or has potential activity against osteoporosis, it also can prevent oxidative damage to osteoblasts in osteoporotic patients. Actein's ability to pathways involved in lipid disorders and carcinogenesis may make it a new agent for preventing and treating these major disorders, it has been shown to inhibit the proliferation of human breast cancer cells, by altering the activity of the ER IP3 receptor and Na,K-ATPase, inducing calcium release and modulating the NF-κB and MEK pathways.
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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.

Need more advice on solubility, usage and handling? Please email to:

The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    J Med Food. 2014 Apr;17(4):414-23.
    Actein isolated from black cohosh promotes the function of osteoblastic MC3T3-E1 cells.[Pubmed: 24552231]
    Actein, isolated from black cohosh, was subjected to in vitro experiments to investigate its functional bioactivities in osteoblastic MC3T3-E1 cells.
    Actein caused a significant elevation of alkaline phosphatase activity, collagen synthesis, osteocalcin production, mineralization, and glutathione content in the cells, suggesting that Actein has a stimulatory effect on osteoblastic bone formation or has potential activity against osteoporosis. We investigated the protective effects of Actein on mitochondrial electron transport inhibitor, antimycin A induced toxicity in osteoblastic MC3T3-E1 cells. Exposure of MC3T3-E1 cells to antimycin A caused significant decrease in cell viability and mineralization. However, pretreatment with Actein prior to antimycin A exposure significantly reduced antimycin A-induced cell damage by preventing mitochondrial membrane potential dissipation, complex IV inactivation, cardiolipin oxidation, ROS release, and nitrotyrosine increase, suggesting that Actein may be useful for protecting mitochondria against a burst of oxidative stress. In addition, Actein increased the phosphorylation of CREB (cAMP-response element-binding protein) inhibited by antimycin A and decreased the production of TNF-α induced by antimycin A.
    These findings suggest that Actein could prevent oxidative damage to osteoblasts in osteoporotic patients.
    Fundam Clin Pharmacol. 2009 Jun;23(3):311-21.
    Actein activates stress- and statin-associated responses and is bioavailable in Sprague-Dawley rats.[Pubmed: 19527300]
    The purpose of this study was to assess in rats the pharmacological parameters and effects on gene expression in the liver of the triterpene glycoside Actein. Actein, an active component from the herb black cohosh, has been shown to inhibit the proliferation of human breast cancer cells.
    To conduct our assessment, we determined the molecular effects of Actein on livers from Sprague-Dawley rats treated with Actein at 35.7 mg/kg for 6 and 24 h. Chemogenomic analyses indicated that Actein elicited stress and statin-associated responses in the liver; Actein altered expression of cholesterol and fatty acid biosynthetic genes, p53 pathway genes, CCND1 and ID3. Real-time RT-PCR validated that Actein induced three time-dependent patterns of gene expression in the liver: (i) a decrease followed by a significant increase of HMGCS1, HMGCR, HSD17B7, NQO1, S100A9; (ii) a progressive increase of BZRP and CYP7A1 and (iii) a significant increase followed by a decrease of CCND1 and ID3. Consistent with Actein's statin- and stress-associated responses, Actein reduced free fatty acid and cholesterol content in the liver by 0.6-fold at 24 h and inhibited the growth of human HepG2 liver cancer cells. To determine the bioavailability of Actein, we collected serum samples for pharmacokinetic analysis at various times up to 24 h. The serum level of Actein peaked at 2.4 microg/mL at 6 h.
    Actein's ability to alter pathways involved in lipid disorders and carcinogenesis may make it a new agent for preventing and treating these major disorders.
    Fitoterapia. 2013 Dec;91:28-38.
    Actein induces calcium release in human breast cancer cells.[Pubmed: 23939423]
    The triterpene glycoside Actein from the herb black cohosh preferentially inhibits the growth of breast cancer cells and activates the ER stress response. The ER IP3 receptor and Na,K-ATPase form a signaling microdomain. Since Actein is lipophilic, its action may be limited by bioavailability. To develop Actein to prevent and treat cancer, we examined the primary targets and combinations with chemotherapy agents, as well as the ability of nanoparticles to enhance the activity.
    To reveal signaling pathways, we treated human breast and colon cancer, as well as 293T and 293T (NF-κB), cells with Actein, and measured effects using the MTT, luciferase promoter, Western blot and histology assays. To assess effects on calcium release, we preloaded cells with the calcium sensitive dye Fura-2. To enhance bioavailability, we conjugated Actein to nanoparticle liposomes. Actein strongly inhibited the growth of human breast cancer cells and induced a dose dependent release of calcium into the cytoplasm. The ER IP3 receptor antagonist heparin blocked this release, indicating that the receptor is required for activity. Heparin partially blocked the growth inhibitory effect, while the MEK inhibitor U0126 enhanced it. Consistent with this, Actein synergized with the ER mobilizer thapsigargin. Further, Actein preferentially inhibited the growth of 293T (NF-κB) cells. Nanoparticle liposomes increased the growth inhibitory activity of Actein.
    Actein alters the activity of the ER IP3 receptor and Na,K-ATPase, induces calcium release and modulates the NF-κB and MEK pathways and may be worthwhile to explore to prevent and treat breast cancer.
    Biochem Biophys Res Commun. 2008 Oct 31;375(4):608-13.
    Actein inhibits the Na+-K+-ATPase and enhances the growth inhibitory effect of digitoxin on human breast cancer cells.[Pubmed: 18755149]
    The Na+K+-ATPase is a known target of cardiac glycosides such as digitoxin and ouabain.
    We determined that the enzyme also is a target of the structurally-related triterpene glycoside Actein, present in the herb black cohosh. Actein's inhibition of Na+-K+-ATPase activity was less potent than that of digitoxin, but Actein potentiated digitoxin's inhibitory effect on Na+-K+-ATPase activity and MDA-MB-453 breast cancer cell growth. We observed different degrees of signal amplification for the two compounds. Actein's inhibitory effect on ATPase activity was amplified 2-fold for cell growth inhibition, whereas digitoxin's signal was amplified 20-fold. Actein induced a biphasic response in proteins downstream of ATPase: low dose and short duration of treatment upregulated NF-kappaB promoter activity, p-ERK, p-Akt and cyclin D1 protein levels, whereas higher doses and longer exposure inhibited these activities.
    Actein and digitoxin may be a useful synergistic combination for cancer chemoprevention and/or therapy.

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