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1-O-Acetylbritannilactone
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Product Name 1-O-Acetylbritannilactone
Price: $218 / 20mg
CAS No.: 33627-41-7
Catalog No.: CFN89438
Molecular Formula: C17H24O5
Molecular Weight: 308.36 g/mol
Purity: >=98%
Type of Compound: Sesquiterpenoids
Physical Desc.: Powder
Source: The flower heads of Inula britannica.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Download: COA    MSDS
Similar structural: Comparison
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
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Biological Activity
Description: 1-O-Acetylbritannilactone has anticancer activity, it suppresses angiogenesis and lung cancer cell growth possibly via regulating the VEGFR-Src-FAK signaling, it also can combine with gemcitabine elicits a potent apoptosis of lung cancer cell. 1-O-Acetylbritannilactone may serve as a novel therapeutic intervention for various cardiovascular diseases, including chronic ischemia, by regulating VEGF signaling and modulating angiogenesis; it is a potent inhibitor of LPS-stimulated VSMC inflammatory responses through blockade of NF-kappaB activity and inhibition of inflammatory gene COX-2 expression. 1-O-Acetylbritannilactone may act as potent natural skin-lightening agents, it exhibits anti-melanogenic activity by suppression of tyrosinase expression via ERK and Akt signaling.
Targets: VEGFR | Src | FAK | ERK | Akt | Bcl-2/Bax | Caspase | p38MAPK | cAMP | p65 | NF-kB | Tyrosinase | COX | PGE
In vitro:
Pharmazie. 2016 Apr;71(4):213-7.
The combination use of 1-O-acetylbritannilactone (ABL) and gemcitabine inhibits cell growth and induces cell apoptosis in lung adenocarcinoma cells.[Pubmed: 27209702]
1-O-Acetylbritannilactone (ABL), a natural chemical component obtained from Chinese traditional medicine, Inula britannica, has been demonstrated to have anticancer activities.
METHODS AND RESULTS:
In the present study, we evaluated the anti-proliferative and the pro-apoptotic abilities of ABL alone or in combination with gemcitabine in human NSCLC cell line. A549 cells were treated, in vitro, with ABL, gemcitabine, and the combination of ABL and gemcitabine for 72 h. Our results showed ABL and gemcitabine inhibited cell growth and induced apoptosis of A549 cells. These effects after the combination of ABL and gemcitabine were superior to those of each alone. Furthermore, signal transduction analysis revealed NF-κB expression was significantly decreased by ABL and the combination treatment. IκBα and Bax levels were up regulated whereas Bcl-2 was substantially downregulated after all treatments.
CONCLUSIONS:
Our findings suggest that ABL combined with gemcitabine elicits a potent apoptosis of lung cancer cell and hence ABL has the potential to be developed as a chemotherapeutic agent.
Arch Pharm Res. 2014 May;37(5):567-74.
Hypo-pigmenting effect of sesquiterpenes from Inula britannica in B16 melanoma cells.[Pubmed: 24346861 ]

METHODS AND RESULTS:
A bioassay-guided isolation of the chloroform fraction of the I. britannica using an in vitro melanogenesis inhibition assay led to the isolation of sesquiterpenes, 1-O-Acetylbritannilactone (1), britannilactone (2) and neobritannilactone B (3). Compounds 1 and 2 significantly reduced melanin production in a dose-dependent manner with IC50 values of 13.3 and 15.5 μM, respectively, whereas compound 3 was found to be cytotoxic. Compound 1 also inhibited the tyrosinase activity only in cell based-systems. Western blot analysis indicated that compound 1 inhibited melanogenesis by activating extracellular signal-regulated kinase (ERK) and Akt signaling and also inhibiting cAMP related binding protein, which regulates its downstream pathway, including tyrosinase, tyrosinase related protein-1 and TRP-2.
CONCLUSIONS:
These results demonstrated that compound 1, a major sesquiterpene from the flowers of I. britannica, exhibited anti-melanogenic activity by suppression of tyrosinase expression via ERK and Akt signaling. Taken together, our results suggest that these compounds may act as potent natural skin-lightening agents.
In vivo:
Biochem Biophys Res Commun. 2015 Aug 21;464(2):422-7.
1-o-acetylbritannilactone (ABL) inhibits angiogenesis and lung cancer cell growth through regulating VEGF-Src-FAK signaling.[Pubmed: 26102035 ]
The search for safe, effective and affordable therapeutics against non-small cell lung cancer (NSCLC) and other lung cancers is important.
METHODS AND RESULTS:
Here we explored the potential effect of 1-O-Acetylbritannilactone (ABL), a novel extract from Inula britannica-F, on angiogenesis and lung cancer cell growth. We demonstrated that ABL dose-dependently inhibited vascular endothelial growth factor (VEGF)-induced proliferation, migration, and capillary structure formation of cultured human umbilical vascular endothelial cells (HUVECs). In vivo, ABL administration suppressed VEGF-induced new vasculature formation in Matrigel plugs. For the mechanism investigations, we found that ABL largely inhibited VEGF-mediated activation of Src kinase and focal adhesion kinase (FAK) in HUVECs. Furthermore, treatment of A549 NSCLC cells with ABL resulted in cell growth inhibition and Src-FAK in-activation. Significantly, administration of a single dose of ABL (12 mg/kg/day) remarkably suppressed growth of A549 xenografts in nude mice. In vivo microvessels formation and Src activation were also significantly inhibited in ABL-treated xenograft tumors.
CONCLUSIONS:
Taken together, our findings suggest that ABL suppresses angiogenesis and lung cancer cell growth possibly via regulating the VEGFR-Src-FAK signaling.
1-O-Acetylbritannilactone Description
Source: The flower heads of Inula britannica.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Storage: 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: service@chemfaces.com

After receiving: 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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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.243 mL 16.2148 mL 32.4296 mL 64.8593 mL 81.0741 mL
5 mM 0.6486 mL 3.243 mL 6.4859 mL 12.9719 mL 16.2148 mL
10 mM 0.3243 mL 1.6215 mL 3.243 mL 6.4859 mL 8.1074 mL
50 mM 0.0649 mL 0.3243 mL 0.6486 mL 1.2972 mL 1.6215 mL
100 mM 0.0324 mL 0.1621 mL 0.3243 mL 0.6486 mL 0.8107 mL
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
Protocol
Kinase Assay:
PLoS One. 2016 Feb 10;11(2):e0148968.
Acetylbritannilactone Modulates Vascular Endothelial Growth Factor Signaling and Regulates Angiogenesis in Endothelial Cells.[Pubmed: 26863518 ]
The present study was conducted to determine the effects of 1-O-Acetylbritannilactone (ABL), a compound extracted from Inula britannica L., on vascular endothelial growth factor (VEGF) signaling and angiogenesis in endothelial cells (ECs).
METHODS AND RESULTS:
We showed that ABL promotes VEGF-induced cell proliferation, growth, migration, and tube formation in cultured human ECs. Furthermore, the modulatory effect of ABL on VEGF-induced Akt, MAPK p42/44, and p38 phosphorylation, as well as on upstream VEGFR-2 phosphorylation, were associated with VEGF-dependent Matrigel angiogenesis in vivo. In addition, animals treated with ABL (26 mg/kg/day) recovered blood flow significantly earlier than control animals, suggesting that ABL affects ischemia-mediated angiogenesis and arteriogenesis in vivo. Finally, we demonstrated that ABL strongly reduced the levels of VEGFR-2 on the cell surface, enhanced VEGFR-2 endocytosis, which consistent with inhibited VE-cadherin, a negative regulator of VEGF signaling associated with VEGFR-2 complex formation, but did not alter VE-cadherin or VEGFR-2 expression in ECs.
CONCLUSIONS:
Our results suggest that ABL may serve as a novel therapeutic intervention for various cardiovascular diseases, including chronic ischemia, by regulating VEGF signaling and modulating angiogenesis.
Eur J Pharmacol. 2007 Dec 22;577(1-3):28-34.
Acetylbritannilactone suppresses lipopolysaccharide-induced vascular smooth muscle cell inflammatory response.[Pubmed: 17915214 ]
To investigate the mechanism of action by which a new anti-inflammatory active compound, 1-O-Acetylbritannilactone (ABL) isolated from Inula britannica-F., inhibits inflammatory responses in vascular smooth muscle cells (VSMCs).
METHODS AND RESULTS:
Enzyme immunoassay was used to measure the levels of prostandin E(2) (PGE(2)) production. Immunocytochemistry staining and Western blot analysis were performed to detect the nuclear translocation of nuclear factor-kappaB (NF-kappaB) p65 and the expression of IkappaB-alpha, pIkappaB-alpha and cyclooxygenase-2 (COX-2). Electrophoretic mobility shift assays (EMSA) were used to detect DNA-binding activity of NF-kappaB in VSMCs. ABL (5, 10, 20 micrommol/l) had several concentration-dependent effects, including inhibition of lipopolysaccharide (LPS)-induced PGE(2) production and COX-2 expression, and blockade of NF-kappaB activation and translocation. These effects were owing to reductions in IkappaB-alpha phosphorylation and degradation induced by LPS. In addition, ABL directly inhibited the binding of active NF-kappaB to specific DNA cis-element.
CONCLUSIONS:
These results indicate that ABL is a potent inhibitor of LPS-stimulated VSMC inflammatory responses through blockade of NF-kappaB activity and inhibition of inflammatory gene COX-2 expression.
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