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Alantolactone
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Product Name Alantolactone
Price: $30 / 20mg
CAS No.: 546-43-0
Catalog No.: CFN99934
Molecular Formula: C15H20O2
Molecular Weight: 232.32 g/mol
Purity: >=98%
Type of Compound: Sesquiterpenoids
Physical Desc.: Powder
Source: The roots of Inula helenium L.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Download: COA    MSDS    SDF    Manual
Similar structural: Comparison (Web)  (SDF)
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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: Alantolactone, an allergenic sesquiterpene lactone, has significant antitumor effects on malignant tumor cells, it can suppress inducible nitric oxide synthase and cyclooxygenase-2 expression by down-regulating NF-κB, MAPK and AP-1 via the MyD88 signaling pathway in LPS-activated RAW 264.7 cells, and inhibit cell proliferation by interrupting the interaction between Cripto-1 and activin receptor type II A in activin signaling pathway.
Targets: Caspase | PARP | NF-kB | TNF-α | IkB | p65 | Bcr-Abl | STAT | IL Receptor | P450 (e.g. CYP17) | CDK | Bcl-2/Bax | IKK | MyD88 | COX
In vitro:
Apoptosis. 2013 Sep;18(9):1060-70.
Alantolactone induces apoptosis in chronic myelogenous leukemia sensitive or resistant to imatinib through NF-κB inhibition and Bcr/Abl protein deletion.[Pubmed: 23613107 ]
Alantolactone, an allergenic sesquiterpene lactone, has recently been found to have significant antitumor effects on malignant tumor cells. Here, we investigated the potential effect of Alantolactone on Bcr/Abl+ imatinib-sensitive and -resistant cells.
METHODS AND RESULTS:
Alantolactone treatment resulted in obvious apoptosis in both imatinib-sensitive and -resistant K562 cells, as shown by the increase in Annexin V-positive cells, caspase-3 activation, poly(ADP-ribose) polymerase-1 (PARP-1) cleavage and mitochondrial membrane potential collapse. Alantolactone significantly inhibited NF-κB-dependent reporter gene activity, decreased the DNA-binding activity of NF-ОκB, and blocked TNF-α-induced IκBα phosphorylation. Of interest, the oncogenic Bcr/Abl fusion protein but not its mRNA levels were quickly reduced upon Alantolactone exposure in imatinib-sensitive and -resistant K562 cells. Bcr/Abl knockdown enhanced the apoptosis driven by Alantolactone. Bcr/Abl protein reduction could not be reversed by the addition of proteasome or caspase-3 inhibitors. The overexpression of p65 inhibited Alantolactone-induced apoptosis, whereas p65 or Bcr/Abl silencing enhanced its apoptotic-inducing effect. Furthermore, Bcr/Abl-transfected 32D cells showed more sensitivity to Alantolactone than vector-transfected control cells, and the Bcr/Abl protein was depleted, as observed in K562 cells. Finally, Alantolactone-induced apoptosis was also observed in primary CD34+ CML leukemic cells.
CONCLUSIONS:
Collectively, these findings suggest that Alantolactone is a promising potent agent to fight against CML cells via the inhibition of the NF-κB signaling pathway and depletion of the Bcr/Abl protein.
In vivo:
Cancer Lett . 2015 Feb 1;357(1):393-403.
Alantolactone selectively suppresses STAT3 activation and exhibits potent anticancer activity in MDA-MB-231 cells[Pubmed: 25434800]
Abstract The important goal of cancer drug discovery is to develop therapeutic agents that are effective, safe, and affordable. In the present study, we demonstrated that Alantolactone, which is a sesquiterpene lactone, has potential activity against triple-negative breast cancer MDA-MB-231 cells by suppressing the signal transducer and activator of transcription 3 (STAT3) signaling pathway. Alantolactone effectively suppressed both constitutive and inducible STAT3 activation at tyrosine 705. Alantolactone decreased STAT3 translocation to the nucleus, its DNA-binding, and STAT3 target gene expression. Alantolactone significantly inhibits STAT3 activation with a marginal effect on MAPKs and on NF-κB transcription; however, this effect is not mediated by inhibiting STAT3 upstream kinases. Although SHP-1, SHP-2, and PTEN, which are protein tyrosine phosphatases (PTPs), were not affected by Alantolactone, the treatment with a PTP inhibitor reversed the Alantolactone-induced suppression of STAT3 activation, indicating that PTP plays an important role in the action of Alantolactone. Finally, Alantolactone treatment resulted in the inhibition of migration, invasion, adhesion, and colony formation. The in vivo administration of Alantolactone inhibited the growth of human breast xenograft tumors. These results provide preclinical evidence to continue the development of Alantolactone as a STAT3 inhibitor and as a potential therapeutic agent against breast cancer. Keywords: Alantolactone; MDA-MB-231 cells; STAT3; Sesquiterpene lactone; Triple-negative breast cancer (TNBC).
Alantolactone Description
Source: The roots of Inula helenium L.
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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Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

Cell. 2018 Jan 11;172(1-2):249-261.e12.
doi: 10.1016/j.cell.2017.12.019.
IF=36.216(2019)

PMID: 29328914

Cell Metab. 2020 Mar 3;31(3):534-548.e5.
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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 4.3044 mL 21.522 mL 43.0441 mL 86.0882 mL 107.6102 mL
5 mM 0.8609 mL 4.3044 mL 8.6088 mL 17.2176 mL 21.522 mL
10 mM 0.4304 mL 2.1522 mL 4.3044 mL 8.6088 mL 10.761 mL
50 mM 0.0861 mL 0.4304 mL 0.8609 mL 1.7218 mL 2.1522 mL
100 mM 0.043 mL 0.2152 mL 0.4304 mL 0.8609 mL 1.0761 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:
J Ethnopharmacol. 2015 Apr 7.
Mechanism-based inhibition of Alantolactone on human cytochrome P450 3A4 in vitro and activity of hepatic cytochrome P450 in mice.[Pubmed: 25858508]
Alantolactone (AL), one of the main active ingredients in Inula helenium L., has been included in various prescriptions of traditional Chinese medicine. The effects of Alantolactone on cytochrome P450 (CYP450) were still unclear. This study evaluated the inhibitory effect of Alantolactone on cytochrome P450s in vitro and in vivo.
METHODS AND RESULTS:
The inhibitory effects of Alantolactone on the CYPs activity were evaluated in human liver microsomes (HLMs) and recombinant cDNA-expressed enzymes incubation system, and then determined by LC-MS/MS based CYPs probe substrate assay. C57BL/6 mice were treated Alantolactone orally (0, 25, 50, 100mg/kg) for 15 days. The inhibitory effects of Alantolactone on major Cyps in mice were examined at both the mRNA and enzyme activity levels. Alantolactone showed a potent inhibitory effect on CYP3A4 activity with IC50 values of 3.599 (HLMs) and 3.90 (recombinant CYP3A4) μM, respectively. Alantolactone strongly decreased CYP3A4 activity in a dose-dependent but not time-dependent way in HLMs. Results from typical Lineweaver-Burk plots showed that Alantolactone could inhibit CYP3A4 activity noncompetitively, with a Ki value of 1.09μM in HLMs. Moreover, activity of CYP2C19 could also be inhibited by Alantolactone with IC50 of 36.82μM. Other CYP450 isoforms were not markedly affected by Alantolactone. The inhibition was also validated by in vivo study of mice. Alantolactone significantly decreased mRNA expression of Cyp2c and 3a family.
CONCLUSIONS:
The study indicates that herb-drug interaction should be paid more attention between Alantolactone and drugs metabolized by CYP3A4.
Cell Research:
Phytother Res. 2015 Apr 17.
Alantolactone from Saussurea lappa Exerts Antiinflammatory Effects by Inhibiting Chemokine Production and STAT1 Phosphorylation in TNF-α and IFN-γ-induced in HaCaT cells.[Pubmed: 25881570]
Skin inflammation is the most common condition seen in dermatology practice and can be caused by various allergic reactions and certain toxins or chemicals. In the present study, we investigated the antiinflammatory effects of Saussurea lappa, a medicinal herb, and its marker compounds Alantolactone, caryophyllene, costic acid, costunolide, and dehydrocostuslactone in the HaCaT human keratinocyte cell line.
METHODS AND RESULTS:
HaCaT cells were stimulated with tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ), and treated with S. lappa or each of five marker compounds. Chemokine production and expression were analyzed by enzyme-linked immunosorbent assay and reverse transcription-polymerase chain reaction, respectively. Phosphorylation of signal transducer and activator of transcription (STAT) 1 was determined by immunoblotting. Stimulation with TNF-α and IFN-γ significantly increased the production of the following chemokines: thymus-regulated and activation-regulated chemokine (TARC): regulated on activation, normal T-cell expressed and secreted (RANTES): macrophage-derived chemokine (MDC): and interleukin-8 (IL-8). By contrast, S. lappa and the five marker compounds significantly reduced the production of these chemokines by TNF-α and IFN-γ-treated cells. S. lappa and Alantolactone suppressed the TNF-α and IFN-γ-stimulated increase in the phosphorylation of STAT1.
CONCLUSIONS:
Our results demonstrate that Alantolactone from S. lappa suppresses TNF-α and IFN-γ-induced production of RANTES and IL-8 by blocking STAT1 phosphorylation in HaCaT cells.
J Biochem Mol Toxicol. 2015 May;29(5):199-206.
Alantolactone Induces Apoptosis and Cell Cycle Arrest on Lung Squamous Cancer SK-MES-1 Cells.[Pubmed: 25597476]
Alantolactone, a sesquiterpene lactone compound, has variety of pharmacological properties, including anti-inflammatory and antineoplastic effects.
METHODS AND RESULTS:
In our study, Alantolactone inhibited cancer cell proliferation. To explore the mechanisms underlying its antitumor action, we further examined apoptotic cells and cell cycle distribution using flow cytometry analysis. Alantolactone triggered apoptosis and induced cell cycle G1/G0 phase arrest. Furthermore, the expressions of caspases-8, -9, -3, PARP, and Bax were significantly upregulated, while antiapoptotic factor Bcl-2 expression was inhibited. In addition, the expressions of cyclin-dependent kinase 4 (CDK4), CDK6, cyclin D3, and cyclin D1 were downregulated by Alantolactone.
CONCLUSIONS:
Therefore, our findings indicated that Alantolactone has an antiproliferative role on lung squamous cancer cells, and it may be a promising chemotherapeutic agent for squamous lung cancer SK-MES-1 cells.
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