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Alpinetin
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Product Name Alpinetin
Price: $30 / 20mg
CAS No.: 36052-37-6
Catalog No.: CFN98489
Molecular Formula: C16H14O4
Molecular Weight: 270.3 g/mol
Purity: >=98%
Type of Compound: Flavonoids
Physical Desc.: Powder
Source: The fruits of Alpinia katsumadai.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Download: COA    MSDS    SDF    Manual
Similar structural: Comparison (Web)  (SDF)
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Size /Price /Stock 10 mM * 1 mL in DMSO / $8.9 / In-stock
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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
Related Libraries
Biological Activity
Description: Alpinetin has antibacterial, anti-inflammatory, and anti-cancer activities; it inhibits proliferation ,regulates of the Bcl-2 family and XIAP expression, releases of cytochrome c and activates caspases.
Targets: LDL | PPAR | TLR | NF-kB | ERK | JNK | IkB | TNF-α | p38MAPK | IL Receptor | Bcl-2/Bax | Caspase | Nrf2 | HO-1 | ROS | Calcium Channel | PKC | IKK
In vitro:
Immunopharmacol Immunotoxicol. 2014 Aug;36(4):290-6.
Immunosuppressive activity of alpinetin on activation and cytokines secretion of murine T lymphocytes.[Pubmed: 24964870]
Alpinetin, a flavonoid compound extracted from the seeds of Alpinia katsumadai Hayata, has been known to possess antibacterial, anti-inflammatory and other important therapeutic activities.
METHODS AND RESULTS:
In the current study, we investigated Alpinetin for its immunosuppressive effect on activation and cytokines secretion of murine T lymphocytes. The data showed that Alpinetin markedly suppressed ConA-induced murine splenocyte proliferation, Th1/Th2 cytokines production, CD4(+) T-cell populations and ratio of CD4(+)/CD8(+). This inspired us to further study the effects of Alpinetin in vivo. The results showed that administration of Alpinetin suppressed T-cell-mediated delayed-type hypersensitivity reaction in mice. In addition, we studied signal transduction pathways about T-cell activation on puried murine T lymphocytes by Western-blot assay. The data revealed that Alpinetin could shock the activation of NF-κB, NFAT2 signal transduction pathways.
CONCLUSIONS:
These observations indicated that Alpinetin have potential effects in downregulating the immune system and might be developed as a useful immunosuppressive agent in treating undesired immune responses.
Int J Mol Med. 2012 Apr;29(4):607-12.
Antiproliferative effect of alpinetin in BxPC-3 pancreatic cancer cells.[Pubmed: 22246103 ]
Alpinetin is a novel plant flavonoid derived from Alpinia katsumadai Hayata, found to possess strong anticancer effects. However, the antitumor effect of Alpinetin on pancreatic cancer cells and the detailed mechanism remain unclear. The aim of this study was to investigate Alpinetin's beneficial effect on pancreatic cancer and the possible molecular mechanism involved.
METHODS AND RESULTS:
Pancreatic cancer cell lines were treated with Alpinetin at various doses and for different times, and the effect of Alpinetin on cell growth inhibition, apoptosis and the cell cycle was determined. The expression of Bcl-2, Bcl-xL, XIAP and Bax, the activity of caspases and the levels of cytochrome c released were measured. The results showed that Alpinetin inhibited the viability of three pancreatic cancer cell lines and induced apoptosis of BxPC-3 cells in a dose- and time-dependent manner. This was accompanied by regulation of the expression of Bcl-2, Bcl-xL, Bax and XIAP. Furthermore, Alpinetin treatment led to the release of cytochrome c and activation of caspases-3, -8 and -9 proteins.
CONCLUSIONS:
Taken together, our studies indicate that Alpinetin inhibited the proliferation of pancreatic cancer cells possibly through the regulation of the Bcl-2 family and XIAP expression, release of cytochrome c and the activation of caspases. Alpinetin may serve as a potential agent for the development of pancreatic cancer cell therapies.
J Cardiovasc Pharmacol. 2001 May;37(5):596-606.
Vasorelaxant effects of cardamonin and alpinetin from Alpinia henryi K. Schum.[Pubmed: 11336110]
The vascular effects of cardamonin and Alpinetin from Alpinia henryi K. Schum. were examined in the rat isolated mesenteric arteries.
METHODS AND RESULTS:
1H and 13C nuclear magnetic resonance spectra showed that cardamonin is present in trans-form, and single-crystal radiographic structure revealed that Alpinetin is present in S configuration. Both cardamonin and Alpinetin produced a rightward shift in the concentration-response curve for phenylephrine in a noncompetitive manner, and they induced relaxation of phenylephrine-preconstricted arteries with respective mean inhibitory concentrations (IC50) of 9.3+/-0.6 microM and 27.5+/-2.8 microM. Both compounds also relaxed arteries preconstricted by endothelin I or U46619. Their relaxant effects were decreased in endothelium-removed rings. Pretreatment with N(G)-nitro-L-arginine methyl ester or methylene blue inhibited relaxation induced by both agents, and pretreatment with L-arginine reversed the effect of N(G)-nitro-L-arginine methyl ester on cardamonin-induced endothelium-dependent relaxation. The relaxant effects of cardamonin and Alpinetin were unaffected by indomethacin (3 microM). Cardamonin and Alpinetin inhibited 60 mM K+-induced contraction with respective IC50 of 11.5+/-0.3 microM and 37.9+/-3.6 microM. In addition, both agents inhibited the transient contraction induced by 3 microM phenylephrine or by 10 mM caffeine in Ca2+-free Krebs solution. Finally, these two agents also concentration dependently relax the arteries preconstricted by 1 microM phorbol 12,13-diacetate in Ca2+-free Krebs solution.
CONCLUSIONS:
These results indicate that purified cardamonin and Alpinetin from A. henryi K. Schum. relaxed rat mesenteric arteries through multiple mechanisms. They induced both endothelium-dependent and -independent relaxation; the former is likely mediated by nitric oxide whereas the latter is probably mediated through nonselective inhibition of Ca2+ influx and intracellular Ca2+ release and inhibition of the protein kinase C-dependent contractile mechanism.
In vivo:
Int Immunopharmacol. 2015 Oct;28(2):1003-8.
Alpinetin inhibits lipopolysaccharide-induced acute kidney injury in mice.[Pubmed: 26321118]
Alpinetin, a novel plant flavonoid isolated from Alpinia katsumadai Hayata, has been demonstrated to have anti-inflammatory and antioxidant effects. However, the effects of Alpinetin on lipopolysaccharide (LPS)-induced acute kidney injury have not been reported.
METHODS AND RESULTS:
In the present study, we investigated the protective effects and the underlying mechanism of Alpinetin against LPS-induced acute kidney injury in mice. The results showed that Alpinetin inhibited LPS-induced kidney histopathologic changes, blood urea nitrogen (BUN) and creatinine levels. Alpinetin also inhibited LPS-induced ROS, MDA, and inflammatory cytokines TNF-α, IL-6 and IL-1β production in kidney tissues. Meanwhile, Western blot analysis showed that Alpinetin suppressed LPS-induced TLR4 expression and NF-κB activation in kidney tissues. In addition, Alpinetin was found to up-regulate the expression of Nrf2 and HO-1 in a dose-dependent manner.
CONCLUSIONS:
In conclusion, Alpinetin protected LPS-induced kidney injury through activating Nrf2 and inhibiting TLR4 expression.
Alpinetin Description
Source: The fruits of Alpinia katsumadai.
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.
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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.6996 mL 18.498 mL 36.9959 mL 73.9919 mL 92.4898 mL
5 mM 0.7399 mL 3.6996 mL 7.3992 mL 14.7984 mL 18.498 mL
10 mM 0.37 mL 1.8498 mL 3.6996 mL 7.3992 mL 9.249 mL
50 mM 0.074 mL 0.37 mL 0.7399 mL 1.4798 mL 1.8498 mL
100 mM 0.037 mL 0.185 mL 0.37 mL 0.7399 mL 0.9249 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:
Biotechnol Appl Biochem. 2014 Dec 11.
Alpinetin enhances cholesterol efflux and inhibits lipid accumulation in oxidized low-density lipoprotein-loaded human macrophages.[Pubmed: 25496323]
Alpinetin is a natural flavonoid abundantly present in the ginger family.
METHODS AND RESULTS:
Here, we investigated the effect of Alpinetin on cholesterol efflux and lipid accumulation in oxidized low-density lipoprotein (ox-LDL)-treated THP-1 macrophages and human peripheral blood monocyte-derived macrophages (HMDMs). After exposing THP-1 macrophages to Alpinetin, cholesterol efflux was determined by liquid scintillator. The mRNA and protein levels of peroxisome proliferator-activated receptor gamma (PPAR-γ), liver X receptor alpha (LXR-α), ATP-binding cassette transporter A1 (ABCA1), and ABCG1 and scavenger receptor class B member 1 were determined by reverse-transcriptase PCR (RT-PCR) and Western blot analysis, respectively. Alpinetin promoted apolipoprotein A-I- and high-density-lipoprotein-mediated cholesterol efflux and elevated PPAR-γ and LXR-α mRNA and protein expression in a dose-dependent fashion in ox-LDL-treated THP-1 macrophages and HMDMs. Small interfering RNA-mediated silencing of PPAR-γ or LXR-α dose dependently reversed Alpinetin-increased cholesterol efflux in THP-1 macrophages, indicating the involvement of PPAR-γ and LXR-α in Alpinetin-promoted cholesterol efflux. Alpinetin inhibited ox-LDL-induced lipid accumulation and enhanced the expression of ABCA1 and ABCG1 mRNA and protein, which was reversed by specific knockdown of PPAR-γ or LXR-α.
CONCLUSIONS:
Taken together, our results reveal that Alpinetin exhibits positive effects on cholesterol efflux and inhibits ox-LDL-induced lipid accumulation, which might be through PPAR-γ/LXR-α/ABCA1/ABCG1 pathway.
Eur J Pharmacol. 2013 Dec 5;721(1-3):96-102.
Alpinetin inhibits LPS-induced inflammatory mediator response by activating PPAR-γ in THP-1-derived macrophages.[Pubmed: 24104193]
Alpinetin, a novel plant flavonoid derived from Alpinia katsumadai Hayata, has been reported to have anti-inflammatory properties. However, the anti-inflammatory mechanism of Alpinetin has not been fully elucidated.
METHODS AND RESULTS:
The purpose of this study was to investigate the anti-inflammatory mechanism of Alpinetin in modifying lipopolysaccharide (LPS)-induced signaling pathways in human THP-1 macrophages. The cells were stimulated with LPS in the presence or absence of Alpinetin. The pro-inflammatory cytokines were evaluated by ELISA and qRT-PCR. Toll-like receptor 4 (TLR4), nuclear factor-κB (NF-κB), inhibitory kappa B (IκBα) protein, p38, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and PPAR-γ were determined by Western blotting. The results showed that Alpinetin inhibited TNF-α, IL-6 and IL-1β expression in LPS-stimulated human THP-1 macrophages in a dose-dependent manner. Western blot analysis showed that Alpinetin suppressed LPS-induced NF-κB activation, IκBα degradation, phosphorylation of ERK, JNK and P38. Furthermore, Alpinetin could significantly down-regulated the expression of TLR4 stimulating by LPS. We also found that Alpinetin could activate PPAR-γ and the anti-inflammatory effects of Alpinetin can be reversed by GW9662, a specific antagonist for PPAR-γ.
CONCLUSIONS:
These results suggest that Alpinetin activates PPAR-γ, thereby attenuating TLR4 expression and TLR4 mediated NF-κB and MAPK activation and the release of pro-inflammatory cytokines. These findings suggest that Alpinetin may be a therapeutic agent against inflammatory diseases.
Cell Research:
Oncol Rep. 2012 Apr;27(4):1090-6.
Alpinetin suppresses proliferation of human hepatoma cells by the activation of MKK7 and elevates sensitization to cis-diammined dichloridoplatium.[Pubmed: 22159816]
Alpinetin is a type of novel plant flavonoid derived from Alpinia katsumadai Hayata, found to possess strong anti-hepatoma effects. However, the detailed antitumor mechanism of Alpinetin remains unclear. Mitogen-activated protein kinase kinase-7 (MKK7) can regulate cellular growth, differentiation and apoptosis.
METHODS AND RESULTS:
The aim of this study was to investigate the role of MKK7 in the anti-hepatoma effect mediated by Alpinetin. HepG2 cells were treated with Alpinetin at various doses and for different times, and the levels of phosphorylated MKK7 (p-MKK7) and total MKK7 were tested by RT-PCR and western blotting. Following transient transfection with RNA interference, cell viability and cell cycle stage were determined using methyl thiazolyl tetrazolium assay and flow cytometry, in order to assess the antitumor action of Alpinetin. In addition, chemosensitization to cis-diammined dichloridoplatium (CDDP) by Alpinetin was assessed by cell counting array and the cell growth inhibitory rate was calculated. The results showed that Alpinetin suppressed HepG2 cell proliferation and arrested cells in the G0/G1 phase by up-regulating the expression levels of p-MKK7. On the contrary, inhibiting the expression of MKK7 reversed the antitumor effect of Alpinetin. Moreover, Alpinetin enhanced the sensitivity of HepG2 hepatoma cells to the chemotherapeutic agent CDDP.
CONCLUSIONS:
Taken together, our studies indicate that activation of MKK7 mediates the anti-hepatoma effect of Alpinetin. MKK7 may be a putative target for molecular therapy against hepatoma and Alpinetin could serve as a potential agent for the development of hepatoma therapy.
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