Capillarisin

CAS# 56365-38-9

Capillarisin

Catalog No. BCN2461----Order now to get a substantial discount!

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Chemical structure

Capillarisin

3D structure

Chemical Properties of Capillarisin

Cas No. 56365-38-9 SDF Download SDF
PubChem ID 5281342 Appearance Powder
Formula C16H12O7 M.Wt 316.26
Type of Compound Flavonoids Storage Desiccate at -20°C
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Chemical Name 5,7-dihydroxy-2-(4-hydroxyphenoxy)-6-methoxychromen-4-one
SMILES COC1=C(C=C2C(=C1O)C(=O)C=C(O2)OC3=CC=C(C=C3)O)O
Standard InChIKey NTKNGUAZSFAKEE-UHFFFAOYSA-N
Standard InChI InChI=1S/C16H12O7/c1-21-16-11(19)6-12-14(15(16)20)10(18)7-13(23-12)22-9-4-2-8(17)3-5-9/h2-7,17,19-20H,1H3
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Capillarisin

The herbs of Artemisia capillaris Thunb.

Biological Activity of Capillarisin

Description1. Capillarisin has anti-inflammatory activity, can inhibit LPS-induced inflammation by blocking TLR4-mediated NF-κB and MAPKs activation in BV2 microglia. 2. Capillarisin possesses promising anti-hyperalgesic and anti-allodynic effects through the inhibition of various inflammatory pain signaling. 3. Capillarisin is a novel blocker of STAT3 activation and thus may have a potential in negative regulation of growth, metastasis, and chemoresistance of tumor cells. 4. Capillarisin inhibits cancer cell growth of osteosarcoma cells by inducing apoptosis accompanied with G0/G1-phase cell cycle arrest and loss in mitochondrial membrane potential.
TargetsTLR | NF-kB | MAPK | STAT | TNF-α | IL Receptor | NO | PGE | AP-1 | ERK | NOS | COX | MMP(e.g.TIMP) | VEGFR | JNK | Bcl-2/Bax

Capillarisin Dilution Calculator

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Capillarisin Molarity Calculator

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Preparing Stock Solutions of Capillarisin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.162 mL 15.8098 mL 31.6196 mL 63.2391 mL 79.0489 mL
5 mM 0.6324 mL 3.162 mL 6.3239 mL 12.6478 mL 15.8098 mL
10 mM 0.3162 mL 1.581 mL 3.162 mL 6.3239 mL 7.9049 mL
50 mM 0.0632 mL 0.3162 mL 0.6324 mL 1.2648 mL 1.581 mL
100 mM 0.0316 mL 0.1581 mL 0.3162 mL 0.6324 mL 0.7905 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Capillarisin

Capillarisin Exhibits Anticancer Effects by Inducing Apoptosis, Cell Cycle Arrest and Mitochondrial Membrane Potential Loss in Osteosarcoma Cancer Cells (HOS).[Pubmed:25368903]

Drug Res (Stuttg). 2015 Aug;65(8):422-7.

The aim of the present study was to assess the anticancer activity of Capillarisin against human osteosarcoma (HOS) cancer cells in vitro. Cell viability after Capillarisin drug treatment and evaluated by MTT assay. The extent of cell death induced by Capillarisin was estimated by using lactate dehydrogenase (LDH) assay. The effect of Capillarisin on cell cycle phase distribution and mitochondrial membrane potential (LambdaPsim) was demonstrated via flow cytometry using propidium iodide (PI) and rhodamine-123 (Rh-123) DNA-binding fluorescent dyes respectively. Fluorescence microscopy was employed to examine the morphological changes in osteosarcoma cancer cells and presence of apoptotic bodies following Capillarisin treatment. The results of this study revealed that Capillarisin induced dose-dependent growth inhibition of these cancer cells after 12-h of incubation. Further, Capillarisin induced significant release of LDH from these cell cultures and this LDH release was much more noticeable at higher concentrations of Capillarisin. Hoechst 33258 staining revealed characteristic morphological features of apoptosis triggered by Capillarisin treatment. Cell cycle analysis revealed that Capillarisin induced dose-dependent G0/G1-phase cell cycle arrest. Capillarisin also trigerred a progressive and dose-dependent reduction in the mitochondrial membrane potential. In conclusion, Capillarisin inhibits cancer cell growth of osteosarcoma cells by inducing apoptosis accompanied with G0/G1-phase cell cycle arrest and loss in mitochondrial membrane potential.

Capillarisin inhibits iNOS, COX-2 expression, and proinflammatory cytokines in LPS-induced RAW 264.7 macrophages via the suppression of ERK, JNK, and NF-kappaB activation.[Pubmed:23131135]

Immunopharmacol Immunotoxicol. 2013 Feb;35(1):34-42.

The aerial parts of Artemisia capillaris (Compositae) have been used in traditional Korean medicine as a cholagogic, antipyretic, anti-inflammatory, and diuretic purposes. In our previous study, ethanolic extracts of the plant demonstrated a marked anti-inflammatory effect in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells (J. Korean Soc. Appl. Biol. Chem., 2010, 53, 275-282). In the present study, Capillarisin (CPS), a flavone, main constituent of A. capillaris, was examined for its anti-inflammatory activity in the cells. We found that CPS highly suppressed LPS-induced nitric oxide (NO) without exerting cytotoxic effects on RAW 264.7 cells. CPS inhibited the expression of LPS-induced inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein and their mRNA in a dose-dependent manner. Also, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-1beta, and prostaglandin E(2) (PGE(2)) secretion were decreased by CPS in LPS-stimulated macrophages. As a result, CPS inhibited proinflammatory cytokines, iNOS, and COX-2, which is attributed to the suppression of LPS-induced ERK, JNK, and nuclear factor-kappaB (NF-kappaB) activation. Therefore, we demonstrate here that CPS potentially inhibits the biomarkers related to inflammation through the abrogation of ERK, JNK, and NF-kappaB p65 activation, and it may be a potential therapeutic candidate for the treatment of inflammatory diseases.

Anti-hyperalgesic and anti-allodynic activities of capillarisin via suppression of inflammatory signaling in animal model.[Pubmed:24495472]

J Ethnopharmacol. 2014 Mar 28;152(3):478-86.

ETHNOPHARMACOLOGICAL RELEVANCE: Artemisia capillaris has widespread traditional and pharmacological applications such as analgesic, anti-inflammatory, anti-pyretic, enhance immunity and anti-tumor activity properties. To evaluate the pharmacological activities of this plant, Capillarisin, one of the potent constituent of Artemisia capillaris was studied based on anti-hyperalgesic and anti-allodynic effects with detailed mechanism. It can be assumed that measurement of anti-nociceptive effects of Capillarisin is one of the parameter for the evaluation of this herb. Capillarisin has extensive pharmacological properties and has been considered to have promising ant-inflammatory and anti-nociceptive activities. The aim of the current study is to investigate the effect of Capillarisin and underlying molecular mechanisms of action in preventing acute and subchronic inflammatory pain. MATERIALS AND METHODS: The inflammatory pain was induced after 40 min or 1h of administration of vehicle, 70% EtOH extract of Artemisia capillaris (100mg/kg) or Capillarisin (20 and 80 mg/kg) by intraplantar (i.p.l.) injections of CFA and carrageenan in ICR mice, respectively. Mechanical hyperalgesia and allodynia were evaluated in both acute and subchronic models. Further analysis was performed in CFA-induced mice exploring various molecular and signaling pathways such as NF-kappaB, AP-1, and ERK-CREB involved in the persistent pain sensations. RESULTS: In acute model, mechanical hyperalgesia and allodynia were evaluated after every 2h until 6h of CFA and after 4h of carrageenan injections. Whereas, in subchronic inflammatory pain model, mechanical hyperalgesia and paw edema were measured after 4h of CFA injection and every day after 4h of daily treatment until 5 days with interval of day four in order to assess the tolerance effect of Capillarisin. Further analysis was performed in CFA-induced mice exploring various molecular and signaling pathways such as NF-kappaB, AP-1 and ERK-CREB involved in the persistent of pain sensations. Pre-treatment of Capillarisin strongly inhibited NF-kappaB mediated genes (iNOS, COX-2), involved in pain. The plasma leading nitrite production was significantly reduced by Capillarisin. Moreover, i.p. administration of Capillarisin markedly suppressed the adenosine 5-triphosphate (ATP) in plasma and substance P in CFA-induced paw tissue. CONCLUSIONS: The present study indicates that Capillarisin possessed promising anti-hyperalgesic and anti-allodynic effects through the inhibition of various inflammatory pain signaling, suggesting that Capillarisin constitutes a significant component for the treatment of inflammatory pain.

Capillarisin Suppresses Lipopolysaccharide-Induced Inflammatory Mediators in BV2 Microglial Cells by Suppressing TLR4-Mediated NF-kappaB and MAPKs Signaling Pathway.[Pubmed:25894679]

Neurochem Res. 2015 Jun;40(6):1095-101.

Capillarisin, one of the major bioactive compounds derived from Artemisia capillaries Thunb, has been reported to have extensive pharmacological properties, such as ant-inflammatory and anti-nociceptive activities. However, the molecular mechanisms responsible for the anti-inflammatory activity of Capillarisin have not been elucidated in microglia. In the present study, we investigated the anti-inflammatory effects and molecular mechanisms of Capillarisin on LPS-stimulated BV2 microglial cells. The effects of Capillarisin on inflammatory mediators TNF-alpha, IL-6, IL-1beta, NO and PGE2 were detected. The effects of Capillarisin on NF-kappaB and MAPK activation were detected by western blotting. The results showed that Capillarisin suppressed LPS-induced TNF-alpha, IL-6, IL-1beta, NO and PGE2 production in a dose-dependent manner. Capillarisin also inhibited LPS-induced TLR4 expression, NF-kappaB and MAPKs activation in BV2 microglia. In conclusion, Capillarisin inhibited LPS-induced inflammation by blocking TLR4-mediated NF-kappaB and MAPKs activation in BV2 microglia.

Capillarisin inhibits constitutive and inducible STAT3 activation through induction of SHP-1 and SHP-2 tyrosine phosphatases.[Pubmed:24333736]

Cancer Lett. 2014 Apr 1;345(1):140-8.

Signal transducers and activators of transcription (STAT)-3 is a latent cytosolic transcription factor that has been closely associated with survival, proliferation, chemoresistance, and metastasis of tumor cells. Whether the anti-proliferative, pro-apoptotic, and anti-metastatic effects of Capillarisin (CPS), derived from Artemisia capillaris (Compositae), are linked to its capability to inhibit STAT3 activation was investigated. We found that CPS specifically inhibited both constitutive and inducible STAT3 activation at tyrosine residue 705 but not at serine residue 727 in human multiple myeloma cells. Besides the inhibition of STAT3 phosphorylation, CPS also abrogated STAT3 constitutive activity and nuclear translocation. The suppression of STAT3 was mediated through the inhibition of activation of upstream JAK1, JAK2, and c-Src kinases. Treatment with the protein tyrosine phosphatase (PTP) inhibitor pervanadate treatment reversed the CPS-induced down-regulation of JAK1/2 and STAT3, thereby suggesting the involvement of a PTP. Indeed, knockdown of the SHP-1 and SHP-2 genes by small interfering RNA suppressed the ability of CPS to inhibit JAK1 and STAT3 activation, suggesting the critical role of both SHP-1 and SHP-2 in its possible mechanism of action. CPS downregulated the expression of STAT3-regulated antiapoptotic and proliferative gene products; and this correlated with suppression of cell viability, the accumulation of cells in sub-G1 phase of cell cycle and induction of apoptosis. Moreover, CPS potentiated bortezomib-induced apoptotic effects in MM cells, and this correlated with down-regulation of various gene products that mediate cell proliferation (Cyclin D1 and COX-2), cell survival (Bcl-2, Bcl-xl, IAP1, IAP2, and Survivin), invasion (MMP-9), and angiogenesis (VEGF). Thus, overall, our results suggest that CPS is a novel blocker of STAT3 activation and thus may have a potential in negative regulation of growth, metastasis, and chemoresistance of tumor cells.

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