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1-Hydroxy-2,3,5-trimethoxyxanthone
1-Hydroxy-2,3,5-trimethoxyxanthone
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Product Name 1-Hydroxy-2,3,5-trimethoxyxanthone
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CAS No.: 22804-49-5
Catalog No.: CFN96272
Molecular Formula: C16H14O6
Molecular Weight: 302.3 g/mol
Purity: >=98%
Type of Compound: Xanthones
Physical Desc.: Yellow powder
Source: The herbs of Halenia elliptica D. Don
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Download: COA    MSDS
Similar structural: Comparison (Web)  (SDF)
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Biological Activity
Description: 1-Hydroxy-2,3,5-trimethoxyxanthone (HM-1) has vasodilator action ,which involves both an endothelium-dependent mechanism involving NO and an endothelium-independent mechanism by inhibiting Ca(2+) influx through L-type voltage-operated Ca(2+) channels; a minor contribution to the effects of HM-1 may be related to inhibition of the protein kinase C-mediated release of intracellular Ca(2+) stores. HM-1,at the concentration of 1 ug/mL, can effectively inhibit the osteoclast differentiation in a co-culture system with mouse osteoblastic calvarial cells and bone marrow cells; it also can protect mice from the acute lung injury induced by ipopolysaccharide (LPS), which is relative to the increasing of IκB-α protein expression and the suppressing of inducible nitric oxide synthase and cyclooxygenase-Ⅱ protein expression.
Targets: NO | 5-HT Receptor | Calcium Channel | COX | NOS | IkB | IKK
In vitro:
Life Sci. 2007 Sep 1;81(12):1016-23
Mechanisms of the vasorelaxant effect of 1-hydroxy-2, 3, 5-trimethoxy-xanthone, isolated from a Tibetan herb, Halenia elliptica, on rat coronary artery.[Pubmed: 17822718]
1-Hydroxy-2,3,5-trimethoxyxanthone(HM-1) is a xanthone isolated from Halenia elliptica, a Tibetan medicinal herb.
METHODS AND RESULTS:
HM-1 (0.33-42.1 microM) produced a concentration-dependent relaxation in rat coronary artery rings pre-contracted with 1 microM 5-hydroxytryptamine (5-HT), with an EC(50) of 1.67+/-0.27 microM. Removal of the endothelium significantly affected the vasodilator potency of HM-1, resulting in 46% decrease in E(max) value. The endothelium-dependent effects of HM-1 was confirmed when its vasorelaxant effect was inhibited after addition of nitric oxide synthase (NOS) inhibitor N(omega)-nitro-l-arginine methyl ester (100 microM) or the soluble guanylate cyclase inhibitor 1H-[1, 2, 4] oxadiazolo [4,3-alpha] quinoxalin-1-one (ODQ, 10 microM). Atropine (100 nM), flurbiprofen (10 microM), propranolol (100 microM), pyrilamine (10 microM), cimetidine (10 microM) and SQ22536 (100 microM) had no effect on the vasorelaxant activity of HM-1 indicated the non-involvement of other receptor/enzyme systems. In endothelium-denuded coronary artery rings, the vasorelaxant effect of HM-1 was unaffected by potassium channel blockers such as tetraethylammonium (10 mM), iberiotoxin (100 nM), barium chloride (100 microM) and 4-aminopyridine (1 mM). The involvement of Ca(2+) channel in 5-HT-primed artery ring preparations incubated with Ca(2+)-free buffer was confirmed when HM-1 (9.93 microM) partially abolished the CaCl(2)-induced vasoconstriction (87% inhibition in intact-endothelium artery rings; 50% inhibition in endothelium-denuded rings). In the KCl-primed preparations incubated with Ca(2+)-free buffer, HM-1 (9.93 microM) produced a 27.3% inhibition in endothelium-denuded rings. HM-1 (3.31-33.1 microM) had minimal relaxant effects (14.4%-20.3%) on the contractile response generated by 10 microM phorbol 12,13-diacetate (PDA) in Ca(2+)-free solutions, suggesting minimal effects on intracellular Ca(2+) mechanisms.
CONCLUSIONS:
These findings suggest the vasodilator action of HM-1 involved both an endothelium-dependent mechanism involving NO and an endothelium-independent mechanism by inhibiting Ca(2+) influx through L-type voltage-operated Ca(2+) channels; a minor contribution to the effects of HM-1 may be related to inhibition of the protein kinase C-mediated release of intracellular Ca(2+) stores.
Arch Pharm Res. 2008 Jul;31(7):850-5.
Inhibitors of bone resorption from Halenia corniculata.[Pubmed: 18704326]

METHODS AND RESULTS:
Eleven xanthones (1-11), three flavonoids (12-14) and three secoiridoids (15-17) were isolated from the aerial parts of Halenia corniculata. Among those compounds, 1-hydroxy-2,3,4,5-tetramethoxyxanthone (1), 1-hydroxy-2,3,4,7-tetramethoxyxanthone (2), 1-hydroxy-2,3,4,5,7-pentamethoxyxanthone (3), 1-Hydroxy-2,3,5-trimethoxyxanthone (4), 1,8-dihydroxy-3,5-dimethoxyxanthone (7), and luteolin (12), at the concentration of 1 microg/mL, effectively inhibited the osteoclast differentiation in a co-culture system with mouse osteoblastic calvarial cells and bone marrow cells. Notably, compounds 1, 3, and 4 exhibited, in a dose-dependent manner, significant inhibition of osteoclast differentiation even at a low concentration (0.01 microg/mL). All the inhibitory compounds, except for compound 7, significantly reduced the pit formation on the dentine slice compared with the control group.
CONCLUSIONS:
For the survival of the mature osteoclasts, compounds 1-4 and 12 (1 microg/mL), significantly decreased the survival number through induction of cell apoptosis, and compound 4 exhibited a significant inhibitory effect on osteoclast survival even at the low concentration of 0.1 microg/mL.
1-Hydroxy-2,3,5-trimethoxyxanthone Description
Source: The herbs of Halenia elliptica D. Don
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.

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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.308 mL 16.5399 mL 33.0797 mL 66.1594 mL 82.6993 mL
5 mM 0.6616 mL 3.308 mL 6.6159 mL 13.2319 mL 16.5399 mL
10 mM 0.3308 mL 1.654 mL 3.308 mL 6.6159 mL 8.2699 mL
50 mM 0.0662 mL 0.3308 mL 0.6616 mL 1.3232 mL 1.654 mL
100 mM 0.0331 mL 0.1654 mL 0.3308 mL 0.6616 mL 0.827 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
Animal Research:
Chinese Traditional & Herbal Drugs, 2007, 38(9):1355-9.
Protection of 1-hydroxy-2, 3, 5-trimethoxyxanthone on acute lung injury of mice induced by lipopolysaccharide[Reference: WebLink]
To investigate the protective effects of 1-Hydroxy-2,3,5-trimethoxyxanthone(QGS) on acute lung injury of mice induced by ip lipopolysaccharide (LPS).
METHODS AND RESULTS:
Mice were pretreated with QGS for 7 d. Murine models of acute lung injury were duplicated by injection of LPS 20 mg/kg intraperitoneally. In 12 h, the lung weight index was observed and the NO level in the bronchoalveolar lavage fluid (BALF) was measured with kits. The lung was also assessd for the expression of I-κB, inducible nitric oxide synthase (iNOS), and cyclooxygenase-II (COX-2) using Western blotting analysis. Lung pathological changes were also observed by HE in each group. The lung weight index of injury lung in mice induced by LPS was decreased in 500 mg/kg QGS group (P< 0.05), the NO level in BALF of mice induced by LPS was decreased significantly in 250 and 500 mg/kg QGS groups with the inhibitory rate of 37% and 48.1%, respectively. Meanwhile the protein expression of IκB-α in lung tissue was increased remarkably but the expression of iNOS and COX-2 was suppressed in 500 mg/kg QGS group.
CONCLUSIONS:
QGS could protect mice from the acute lung injury induced by LPS, which is relative to the increasing of IκB-α protein expression and the suppressing of iNOS and COX-2 protein expression.
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