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1,7-Dihydroxy-3-methoxy-2-prenylxanthone

CAS# 77741-58-3

1,7-Dihydroxy-3-methoxy-2-prenylxanthone

Catalog No. BCN1354----Order now to get a substantial discount!

Product Name & Size Price Stock
1,7-Dihydroxy-3-methoxy-2-prenylxanthone: 5mg $748 In Stock
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Quality Control of 1,7-Dihydroxy-3-methoxy-2-prenylxanthone

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Chemical structure

1,7-Dihydroxy-3-methoxy-2-prenylxanthone

3D structure

Chemical Properties of 1,7-Dihydroxy-3-methoxy-2-prenylxanthone

Cas No. 77741-58-3 SDF Download SDF
PubChem ID 509269 Appearance Yellow powder
Formula C19H18O5 M.Wt 326.4
Type of Compound Xanthones Storage Desiccate at -20°C
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Chemical Name 1,7-dihydroxy-3-methoxy-2-(3-methylbut-2-enyl)xanthen-9-one
SMILES CC(=CCC1=C(C=C2C(=C1O)C(=O)C3=C(O2)C=CC(=C3)O)OC)C
Standard InChIKey JKOMBLYQDHTFJC-UHFFFAOYSA-N
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 1,7-Dihydroxy-3-methoxy-2-prenylxanthone

The fruits of Garcinia mangostana

1,7-Dihydroxy-3-methoxy-2-prenylxanthone Dilution Calculator

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1,7-Dihydroxy-3-methoxy-2-prenylxanthone Molarity Calculator

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Preparing Stock Solutions of 1,7-Dihydroxy-3-methoxy-2-prenylxanthone

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.0637 mL 15.3186 mL 30.6373 mL 61.2745 mL 76.5931 mL
5 mM 0.6127 mL 3.0637 mL 6.1275 mL 12.2549 mL 15.3186 mL
10 mM 0.3064 mL 1.5319 mL 3.0637 mL 6.1275 mL 7.6593 mL
50 mM 0.0613 mL 0.3064 mL 0.6127 mL 1.2255 mL 1.5319 mL
100 mM 0.0306 mL 0.1532 mL 0.3064 mL 0.6127 mL 0.7659 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 1,7-Dihydroxy-3-methoxy-2-prenylxanthone

No significant difference between chiari malformation type 1.5 and type I.[Pubmed:28384597]

Clin Neurol Neurosurg. 2017 Jun;157:34-39.

OBJECTIVE: Chiari malformation Type 1.5 (CM 1.5) was defined as the association of Chiari malformation Type I (CM I) and brainstem herniation. The objective was to demonstrate the difference of clinical features and surgical outcomes between CM 1.5 and CM I. PATIENTS AND METHODS: All CM 1.5 and CM I adult patients who underwent posterior fossa decompression with duraplasty at our institution between 2006 and 2010 were retrospectively reviewed. Clinical characteristics, imaging features, and long-term outcomes were compared between CM 1.5 and CM I patients. RESULTS: A total of 142 adult patients were enrolled, including 27 CM 1.5 and 115 CM I patients. The average follow-up period was 102 months. Age at diagnosis was significantly younger in CM 1.5 group than CM I group (p=0.039). And the degree of tonsillar herniation was significantly more severe in CM 1.5 group than CM I group (p<0.001). There was no significant difference in other clinical and imaging characteristics. Moreover, improvement of symptoms was observed in 21 CM 1.5 patients (77.8%) and 94 CM I patients (81.7%), and no significant difference was detected (p=0.637). There was no significant difference in the resolution of syringomyelia between CM 1.5 (72.7%) and CM I (76.5%) patients, either (p=0. 710). CONCLUSIONS: Although CM 1.5 patients presented with brainstem herniation and more severe tonsillar herniation, other clinical and imaging features and surgical outcomes were similar with CM I patients. We think CM 1.5 is just a subtype of CM I, rather than a unique type of Chiari malformations.

Neuropathy of type 1 diabetes in the Arab world: A systematic review and meta-analysis.[Pubmed:28384559]

Diabetes Res Clin Pract. 2017 May;127:172-180.

AIMS: Although type 1 diabetes (T1D) is a common disease in the Arab nations, there is no data available on the prevalence of peripheral neuropathy (PN) among T1D subjects in Arab countries. The aim of this study is to analyze the prevalence of PN in T1D subjects via published literature and to draw attention to the dearth of the published work in this serious complication of T1D. METHODS: A meta-analysis was performed on studies representing different Arab countries with a total number of 2243 T1D subjects. RESULTS: The pooled prevalence of PN among T1D subjects in the Arab region was estimated as 18% with 95% confidence intervals (CI): 0.09-0.34. The PN prevalence was significantly higher in the >16-yr age group, with 59.1% (95% CI: 0.45-0.72) compared to 9.5% (95% CI: 0.05-0.19) in the <16-yr age group. Furthermore, the PN prevalence was significantly higher in the group with more than 10-yr T1D, 35% (95% CI: 0.15-0.62) than in the group with less than 10-yr T1D, 9.4% (95% CI: 0.04-0.21). CONCLUSION: In Arab countries, PN is common in adults and children with T1D, but prevalence varies widely. Older age Arab people (>16years) with T1D are affected more with PN than younger age Arab people (<16years). PN is more frequently present in Arab subjects with a longer duration of T1D diabetes than in those with shorter duration.

Poly-(ADP-Ribose) Polymerase-1 Promotes Prothrombin Gene Transcription and Produces Des-Gamma-Carboxy Prothrombin in Hepatocellular Carcinoma.[Pubmed:28384634]

Digestion. 2017;95(3):242-251.

BACKGROUND AND AIM: Although des-gamma-carboxy prothrombin (DCP) is a well-known tumor marker for hepatocellular carcinoma (HCC), the mechanism of DCP production is unclear. This study aimed to investigate the mechanism how DCP is produced in HCC cells. METHODS: Levels of mRNA and DCP were analyzed by real-time polymerase chain reaction and electro-chemiluminescence immunoassay respectively. Secreted alkaline phosphatase (SEAP) expression vectors including deletion mutants of the prothrombin gene promoter were constructed for reporter gene assay. The transcription factors bound to DNA fragments were analyzed by mass spectrometry. An electrophoretic mobility shift assay (EMSA) was performed using a biotin end-labeled DNA. RESULTS: The prothrombin mRNA levels in all 5 DCP producing cell lines were appreciably high. However, those in 2 DCP non-producing cell lines were below detectable levels. A SEAP vector with -2985 to +27 showed a very high transcription activity in DCP-producing Huh-1 cells. However, transcription abruptly decreased when the vector with -2955 to +27 was transfected, and then remained at the similar levels with larger deletion mutants, indicating the existence of a cis-element at -2985 to -2955 (31-bp). Mass spectrometry analysis identified the protein that bound to the 31-bp DNA as poly-(ADP-ribose) polymerase-1 (PARP-1). Knockdown of the PARP-1 gene by small interfering RNA in Huh-1 cells induced marked inhibition of prothrombin gene transcription. The EMSA clearly showed that PARP-1 specifically binds to the 31-bp DNA fragment in the prothrombin gene promoter. CONCLUSIONS: Our data suggest that PARP-1 activates prothrombin gene transcription and that the excessive prothrombin gene transcription induces DCP production in DCP-producing HCC cells.

Very low-dose fluvastatin-valsartan combination decreases parameters of inflammation and oxidative stress in patients with type 1 diabetes mellitus.[Pubmed:28384560]

Diabetes Res Clin Pract. 2017 May;127:181-186.

AIMS: Previously we revealed the effectiveness of a new therapeutic approach with a short-term, very-low dose fluvastatin-valsartan combination on the improvement of arterial function in type 1 diabetes mellitus patients (T1DM). In this study we explored whether this approach influences inflammation and oxidative stress and explored any association of these effects with arterial function improvement. METHODS: This was a supplementary analysis of the two previous double blind randomized studies (included 44 T1DM patients). Treatment group received very-low dose fluvastatin-valsartan, the control group received placebo. Blood samples were collected and inflammation parameters: high-sensitivity CRP (hsCRP), interleukin 6 (IL-6), vascular cell adhesion molecule-1 (VCAM-1) and oxidative stress parameter total antioxidant status (TAS) were measured. RESULTS: Treatment decreased hsCRP values (by 56.5%, P<0.05) and IL-6 values (by 33.6%, P<0.05) and increased TAS values (by 21.1%; P<0.05) after 30days of treatment. High sensitivity CRP and TAS remained decreased 3months after treatment discontinuation. Importantly, the anti-inflammatory and anti-oxidative action significantly correlated with arterial function improvement. CONCLUSIONS: The approach consisting of short-term (30days) treatment with a very low-dose fluvastatin-valsartan combination acts anti-inflammatory and anti-oxidative in T1DM patients. These observations along with the improvement of arterial function support the assumption that this approach could have an important clinical benefit in T1DM patients.

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