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13-Methyl-8,11,13-podocarpatriene-3,12-diol

13-Methyl-8,11,13-podocarpatriene-3,12-diol

Catalog No. BCN1360
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20mg $298 In stock
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Quality Control of 13-Methyl-8,11,13-podocarpatriene-3,12-diol

Chemical structure

13-Methyl-8,11,13-podocarpatriene-3,12-diol

13-Methyl-8,11,13-podocarpatriene-3,12-diol Dilution Calculator

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Chemical Properties of 13-Methyl-8,11,13-podocarpatriene-3,12-diol

Cas No. 769140-74-1 SDF Download SDF
Type of Compound Diterpenoids Appearance Powder
Formula C18H26O2 M.Wt 274.4
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
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.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other courier with RT , or blue ice upon request.

Preparing Stock Solutions of 13-Methyl-8,11,13-podocarpatriene-3,12-diol

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.6443 mL 18.2216 mL 36.4431 mL 72.8863 mL 91.1079 mL
5 mM 0.7289 mL 3.6443 mL 7.2886 mL 14.5773 mL 18.2216 mL
10 mM 0.3644 mL 1.8222 mL 3.6443 mL 7.2886 mL 9.1108 mL
50 mM 0.0729 mL 0.3644 mL 0.7289 mL 1.4577 mL 1.8222 mL
100 mM 0.0364 mL 0.1822 mL 0.3644 mL 0.7289 mL 0.9111 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.

Preparation of 13-Methyl-8,11,13-podocarpatriene-3,12-diol

This product is isolated and purified from the herbs of Jatropha curcas

References on 13-Methyl-8,11,13-podocarpatriene-3,12-diol

In vitro metabolism of benzo[a]pyrene-7,8-dihydrodiol and dibenzo[def,p]chrysene-11,12 diol in rodent and human hepatic microsomes.[Pubmed: 28119020]


Polycyclic aromatic hydrocarbons (PAHs) are contaminants that are ubiquitously found in the environment, produced through combustion of organic matter or petrochemicals, and many of which are procarcinogens. The prototypic PAH, benzo[a]pyrene (B[a]P) and the highly carcinogenic dibenzo[def,p]chrysene (DBC) are metabolically activated by isoforms of the P450 enzyme superfamily producing benzo[a]pyrene-7,8-dihydrodiol (B[a]P diol), dibenzo[def,p]chrysene-11,12 diol (DBC diol). Each of these diols can be further metabolized by cytochrome P450 enzymes to highly reactive diol-epoxide metabolites that readily react with DNA or by phase II conjugation facilitating excretion. To complement prior in vitro metabolism studies with parent B[a]P and DBC, both phase I metabolism and phase II glucuronidation of B[a]P diol and DBC diol were measured in hepatic microsomes from female B6129SF1/J mice, male Sprague-Dawley rats, and female humans. Metabolic parameters, including intrinsic clearance and Michaelis-Menten kinetics were calculated from substrate depletion data. Mice and rats demonstrated similar B[a]P diol phase I metabolic rates. Compared to rodents, human phase I metabolism of B[a]P diol demonstrated lower overall metabolic capacity, lower intrinsic clearance at higher substrate concentrations (>0.14μM), and higher intrinsic clearance at lower substrate concentrations (<0.07μM). Rates of DBC diol metabolism did not saturate in mice or humans and were highest overall in mice. Higher affinity constants and lower capacities were observed for DBC diol glucuronidation compared to B[a]P diol glucuronidation; however, intrinsic clearance values for these compounds were consistent within each species. Kinetic parameters reported here will be used to extend physiologically based pharmacokinetic (PBPK) models to include the disposition of B[a]P and DBC metabolites in animal models and humans to support future human health risk assessments.

Characterization of dibenzo[a,l]pyrene-trans-11,12-diol (dibenzo[def,p]chrysene) glucuronidation by UDP-glucuronosyltransferases.[Pubmed: 21780761]


Dibenzo[a,l]pyrene (DB[a,l]P) (dibenzo[def,p]chrysene) is a highly carcinogenic polycyclic aromatic hydrocarbon (PAH) that has been identified in tobacco smoke and is found in our environment due to incomplete combustion of organic matter. Its metabolites are known to form stable DNA adducts in bacteria and mammalian cells, and can lead to tumors in animal models. Glucuronidation of major metabolites of DB[a,l]P by the uridine-5'-diphosphate glucuronosyltransferase (UGT) family of enzymes is an important route of detoxification of this pro-carcinogen. The focus of the current study was to characterize the glucuronidation of the pro-carcinogenic enantiomers DB[a,l]P-(+)-trans-11S,12S-diol and DB[a,l]P-(-)-trans-11R,12R-diol. Glucuronidation assays with HEK293 cell lines overexpressing individual human UGT enzymes demonstrated that UGTs 1A1, 1A4, 1A7, 1A8, 1A9, 1A10, and 2B7 glucuronidated one or both DB[a,l]P-trans-11,12-diol enantiomers. Three glucuronide conjugates were observed in activity assays with UGTs 1A1 and 1A10, while two glucuronides were formed by UGTs 1A7, 1A8, and 1A9, and one glucuronide was made by UGT1A4 and UGT2B7. Enzyme kinetic analysis indicated that UGT1A9 was the most efficient UGT at forming both the (+)-DB[a,l]P-11-Gluc and (-)-DB[a,l]P-11-Gluc products, while UGTs 1A1 and 1A10 were the most efficient at forming the (+)-DB[a,l]P-12-Gluc product (as determined by k(cat)/K(M)). Incubations with human liver microsomes showed the formation of three diastereomeric glucuronide products: (+)-DB[a,l]P-11-Gluc, (+)-DB[a,l]P-12-Gluc, and (-)-DB[a,l]P-11-Gluc, with an average overall ratio of 31:32:37 in four liver specimens. Human bronchus and trachea tissue homogenates demonstrated glucuronidation activity against both DB[a,l]P-trans-11,12-diol enantiomers, with both tissues producing the (+)-DB[a,l]P-11-Gluc and (+)-DB[a,l]P-12-Gluc with little or no formation of (-)-DB[a,l]P-11-Gluc. These results indicate that multiple UGTs are involved in the stereospecific glucuronidation of DB[a,l]P-trans-11,12-diol in a pattern consistent with their expression in respiratory tract tissues and that glucuronidation may be an important first-line detoxification mechanism of DB[a,l]P metabolites.

Formation and differential repair of covalent DNA adducts generated by treatment of human cells with (+/-)-anti-dibenzo[a,l]pyrene-11,12-diol-13,14-epoxide.[Pubmed: 19053321]


Dibenzo[a,l]pyrene (DBP) is the most potent tumor initiating polycyclic aromatic hydrocarbon tested to date in rodent tumor models. To investigate how DBP adduct formation and removal might influence carcinogenesis, we have examined the effects of treatment of several nucleotide excision repair (NER)-proficient (NER(+)) and -deficient (NER(-)) cell lines with the carcinogenic metabolite (+/-)-anti-DBP-11,12-diol-13,14-epoxide (DBPDE). The treatment of NER(-) cells with (+/-)-anti-DBPDE for 0.5, 1, or 2 h yielded similar total adduct levels, indicating that adduct formation was essentially complete during a 2 h treatment period with no additional adducts produced after replacement of media. In all cell lines, treatment with (+/-)-anti-DBPDE generated five major and at least two minor adducts that were chromatographically identical to those formed by direct treatment of 3'-GMP and 3'-AMP with (+/-)-anti-DBPDE. When adduct levels were assessed in NER(-) cells, the number of adducts/10(9) nucleotides decreased over time, suggesting that DNA replication was ongoing, so we incorporated a normalization strategy based on DNA synthesis. This strategy indicated that DBPDE-DNA adduct levels in NER(-) cells are stable over time. After normalization for DNA synthesis in the NER(+) cells, our data indicated that three adducts showed biphasic repair kinetics. A faster rate of removal was observed during the first 6 h following DBPDE removal followed by a slower rate for up to 34 h. Importantly, two of the major guanine adducts were particularly refractory to removal in the NER(+) cells. Our results suggest that the extreme carcinogenicity of DBPDE may result from the ability of a substantial percentage of two structurally distinct DBPDE-DNA adducts to escape repair.

Facile interstrand migration of the hydrocarbon moiety of a dibenzo[a,l]pyrene 11,12-diol 13,14-epoxide adduct at N2 of deoxyguanosine in a duplex oligonucleotide.[Pubmed: 16881636]


When a synthesized deoxyribonucleotide duplex, 5'-CCATCGCTACC-3'.5'-GGTAGCGATGG-3', containing a trans 14R dibenzo[a,l]pyrene (DB[a,l]P) adduct, corresponding to trans opening of the (+)-(11S,12R)-diol (13R,14S)-epoxide by N (2) of the central G residue, was allowed to stand for 2-6 days at ambient temperature in neutral aqueous solution, three new products were observed on denaturing HPLC. One of these corresponded to loss of the DB[a,l]P moiety from the original adducted strand to give an 11-mer with an unmodified central dG. The other two products resulted from a highly unexpected migration of the hydrocarbon moiety to either dG5 or dG7 of the complementary strand, 5'-GGTAG5CG7ATGG-3'. Enzymatic hydrolysis of the two 11-mer migration products followed by CD spectroscopy of the isolated adducted nucleosides indicated that, in both cases, the hydrocarbon moiety had undergone configurational inversion at C14 to give the cis 14S DB[a,l]P dG adduct. MS/MS and partial enzymatic hydrolysis showed that the major 11-mer had the hydrocarbon at dG7. Two 11-mer oligonucleotides were synthesized with a single cis 14S DB[a,l]P dG adduct either at G7 or at G5 and were found to be chromatographically identical to the major and minor migration products, respectively. Although HPLC evidence suggested that a small extent of hydrocarbon migration from the trans 14S DB[a,l]P dG diastereomer also occurred, the very small amount of presumed migration products from this isomer precluded their detailed characterization. This interstrand migration appears unique to DB[a,l]P adducts and has not been observed for their fjord-region benzo[c]phenanthrene or bay-region benzo[a]pyrene analogues.

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