|Description:||1. Decursinol could significantly suppress the expression levels of inducible nitric oxide synthase mRNA in a concentration-dependent manner.|
2. Decursinol and Decursin inhibit the proliferation and invasion of CT-26 colon carcinoma cells, might via downregulated ERK and JNK phosphorylation.
3. Aspirin-decursinol has neuroprotective effects, may be closely related to the attenuation of ischemia-induced gliosis and maintenance of antioxidants.
|Targets:||NADPH-oxidase | P450 (e.g. CYP17) | ERK | JNK | MMP(e.g.TIMP)|
|Source:||The roots of Angelica gigas|
|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: firstname.lastname@example.org
|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.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||4.0607 mL||20.3037 mL||40.6075 mL||81.215 mL||101.5187 mL|
|5 mM||0.8121 mL||4.0607 mL||8.1215 mL||16.243 mL||20.3037 mL|
|10 mM||0.4061 mL||2.0304 mL||4.0607 mL||8.1215 mL||10.1519 mL|
|50 mM||0.0812 mL||0.4061 mL||0.8121 mL||1.6243 mL||2.0304 mL|
|100 mM||0.0406 mL||0.203 mL||0.4061 mL||0.8121 mL||1.0152 mL|
Planta Med. 2013 Nov;79(16):1536-44.
|In vitro metabolism of pyranocoumarin isomers decursin and decursinol angelate by liver microsomes from man and rodents.[Pubmed: 24026903]|
|First, we conducted liver microsomal incubations of decursin and Decursinol angelate in the presence or absence of NADPH. We found that in the absence of NADPH, decursin was efficiently hydrolyzed to Decursinol by hepatic esterase(s), but Decursinol angelate was not. In contrast, formation of Decursinol from Decursinol angelate was mediated mainly by cytochrome P450(s). Second, we measured the metabolic rate of decursin and Decursinol angelate in liver S9 fractions from mice and humans. We found that human liver S9 fractions metabolized both decursin and Decursinol angelate more slowly than those of the mouse. Third, we characterized the major metabolites of decursin and Decursinol angelate from human liver microsomes incubations using HPLC-UV and LC-MS/MS methods and assessed the in vivo metabolites in mouse plasma from a one-dose PK study. Decursin and Decursinol angelate have different metabolite profiles. Nine metabolites of decursin and nine metabolites of Decursinol angelate were identified in human liver microsome incubations besides Decursinol using a hybrid triple quadruple linear ion trap LC-MS/MS system, and many of them were later verified to be also present in plasma samples from rodent PK studies.|
Planta Med. 2013 Mar;79(3-4):275-80.
|Single oral dose pharmacokinetics of decursin, decursinol angelate, and decursinol in rats.[Pubmed: 23364885]|
|Our previous work convincingly demonstrated that both decursin and Decursinol angelate were rapidly converted to Decursinol in mice after administration by either oral gavage or i. p. injection. In the current study, we compared for the first time the plasma profiles of Decursinol, when equal moles of decursin/Decursinol angelate or Decursinol were given to rats by oral gavage, and investigated the effect of different formulas and other chemicals in Angelica gigas extract on the bioavailability of Decursinol. Our results show that gavage of Decursinol led to a faster attainment of plasma Decursinol peak (Tmax ~ 0.7 h) and much higher peak levels than an equal molar amount administered as decursin/Decursinol angelate mixture or as Angelica gigas ethanol extract, resulting in 2-3 fold higher bioavailability as estimated by the area under the curve of the respective regimens (65 012 vs. 27 033 h · ng/mL for Decursinol and decursin/Decursinol angelate treatment groups, respectively). Compared to a formula based on ethanol-PEG400-Tween80, carboxyl methyl cellulose was a less optimized vehicle. In addition, we detected peak levels of decursin and Decursinol angelate in the plasma of rats administered with decursin/Decursinol angelate or Angelica gigas extract in the nM range (Tmax ~ 0.5 h) with a newly established sensitive UHPLC-MS/MS method. Furthermore, our data support the liver, instead of intestine, as a major organ site where decursin and Decursinol angelate were hydrolyzed to Decursinol with a S9 microsomal in vitro metabolism assay.|
PLoS One. 2015 Feb 19;10(2):e0114992.
|Single oral dose pharmacokinetics of decursin and decursinol angelate in healthy adult men and women.[Pubmed: 25695490]|
|The mean area under the curve (AUC0-48h) for D, DA and Decursinol was estimated as 37, 335 and 27,579 h∙nmol/L, respectively. Gender-wise, men absorbed the parent compounds faster and took shorter time to reach Decursinol peak concentration. The human data supported an extensive conversion of D and DA to Decursinol, even though they metabolized DA slightly slower than rodents. Therefore, the data generated in rodent models concerning anti-cancer efficacy, safety, tissue distribution and pharmacodynamic biomarkers will likely be relevant for human translation.|
Phytother Res. 2011 Jul;25(7):959-64.
|Decursin and decursinol from Angelica gigas inhibit the lung metastasis of murine colon carcinoma.[Pubmed: 21170925]|
|Decursin and Decursinol inhibited the proliferation and invasion of CT-26 colon carcinoma cells. The expressions of matrix metalloproteinase (MMP)-2 and MMP-9 in cells and the activities in the culture medium were also reduced by decursin and Decursinol treatment. In CT-26 cells, the extracellular signal-regulated kinase (ERK) inhibitor inhibited cell proliferation, invasion and MMP-9 expression, and the c-Jun N-terminal kinase (JNK) inhibitor suppressed the expression of both MMPs, as well as cell proliferation and cell invasion. Decursin and Decursinol downregulated ERK and JNK phosphorylation. Moreover, oral administration of decursin and Decursinol reduced the formation of tumor nodules in the lungs and the increase in lung weight caused by CT-26 metastases. Therefore, both decursin and Decursinol may be beneficial antimetastatic agents, targeting MMPs and their upstream signaling molecules.|