Decursinol
Decursinol may be a beneficial antimetastatic agent, targeting MMPs and its upstream signaling molecules; it inhibits the proliferation and invasion of CT-26 colon carcinoma cells, might via downregulated ERK and JNK phosphorylation. Aspirin-decursinol has neuroprotective effects, may be closely related to the attenuation of ischemia-induced gliosis and maintenance of antioxidants.
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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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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.
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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]
The aim of this study is to investigate and compare the metabolic rate and profiles of pyranocoumarin isomers decursin and Decursinol angelate using liver microsomes from humans and rodents, and to characterize the major metabolites of decursin and Decursinol angelate in human liver microsomal incubations using LC-MS/MS.
METHODS AND RESULTS:
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.
CONCLUSIONS:
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.
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 ethanol extract of Angelica gigas Nakai (AGN) root has promising anti-cancer and other bioactivities in rodent models. It is currently believed that the pyranocoumarin isomers decursin (D) and Decursinol angelate (DA) contribute to these activities. We and others have documented that D and DA were rapidly converted to Decursinol (DOH) in rodents. However, our in vitro metabolism studies suggested that D and DA might be metabolized differently in humans.
METHODS AND RESULTS:
To test this hypothesis and address a key question for human translatability of animal model studies of D and DA or AGN extract, we conducted a single oral dose human pharmacokinetic study of D and DA delivered through an AGN-based dietary supplement Cogni.Q (purchased from Quality of Life Labs, Purchase, NY) in twenty healthy subjects, i.e., 10 men and 10 women, each consuming 119 mg D and 77 mg DA from 4 vegicaps. Analyses of plasma samples using UHPLC-MS/MS showed mean time to peak concentration (Tmax) of 2.1, 2.4 and 3.3 h and mean peak concentration (Cmax) of 5.3, 48.1 and 2,480 nmol/L for D, DA and DOH, respectively. The terminal elimination half-life (t1/2) for D and DA was similar (17.4 and 19.3 h) and each was much longer than that of DOH (7.4 h). The mean area under the curve (AUC0-48h) for D, DA and DOH 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 DOH peak concentration. The human data supported an extensive conversion of D and DA to DOH, even though they metabolized DA slightly slower than rodents.
CONCLUSIONS:
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]
The principal objective of the present study was to evaluate the antimetastatic activity of decursin and Decursinol isolated from Angelica gigas.
METHODS AND RESULTS:
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. The phosphatidylinositol-3 kinase (PI3K) inhibitor reduced only the expression of MMP-2. In addition, the invasion of CT-26 cells was inhibited by the treatment with anti-MMP-9 antibody, rather than anti-MMP-2 antibody. These results indicate that MMP-9 expression via ERK and JNK plays a critical role for the invasion of CT26 cells. 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.
CONCLUSIONS:
Therefore, both decursin and Decursinol may be beneficial antimetastatic agents, targeting MMPs and their upstream signaling molecules.
