|Description:||1. Thevetin B is a cardiac glycoside. |
2. Thevetin A and thevetin B are Na+-, K+-dependent adenosinetriphosphatase (Na+,K+-ATPase) (EC 184.108.40.206) inhibitors.
|Targets:||Sodium Channel | ATPase | Potassium Channel|
|Source:||The herbs of Thevetia peruviana|
|Solvent:||DMSO, Pyridine, Methanol, Ethanol, 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: email@example.com
|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||1.1641 mL||5.8207 mL||11.6414 mL||23.2829 mL||29.1036 mL|
|5 mM||0.2328 mL||1.1641 mL||2.3283 mL||4.6566 mL||5.8207 mL|
|10 mM||0.1164 mL||0.5821 mL||1.1641 mL||2.3283 mL||2.9104 mL|
|50 mM||0.0233 mL||0.1164 mL||0.2328 mL||0.4657 mL||0.5821 mL|
|100 mM||0.0116 mL||0.0582 mL||0.1164 mL||0.2328 mL||0.291 mL|
J Pharm Biomed Anal. 1992 Jun;10(6):413-9.
|Determination of thevetin B in serum by fluorescence polarization immunoassay.[Pubmed: 1420463]|
|Thevetin B, a cardiac glycoside of Thevetia neriifolia Juss. seeds, was determined in serum by fluorescence polarization immunoassay. Anti-digitoxin antibody was used, Thevetin B genin being structurally identical to digitoxigenin. Cross-reactivity of 94% was found by this method, for concentrations from 5 to 80 ng ml-1.|
Forensic Sci Int. 2012 Feb 10;215(1-3):146-51.
|Method validation of a survey of thevetia cardiac glycosides in serum samples.[Pubmed: 21376490]|
|A sensitive and specific liquid chromatography tandem mass spectrometry (HPLC-ESI(+)-MS/MS) procedure was developed and validated for the identification and quantification of Thevetin B and further cardiac glycosides in human serum. The seeds of Yellow Oleander (Thevetia peruviana) contain cardiac glycosides that can cause serious intoxication. A mixture of six thevetia glycosides was extracted from these seeds and characterized. Thevetin B, isolated and efficiently purified from that mixture, is the main component and can be used as evidence. Solid phase extraction (SPE) proved to be an effective sample preparation method. Digoxin-d3 was used as the internal standard. Although ion suppression occurs, the limit of detection (LOD) is 0.27 ng/ml serum for Thevetin B. Recovery is higher than 94%, and accuracy and precision were proficient. Method refinement was carried out with regard to developing a general screening method for cardiac glycosides. The assay is linear over the range of 0.5-8 ng/ml serum. Finally, the method was applied to a case of thevetia seed ingestion.|
Can J Physiol Pharmacol. 1977 Apr;55(2):170-9.
|Antagonism of biogenic amine-induced depression of cerebral cortical neurones by Na+, K+-ATPase in inhibitors.[Pubmed: 141320]|
|The effects of iontophoretically applied Na+-, K+-dependent adenosinetriphosphatase (Na+,K+-ATPase) (EC 220.127.116.11) inhibitors (ouabain, digitoxin, digitoxigenin, strophanthin K, strophanthidin, thevetin A and Thevetin B, ethacrynate, and harmaline) on the depression of rat cerebral cortical neurones by noradrenaline, 5-hydroxytryptamine, and histamine have been studied. The inhibitors antagonized depressions of spontaneously active neurones evoked by these amines, but not those evoked by gamma-aminobutyric acid, adenosine, adenosine 5'-monophosphate, or calcium. The antagonistic potencies of the various inhibitors appeared to be proportional to their known potencies as inhibitors of Na+, K+-ATPase. The data therefore support the hypothesis that amines depress central neurones by activating an electrogenic sodium pump.|