(+)-β-HYDRASTINE - CAS 29617-43-4
Category:
Main Product
Product Name:
(+)-β-HYDRASTINE
Catalog Number:
29617-43-4
Synonyms:
ISOCORYNE; D-BETA-HYDRASTINE; (+)-BETA-HYDRASTINE; (1S,9R)-BETA-HYDRASTINE; (1S,9R)-B-hydrastine free base; (1s,9r)-(+)-β-hydrastine
CAS Number:
29617-43-4
Molecular Weight:
383.39
Molecular Formula:
C21H21NO6
COA:
Inquire
MSDS:
Inquire
Canonical SMILES:
CN1CCC2=CC3=C(C=C2C1C4C5=C(C(=C(C=C5)OC)OC)C(=O)O4)OCO3
InChI:
InChI=1S/C21H21NO6/c1-22-7-6-11-8-15-16(27-10-26-15)9-13(11)18(22)19-12-4-5-14(24-2)20(25-3)17(12)21(23)28-19/h4-5,8-9,18-19H,6-7,10H2,1-3H3/t18-,19+/m0/s1
InChIKey:
JZUTXVTYJDCMDU-RBUKOAKNSA-N
Chemical Structure
CAS 29617-43-4 (+)-β-HYDRASTINE

Reference Reading


1.Chiral differentiation of the noscapine and hydrastine stereoisomers by electrospray ionization tandem mass spectrometry.
Nagy T1, Kuki Á, Antal B, Nagy L, Purgel M, Sipos A, Nagy M, Zsuga M, Kéki S. J Mass Spectrom. 2015 Jan;50(1):240-6. doi: 10.1002/jms.3527.
Energy-dependent collision-induced dissociation (CID) of the dimers [2 M + Cat](+) of the noscapine and hydrastine stereoisomers was studied where Cat stands for Li(+), Na(+), K(+) and Cs(+) ions. These dimers were generated 'in situ' from the electrosprayed solution. The survival yield (SY) method was used for distinguishing the noscapine and hydrastine dimers. Significant differences were found between the characteristic collision energies (CE50, i.e. the collision energy necessary to obtain 50% fragmentation) of the homo- (R,R; S,S) and heterochiral (R,S; S,R) stereoisomers. To distinguish the enantiomer pairs L-, D-tyrosine ([M + Tyr + Cat](+)) and L-, D-lysine ([M + Lys + Cat](+)) were used as chiral selectors. Furthermore, these heterodimers [M + amino acid + Cat](+) were also applied to determine the stereoisomeric composition. It was found that the characteristic collision energy (CE50) of the noscapine and hydrastine homodimers ([2 M + Cat](+)) was inversely proportional to the ionic radius of the cations.
2.Hydrastine pharmacokinetics and metabolism after a single oral dose of goldenseal (Hydrastis canadensis) to humans.
Gupta PK1, Barone G1, Gurley BJ1, Fifer EK1, Hendrickson HP2. Drug Metab Dispos. 2015 Apr;43(4):534-52. doi: 10.1124/dmd.114.059410. Epub 2015 Jan 21.
The disposition and metabolism of hydrastine was investigated in 11 healthy subjects following an oral dose of 2.7 g of goldenseal supplement containing 78 mg of hydrastine. Serial blood samples were collected for 48 hours, and urine was collected for 24 hours. Hydrastine serum and urine concentrations were determined by Liquid Chromatography-tandem mass spectrometry (LC-MS/MS). Pharmacokinetic parameters for hydrastine were calculated using noncompartmental methods. The maximal serum concentration (Cmax) was 225 ± 100 ng/ml, Tmax was 1.5 ± 0.3 hours, and area under the curve was 6.4 ± 4.1 ng ⋅ h/ml ⋅ kg. The elimination half-life was 4.8 ± 1.4 hours. Metabolites of hydrastine were identified in serum and urine by using liquid chromatography coupled to high-resolution mass spectrometry. Hydrastine metabolites were identified by various mass spectrometric techniques, such as accurate mass measurement, neutral loss scanning, and product ion scanning using Quadrupole-Time of Flight (Q-ToF) and triple quadrupole instruments.
3.(-)-β-hydrastine suppresses the proliferation and invasion of human lung adenocarcinoma cells by inhibiting PAK4 kinase activity.
Guo B1, Li X1, Song S2, Chen M1, Cheng M2, Zhao D2, Li F1. Oncol Rep. 2016 Apr;35(4):2246-56. doi: 10.3892/or.2016.4594. Epub 2016 Jan 25.
(-)-β-hydrastine is one of the main active components of the medicinal plant, Hydrastis canadensis, which is used in many dietary supplements intended to enhance the immune system. However, whether (-)-β-hydrastine affects the tumor signaling pathway remains unexplored. In the present study, we found that (-)-β-hydrastine inhibited the kinase activity of p21-activated kinase 4 (PAK4), which is involved in the regulation of cytoskeletal reorganization, cell proliferation, gene transcription, oncogenic transformation and cell invasion. In the present study, (-)-β-hydrastine suppressed lung adenocarcinoma cell proliferation by inhibiting expression of cyclin D1/D3 and CDK2/4/6, leading to cell cycle arrest at the G1 phase, in a PAK4 kinase-dependent manner. Moreover, inhibition of PAK4 kinase activity by (-)-β-hydrastine also promoted the early apoptosis of lung adenocarcinoma cells through the mitochondrial apoptosis pathway. In addition, (-)-β-hydrastine significantly suppressed the migration and invasion of human lung adenocarcinoma cells in conjunction with concomitant blockage of the PAK4/LIMK1/cofilin, PAK4/SCG10 and PAK4/MMP2 pathways.