Hernandezine - CAS 6681-13-6
Not Intended for Therapeutic Use. For research use only.
Category:
ADCs
Product Name:
Hernandezine
Catalog Number:
6681-13-6
CAS Number:
6681-13-6
Description:
Anti-tumor effect of hernandezine and other components extracted from Thalictrum glandulosissimum.
Molecular Weight:
652.78
Molecular Formula:
C39H44N2O7
COA:
Inquire
MSDS:
Inquire
Tag:
ADCs Cytotoxin
Chemical Structure
CAS 6681-13-6 Hernandezine

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Reference Reading


1.Inhibitory effects of tetrandrine and hernandezine on Ca2+ mobilization in rat glioma C6 cells.
Imoto K1, Takemura H, Kwan CY, Sakano S, Kaneko M, Ohshika H. Res Commun Mol Pathol Pharmacol. 1997 Feb;95(2):129-46.
The effects of tetrandrine (TET), a Ca2+ antagonist of Chinese herbal origin, and hernandezine (HER), a structural analogue of TET, on Ca2+ mobilization were studied in rat glioma C6 cells. TET and HER alone did not affect the resting cytoplasmic Ca2+ concentration ([Ca2+]i). TET and HER inhibited the peak and sustained elevation of [Ca2+]i induced by bombesin and thapsigargin (TG), a microsomal Ca2+ ATPase inhibitor, in a dose-dependent manner. The doses of TET or HER needed to abolish the sustained and peak increase in [Ca2+]i induced by bombesin and TG were 30 microM and 300 microM, respectively. TET and HER did not increase inositol 1,4,5-trisphosphate (IP3) accumulation by themselves but inhibited IP3 accumulation elevated by bombesin. In permeabilized C6 cells, the addition of IP3 and TG released Ca2+ from intracellular stores. Pretreatment with TET or HER abolished Ca2+ release from intracellular stores induced by bombesin and TG.
2.Hernandezine, a novel AMPK activator induces autophagic cell death in drug-resistant cancers.
Law BY1, Mok SW1, Chan WK1, Xu SW1, Wu AG1, Yao XJ1, Wang JR1, Liu L1, Wong VK1. Oncotarget. 2016 Feb 16;7(7):8090-104. doi: 10.18632/oncotarget.6980.
Drug resistance hinder most cancer chemotherapies and leads to disease recurrence and poor survival of patients. Resistance of cancer cells towards apoptosis is the major cause of these symptomatic behaviours. Here, we showed that isoquinoline alkaloids, including liensinine, isoliensinine, dauricine, cepharanthine and hernandezine, putatively induce cytotoxicity against a repertoire of cancer cell lines (HeLa, A549, MCF-7, PC3, HepG2, Hep3B and H1299). Proven by the use of apoptosis-resistant cellular models and autophagic assays, such isoquinoline alkaloid-induced cytotoxic effect involves energy- and autophagy-related gene 7 (Atg7)-dependent autophagy that resulted from direct activation of AMP activated protein kinase (AMPK). Hernandezine possess the highest efficacy in provoking such cell death when compared with other examined compounds. We confirmed that isoquinoline alkaloid is structurally varied from the existing direct AMPK activators.
3.Plant alkaloids, tetrandrine and hernandezine, inhibit calcium-depletion stimulated calcium entry in human and bovine endothelial cells.
Low AM1, Berdik M, Sormaz L, Gataiance S, Buchanan MR, Kwan CY, Daniel EE. Life Sci. 1996;58(25):2327-35.
Depletion of internal Ca2+ stores causes capacitative Ca2+ entry which occurs through non-selective cation channels sensitive to blockade by SK&F 96365. Recently, alkaloids of Chinese herbal medicinal origin, tetrandrine and hernandezine, have been shown to possess actions including inhibition of Ca2+ channels in non-excitable cell types. In this study, we compared the actions of these novel inhibitors to those of SK&F 96365 in fura-2-loaded endothelial cells from human umbilical vein and bovine pulmonary artery. Depletion of Ca2+ from the internal stores was accomplished in Ca(2+)-free medium using an endoplasmic reticulum Ca2+ pump inhibitor, cyclopiazonic acid (CPA) or receptor agonists, histamine and bradykinin. Stimulation with histamine or bradykinin caused a marked and rapid transient increase in Ca2+ signal whereas CPA caused a smaller amplitude increase of longer duration. Restoring Ca2+ to the medium caused marked and sustained increases in the fluorescence indicating movement of Ca2+ into the cytosol presumably stimulated by the emptied Ca2+ stores.