Digitoxin - CAS 71-63-6
Catalog number: 71-63-6
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
Molecular Weight:
Na+/K+ ATPase
Digitoxin, a cardiac glycoside, is an effective Na+/K+-ATPase inhibitor, the EC50 value of Digitoxin is 0.78 μM that usually comes from the roots of Digitalis purpurea L, targets cancer cells in a time and dose-dependant manner by activating pro-apoptotic
White Solid
(3β,5β)-3-[(O-2,6-Dideoxy-β-D-ribo-hexopyranosyl-(1-4)-O-2,6-dideoxy-β-D-ribo-hexopyranosyl-(1-4)-2,6-dideoxy-β-D-ribo-hexopyranosyl)oxyl]-14-hydroxycard-20(22)-enolide; Digitalin; Digitoxoside;
Soluble in DMSO
Store at -20 °C
Quality Standard:
Enterprise Standard
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Melting Point:
256-257 °C (lit.)
Canonical SMILES:
1.Digitoxin enhances the growth inhibitory effects of thapsigargin and simvastatin on ER negative human breast cancer cells.
Einbond LS1, Wu HA2, Sandu C3, Ford M2, Mighty J4, Antonetti V4, Redenti S4, Ma H2. Fitoterapia. 2016 Mar;109:146-54. doi: 10.1016/j.fitote.2015.12.005. Epub 2015 Dec 12.
BACKGROUND: The cardiac glycoside digitoxin preferentially inhibits the growth of breast cancer cells and targets the Erk pathway. Digitoxin alters the expression of genes that mediate calcium metabolism and IAP genes.
2.Digitoxin improves cardiovascular autonomic control in rats with heart failure.
Fardin NM1, Antonio EL2, Montemor JA2, da Veiga GL1, Tucci PJ2, Campos RR1. Can J Physiol Pharmacol. 2016 Jan 17:1-8. [Epub ahead of print]
The effects of chronic treatment with digitoxin on arterial baroreceptor sensitivity for heart rate (HR) and renal sympathetic nerve activity (rSNA) control, cardiopulmonary reflex, and autonomic HR control in an animal model of heart failure (HF) were evaluated. Wistar rats were treated with digitoxin, which was administered in their daily feed (1 mg/kg per day) for 60 days. The following 3 experimental groups were evaluated: sham, HF, and HF treated with digitoxin (HF + DIG). We observed an increase in rSNA in the HF group (190 ± 29 pps, n = 5) compared with the sham group (98 ± 14 pps, n = 5). Digitoxin treatment prevented an increase in rSNA (98 ± 14 pps, n = 7). Therefore, arterial baroreceptor sensitivity was decreased in the HF group (-1.24 ± 0.07 bpm/mm Hg, n = 8) compared with the sham group (-2.27 ± 0.23 bpm/mm Hg, n = 6). Digitoxin did not alter arterial baroreceptor sensitivity in the HF + DIG group. Finally, the HF group showed an increased low frequency band (LFb: 23 ± 5 ms2, n = 8) and a decreased high frequency band (HFb: 77 ± 5 ms2, n = 8) compared with the sham group (LFb: 14 ± 3 ms2; HFb: 86 ± 3 ms2, n = 9); the HF+DIG group exhibited normalized parameters (LFb: 15 ± 3 ms2; HFb: 85 ± 3 ms2, n = 9).
3.Compound Library Screening Identified Cardiac Glycoside Digitoxin as an Effective Growth Inhibitor of Gefitinib-Resistant Non-Small Cell Lung Cancer via Downregulation of α-Tubulin and Inhibition of Microtubule Formation.
Zhang YZ1, Chen X2, Fan XX3, He JX4, Huang J5, Xiao DK6, Zhou YL7, Zheng SY8, Xu JH9, Yao XJ10, Liu L11, Leung EL12. Molecules. 2016 Mar 18;21(3). pii: E374. doi: 10.3390/molecules21030374.
Non-small-cell lung cancer (NSCLC) dominates over 85% of all lung cancer cases. Epidermal growth factor receptor (EGFR) activating mutation is a common situation in NSCLC. In the clinic, molecular-targeting with Gefitinib as a tyrosine kinase inhibitor (TKI) for EGFR downstream signaling is initially effective. However, drug resistance frequently happens due to additional mutation on EGFR, such as substitution from threonine to methionine at amino acid position 790 (T790M). In this study, we screened a traditional Chinese medicine (TCM) compound library consisting of 800 single compounds in TKI-resistance NSCLC H1975 cells, which contains substitutions from leucine to arginine at amino acid 858 (L858R) and T790M mutation on EGFR. Attractively, among these compounds there are 24 compounds CC50 of which was less than 2.5 μM were identified. We have further investigated the mechanism of the most effective one, Digitoxin. It showed a significantly cytotoxic effect in H1975 cells by causing G2 phase arrest, also remarkably activated 5' adenosine monophosphate-activated protein kinase (AMPK).
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