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Last Updated: 2 years ago

Possible Interaction: Epigallocatechin Gallate and Doxorubicin Hydrochloride

Research Papers that Mention the Interaction

The duo of DOX and EGCG induced autophagic flux and accelerated the formation of autophagosomes.
Biomaterials science  •  2020  |  View Paper
On the one hand, EGCG could reduce the Doxorubicin-induced pro-survival autophagy through decreasing SOX2OT variant 7 to improve the growth inhibition of Doxorubicin.
Journal of experimental & clinical cancer research : CR  •  2018  |  View Paper
Manuscript reports a number of constituents with evident potential in prevention of DOX cardiotoxicity e.g. proanthocyanidins, epigallocatechin-3-gallate , S-allylcysteine, reseveratrol, rutoside etc.
Current clinical pharmacology  •  2014  |  View Paper
Taken together, the current study suggested that EGCG emerges as a chemotherapeutic augmenter and synergistically enhances DOX anticancer effects involving autophagy inhibition in HCC.
PloS one  •  2014  |  View Paper
EGCG in combination with low levels of Dox had a synergistic effect in blocking tumor cell growth.
Flow cytometry results showed that EGCG appeared to enhance retention of Dox by tumor cells to synergistically inhibit tumor growth and eradicate tumors.
In vivo tumor modeling studies with a highly metastatic tumor line, PC-3ML cells, revealed that EGCG (228 mg/kg or 200 μmol/L) appeared to sensitize tumors to Dox.
Similarly, relatively low levels of EGCG (57 mg/kg or 50 μmol/L) plus Dox (0.07 mg/kg or 1 μmol/L) eradicated established tumors (ie, in nonobese diabetic-severe combined immunodeficiencies) that were derived from CD44(hi) tumor-initiating cells isolated from PCa-20a cells.
The polyphenol epigallocatechin-3-gallate (EGCG) in combination with doxorubicin (Dox) exhibits a synergistic activity in blocking the growth and colony-forming ability of human prostate cell lines in vitro.
The American journal of pathology  •  2010  |  View Paper
Consistent with these results, the intracellular retention of rhodamine 123, a P-gp substrate, was increased and the level of P-gp was decreased in cells concurrently treated with DOX and ECG or EGCG.
Furthermore, the administration of DOX in combination with ECG or EGCG markedly enhanced intracellular DOX accumulation, which implies that the catechins inhibited P-glycoprotein (P-gp) efflux pump activity.
These data suggest that tea catechins at non-toxic doses can augment DOX-induced cell killing and sensitize chemoresistant HCC cells to DOX.
EGCG at higher doses had a slight inhibitory effect on cell proliferation …-7404/DOX in vitro and in vivo, whereas the administration of DOX with these compounds at lower doses significantly inhibited HCC cell proliferation in vitro … model, compared with treatment with either agent alone at the same dose.
International journal of oncology  •  2010  |  View Paper
TP and EGCG enhanced the DOX cytotoxicity on KB‐A‐1 cells by 5.2‐and 2.5‐times, respectively, but did not show a modulating effect on KB‐3–1 cells.
When … μg mL−1 (‐)‐epigallocatechin gallate (EGCG) or 40 μg mL−… TP were present simultaneously with doxorubicin (DOX), the IC50 of DOX on KB‐A‐1 cells decreased from 10.3 ± 0.9 … mL−1 to 4.2 ± 0.2 and 2.0 ± 0.1 μg mL−1, respectively.
The Journal of pharmacy and pharmacology  •  2004  |  View Paper
Moreover, EGCG enhanced the growth inhibitory effect of 5-FU and doxorubicin.
Of note, EGCG enhanced 5-FU's and doxorubicin's effect on apoptosis, but not on cell cycle.
Archives of biochemistry and biophysics  •  2020  |  View Paper
CONCLUSION Our results show that EG G, c urcumin, and tannic acid, when combined with dox orubicin, c an exert synergism, mediated by a reduced activity of P-gp.
Phytomedicine : international journal of phytotherapy and phytopharmacology  •  2018  |  View Paper
The rate of apoptosis and ADM concentration in the Eca109/ABCG2 cells following treatment with ADM and EGCG were higher than that with ADM treatment alone, although the mitochondrial membrane potential was significantly lower (P<0.01).
Pathology, research and practice  •  2017  |  View Paper
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