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Last Updated: 2 years ago

Possible Interaction: Epigallocatechin Gallate and Erlotinib

Research Papers that Mention the Interaction

Finally, the combination of EGCG and erlotinib significantly slowed the growth rate of H460 xenografts.
Results: EGCG inhibited cell proliferation in erlotinib-sensitive and -resistant cell lines, including those with c-Met overexpression, and acquired resistance to erlotinib.
The combination of erlotinib and EGCG resulted in greater inhibition of cell proliferation and colony formation than either agent alone.
Clinical Cancer Research  •  2009  |  View Paper
In vitro studies with 5 head and neck cancer cell … revealed that synergistic cell growth inhibition by the combination of EGCG … erlotinib was associated with significantly greater inhibition of pEGFR and pAKT, increased activation of caspases …, 3 and PARP compared to the inhibition induced by EGCG or erlotinib alone.
Our results suggest a synergistic antitumor effect of a combined treatment with EGCG and erlotinib , and provide a promising regimen for future chemoprevention and treatment of SCCHN.
We investigated whether combining EGCG with the EGFR‐tyrosine kinase inhibitor (EGFR‐TKI) erlotinib may augment erlotinib‐induced cell growth inhibition of squamous cell carcinoma of the head and neck (SCCHN) in a mouse xenograft model.
International journal of cancer  •  2008  |  View Paper
Taken together, our results strongly suggest that the combination of erlotinib and EGCG induces apoptosis of SCCHN cells by regulating Bim and Bcl-2 at the posttranscriptional level.
Apoptosis  •  2015  |  View Paper
Characterizing the underlying mechanisms of EGCG and erlotinib synergism will provide an important rationale for chemoprevention or treatment trials using this combination.
However, simultaneous treatment with EGCG and erlotinib strongly inhibited erlotinib-induced expression of p21 and p27 without affecting the expression of Bim.
In addition, combined treatment with erlotinib and EGCG inhibited the protein level of p65 subunit of nuclear factor-κB and its transcriptional target Bcl-2, but failed to do so in cells with ablated p53.
Cancer Prevention Research  •  2009  |  View Paper