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Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
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Methoxy and Ketone Substitutions of Resveratrol Enhance Its Anticancer Activity by Increasing MEK and ERK Binding

Pattharaporn Saelim1,2,3, Zin Zin Ei1,2, Satapat Racha1,2,3

  • 1Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand.

Anticancer Research
|March 27, 2026
PubMed
Abstract

Insights

SM-23, a resveratrol derivative, shows potent anticancer activity against colorectal cancer by inhibiting the MEK/ERK pathway. This novel compound demonstrates enhanced kinase binding and antiproliferative effects, offering a promising therapeutic candidate.

Area of Science:

  • Oncology
  • Molecular Biology
  • Medicinal Chemistry

Background:

  • Colorectal cancer (CRC) is a leading cause of cancer mortality.
  • Recurrence, metastasis, and therapy resistance are key challenges in CRC treatment.
  • Resveratrol (Res) has anticancer properties but suffers from poor stability and bioavailability.

Purpose of the Study:

  • To investigate the anticancer activity of SM-23, a novel resveratrol derivative.
  • To evaluate SM-23's effects on colorectal cancer cells and its mechanism of action.
  • To compare SM-23's binding affinity and efficacy against key cancer signaling pathways with resveratrol.

Main Methods:

  • MTT viability assay to determine IC50 values in HCT116 colon cancer cells.
  • Colony formation assay for cell proliferation assessment.
  • Western blotting for apoptosis-related proteins and kinase phosphorylation.
  • Molecular docking to compare binding affinities of SM-23 and Res to PI3K/AKT and MEK/ERK pathway kinases.

Main Results:

  • Molecular docking revealed enhanced binding of SM-23 to MEK1, ERK, and AKT compared to Res.
  • SM-23 significantly reduced MEK and ERK phosphorylation in HCT116 cells, outperforming Res.
  • SM-23 demonstrated potent antiproliferative activity in colorectal cancer cells.

Conclusions:

  • SM-23 enhances MEK/ERK pathway inhibition via improved kinase binding.
  • SM-23 exhibits significant antiproliferative activity in colorectal cancer cells.
  • SM-23 is identified as a promising MEK/ERK-targeted therapeutic candidate for CRC.
Keywords:
ERKMEKResveratrolSM-23colorectal cancer

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