4-Ethylphenyl sulfate sodium 

4-Ethylphenyl sulfate sodium is an orally active and brain-penetrant gut microbial metabolite. 4-Ethylphenyl sulfate sodium downregulates Bcl2 expression, upregulates Bax expression, and induces cancer cell apoptosis via the endogenous apoptotic pathway. 4-Ethylphenyl sulfate sodium induces G2/M cell cycle arrest and reactive oxygen species (ROS) production. 4-Ethylphenyl sulfate sodium impairs oligodendrocyte maturation, reduces oligodendrocyte-neuron interactions, decreases axonal myelination levels, and shifts the oligodendrocyte population toward immature precursor cells. 4-Ethylphenyl sulfate sodium alters brain region-specific neural activity and functional connectivity in mice, and correlates with anxiety-like behaviors in mice^[1][2].

4-Ethylphenyl sulfate (0.25-10 mM; 24-72 h) sodium reduces the viability of HCT-116 human colorectal adenocarcinoma cells in a time- and dose-dependent manner, with 10 mM reducing viability to 7% after 72 h^[1].
4-Ethylphenyl sulfate (0.25-10 mM; 24-72 h) sodium reduces intracellular ATP levels and impairs metabolic activity in HCT-116 human colorectal adenocarcinoma cells in a time- and dose-dependent manner^[1].
4-Ethylphenyl sulfate (2.5-10 mM; 24-72 h) sodium induces dose- and time-dependent morphological changes characteristic of cell death in HCT-116 human colorectal adenocarcinoma cells^[1].
4-Ethylphenyl sulfate (0.25-10 mM; 10 days) sodium suppresses the colony-forming ability of HCT-116 human colorectal adenocarcinoma cells in a dose-dependent manner^[1].
4-Ethylphenyl sulfate (1.25-10 mM; 48 h) sodium induces apoptosis and induces G2/M phase cell cycle arrest in HCT-116 human colorectal adenocarcinoma cells in a dose-dependent manner^[1].
4-Ethylphenyl sulfate (1.25-10 mM; 48 h) sodium increases superoxide (ROS) production in HCT-116 human colorectal adenocarcinoma cells in a dose-dependent manner^[1].
4-Ethylphenyl sulfate (5 mM; 48 h) sodium increases the Bax/Bcl-2 ratio in HCT-116 human colorectal adenocarcinoma cells in a dose-dependent manner, activating the intrinsic apoptotic pathway^[1].
4-Ethylphenyl sulfate (0.25-10 mM; 24-72 h) sodium exhibits minimal to no toxicity toward CCD 841 CoN normal colon epithelial cells, with only a minor viability reduction at 10 mM after 72 h, confirming selective anticancer activity^[1].
4-Ethylphenyl sulfate sodium binds to HDAC1, HDAC2, HDAC6, and HDAC8 histone deacetylase isoforms, with the highest binding affinity to HDAC1 (-6.3 kcal/mol), suggesting potential epigenetic modulation^[1].
4-Ethylphenyl sulfate (10 μM; 10 days) sodium impairs oligodendrocyte maturation, reduces axon myelination, and alters expression of oligodendrocyte lineage markers in ex vivo organotypic mouse brain slices^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

4-Ethylphenyl sulfate (250 mM; p.o.; free intake in drinking water) sodium impairs oligodendrocyte maturation and reduces myelination in the mouse brain, leading to altered functional connectivity in anxiety-associated circuits and the development of anxiety-like behaviors^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

224.21

C₈H₉NaO₄S

O=S(OC1=CC=C(CC)C=C1)(O[Na])=O

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Archana, et al. Electrochemical sensor based on polydopamine-molecularly imprinted polymer for detection of 4-ethylphenyl sulfate “a novel gut metabolite”: Fabrication, characterization, and performance evaluation in human urine. Microchemical Journal Volume 193, October 2023, 108964.

  [2]. Jaiswal J, et al. Gut Microbial Metabolite 4-Ethylphenylsulfate Is Selectively Deleterious and Anticancer to Colon Cancer Cells. J Med Chem. 2025;68(10):10425-10438.  [Content Brief]

  [3]. Needham BD, et al. A gut-derived metabolite alters brain activity and anxiety behaviour in mice. Nature. 2022;602(7898):647-653.  [Content Brief]