85734-98-1
Chemical Structure
4-Ethylphenyl sulfate
- CAS No.: 85734-98-1
- Formula:C8H10O4S
- Molecular Weight:202.23
IUPAC Name: 4-ethylphenyl hydrogen sulfate
InChIKey: DWZGLEPNCRFCEP-UHFFFAOYSA-N
SMILES: O=S(O)(OC1=CC=C(CC)C=C1)=O
Biological Activity: 4-Ethylphenyl sulfate is an orally active and brain-penetrant gut microbial metabolite. 4-Ethylphenyl sulfate downregulates Bcl2 expression, upregulates Bax expression, and induces cancer cell apoptosis via the endogenous apoptotic pathway. 4-Ethylphenyl sulfate induces G2/M cell cycle arrest and reactive oxygen species (ROS) production. 4-Ethylphenyl sulfate impairs oligodendrocyte maturation, reduces oligodendrocyte-neuron interactions, decreases axonal myelination levels, and shifts the oligodendrocyte population toward immature precursor cells. 4-Ethylphenyl sulfate alters brain region-specific neural activity and functional connectivity in mice, and correlates with anxiety-like behaviors in mice[1][2].
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4-Ethylphenyl sulfate | 4-Ethylphenyl sulfate is an orally active and brain-penetrant gut microbial metabolite. 4-Ethylphenyl sulfate downregulates Bcl2 expression, upregulates Bax expression, and induces cancer cell apoptosis via the endogenous apoptotic pathway. 4-Ethylphenyl sulfate induces G2/M cell cycle arrest and reactive oxygen species (ROS) production. 4-Ethylphenyl sulfate impairs oligodendrocyte maturation, reduces oligodendrocyte-neuron interactions, decreases axonal myelination levels, and shifts the oligodendrocyte population toward immature precursor cells. 4-Ethylphenyl sulfate alters brain region-specific neural activity and functional connectivity in mice, and correlates with anxiety-like behaviors in mice. | |||||||||||||||||||||
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- [1]. 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]
- [2]. Needham BD, et al. A gut-derived metabolite alters brain activity and anxiety behaviour in mice. Nature. 2022;602(7898):647-653. [Content Brief]
Keywords