product name Rifaximin
Description: Rifaximin is a RNA synthesis inhibitor by binding the β subunit of the bacterial DNA-dependent RNA polymerase, it is used to treat travelers diarrhea caused by certain bacteria. Rifaximin, a gut-specific ligand for the human nuclear receptor pregnane-X receptor (PXR), contributes to the maintenance of the intestinal immune homeostasis. Rifaximin abrogates the binding of NF-κB caused by LPS.
References: Eur J Pharmacol. 2011 Oct 1;668(1-2):317-24; J Pharmacol Exp Ther. 2007 Jul;322(1):391-8.
785.88
Formula
C43H51N3O11
CAS No.
80621-81-4
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 47 mg/mL (59.8 mM)
Water: <1 mg/mL
Ethanol: 3 mg/mL (3.8 mM)
Solubility (In vivo)
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19413417
| In Vitro |
In vitro activity: Rifaximin (50 μM) reduces changes in the production of proinflammatory factors caused by LPS stimulation in IEC, such as TNF-α, IL-8, Rantes and PGE2 in normal intestinal epithelial cells. Rifaximin inhibits the LPS-induced cytokine and chemokine expression by suppressing NF-κB DNA-binding activity. Rifaximin (100 μM) effectively decreases the expression of TNFα, IL-8, MIP-3α and Rantes induced by LPS stimulation (100 μg/mL). Rifaximin binds the β subunit of the bacterial DNA-dependent RNA polymerase, inhibiting the initiation of chain formation in RNA synthesis. Rifaximin has a lower MIC against gram-positive bacteria, with an MIC90 at dosages ranging from 0.01 µg/mL to 0.5 µg/mL. Rifaximin has broad-spectrum activity against aerobic and anaerobic gram-positive and gram-negative microorganisms. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Rifaximin is highly concentrated in the intestinal tract compared with rifampicin. Rifaximin treatment results in significant induction of PXR target genes in the intestine of hPXR mice, but not in wild-type and Pxr-null mice. Rifaximin-mediated activation of human PXR, but not the other xenobiotic nuclear receptors constitutive androstane receptor, peroxisome proliferator-activated receptor (PPAR)alpha, PPARgamma, and farnesoid X receptor. Rifaximin could lead to PXR-dependent hepatocellular fatty degeneration as a result of activation of genes involved in lipid uptake, thus indicating a potential adverse effect of rifaximin on liver function after long-term exposure. |
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| Formulation & Dosage | |
| References | Eur J Pharmacol. 2011 Oct 1;668(1-2):317-24; J Pharmacol Exp Ther. 2007 Jul;322(1):391-8. |
