product name Clarithromycin
Description: Clarithromycin is a potent macrolide antibiotic and a CYP3A4 inhibitor, used for treatment of a number of bacterial infections. It is used to treat pharyngitis, tonsillitis, acute maxillary sinusitis, acute bacterial exacerbation of chronic bronchitis, pneumonia (especially atypical pneumonias associated with Chlamydophila pneumoniae), skin and skin structure infections. Clarithromycin prevents bacteria from growing by interfering with their protein synthesis.
References: J Antimicrob Chemother. 2002 May;49(5):745-55; Antimicrob Agents Chemother. 2001 Jan;45(1):44-7.
747.95
Formula
C38H69NO13
CAS No.
81103-11-9
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 25 mg/mL (33.4 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
A-56268
other peoduct :
| In Vitro |
In vitro activity: Clarithromycin suppresses this production in a dose-dependent manner in both monocytes and THP-1 cells. Clarithromycin regulates three other promoters that have either the NF-kappa B or the AP-1 binding sequences: two synthetic (pAP-1-Luc and pNF-kappa B-Luc) and one naturally occurring (ELAM-Luc). Clarithromycin suppresses NF-kappaB activation induced by TNF-alpha in U-937 and Jurkat cells in a concentration-related manner. Clarithromycin inhibits NF-kappaB activation induced by TNF-alpha in U-937, Jurkat, and A549 cells and PBMC and by SEA in PBMC. Clarithromycin prevents NF-kappaB-dependent reporter gene expression in U-937 cells. Clarithromycin results in a significant suppression of production of each cytokine in 71% and a significant increase in 29% of the human monocytes. Clarithromycin inhibits tumor necrosis factor (TNF)-alpha-induced IL-8 gene expression in a dose- and incubation time-dependent manner. Clarithromycin represses AP-1 binding in TNF-alpha-treated BET-1A cells. Clarithromycin represses IL-8 gene transcription mainly via the AP-1 binding site in human bronchial epithelial cells. Clarithromycin suppresses IL-1 beta gene expression in human nasal epithelial cells stimulated by H. influenzae endotoxin (HIE). Clarithromycin suppresses intercellular adhesion molecule-1 gene expression in nasal fibroblasts stimulated by IL-1 beta. Clarithromycin reduces DNA-binding activity of NF-kappa B in both human nasal epithelial cells and fibroblasts stimulated by HIE or IL-1 beta, respectively Kinase Assay: Cell Assay: |
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| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | J Antimicrob Chemother. 2002 May;49(5):745-55; Antimicrob Agents Chemother. 2001 Jan;45(1):44-7. |
