product name Cefdinir
Description: Cefdinir (also known as FK 482, PD 134393, CI-983) is an oral cephalosporin antibiotic, used to treat bacterial infections in many different parts of the body. Cefdinir, a new oral 2-amino-5-thiazolyl cephalosporin, inhibits the luminol-amplified chemiluminescence (LACL) response of human neutrophils stimulated by PMA but not opsonized zymosan, in a concentration-dependent but not time-dependent manner. Cefdinir inhibits LACL generation in cell-free systems consisting of H2O2, NaI, and either horseradish peroxidase or amyeloperoxidase-containing neutrophil extract. Cefdinir impairs LACL response induced by the calcium ionophore A23187 and FMLP, and this impairment is increased in cytochalasin B-treated neutrophils.
References: J Immunol. 1994 Mar 1;152(5):2447-55; Antimicrob Agents Chemother. 2003 Feb;47(2):689-96.
395.41
Formula
C14H13N5O5S2
CAS No.
91832-40-5
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 79 mg/mL (199.8 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
FK 482, PD 134393, CI-983
other peoduct :
| In Vitro |
In vitro activity: Cefdinir, a new oral 2-amino-5-thiazolyl cephalosporin, inhibits the luminol-amplified chemiluminescence (LACL) response of human neutrophils stimulated by PMA but not opsonized zymosan, in a concentration-dependent but not time-dependent manner. Cefdinir inhibits LACL generation in cell-free systems consisting of H2O2, NaI, and either horseradish peroxidase or amyeloperoxidase-containing neutrophil extract. Cefdinir impairs LACL response induced by the calcium ionophore A23187 and FMLP, and this impairment is increased in cytochalasin B-treated neutrophils. Cefdinir directly inhibits the activity of myeloperoxidase-containing neutrophil extract released into the extracellular medium during neutrophil stimulation by soluble mediators, but has no effect on that released into the phagolysosome during phagocytosis. Cefdinir demonstrates excellent activity against a wide range of gram-positive and gram-negative bacteria. Cefdinir is resistant to a broad variety of β-lactamases and exhibits a β-lactam stability profile generally better than those observed with cefaclor and cefuroxime. Cefdinir elimination is primarily mediated by the kidney. Cefdinir interacts with the dipeptide transporters PEPT1 and PEPT2. Cefdinir tubular reabsorption is substantial, that Cefdinir tubular secretion is inhibitable by probenecid, and that this secretion is probably mediated by the renal organic anion secretory pathway. Kinase Assay: Cell Assay: |
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| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | J Immunol. 1994 Mar 1;152(5):2447-55; Antimicrob Agents Chemother. 2003 Feb;47(2):689-96. |
