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Cefdinir(FK-482 CI-983)
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Cefdinir(FK-482 CI-983)图片
CAS NO:91832-40-5
规格:≥98%
包装与价格:
包装价格(元)
100mg电议
250mg电议
500mg电议
1g电议
2g电议
10g电议

产品介绍
理化性质和储存条件
Molecular Weight (MW)395.41
FormulaC14H13N5O5S2
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
Other info
Chemical Name: (6R,7R)-7-[[(2Z)-2-(2-amino-1,3-thiazol-4-yl)-2-hydroxyiminoacetyl]amino]-3-ethenyl-8-oxo-5-thia-1-azabicyclo[4.2.0]oct-2-ene-2-carboxylic acid
InChi Key: RTXOFQZKPXMALH-GHXIOONMSA-N
InChi Code: InChI=1S/C14H13N5O5S2/c1-2-5-3-25-12-8(11(21)19(12)9(5)13(22)23)17-10(20)7(18-24)6-4-26-14(15)16-6/h2,4,8,12,24H,1,3H2,(H2,15,16)(H,17,20)(H,22,23)/b18-7-/t8-,12-/m1/s1
SMILES Code: C=CC1=C(N2[C@@H]([C@@H](C2=O)NC(=O)/C(=N\O)/C3=CSC(=N3)N)SC1)C(=O)O
SynonymsFK 482, PD 134393, CI-983; PD-134393; PD134393; Omnicef; CFDN; Cefdinirum; Cefdinyl; CI 983; CI983; FK482; FK-482
实验参考方法
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.

In Vivo
Animal model
Formulation & Dosage
ReferencesJ Immunol. 1994 Mar 1;152(5):2447-55; Antimicrob Agents Chemother. 2003 Feb;47(2):689-96.