Cefodizime has marginal but variable inhibitory activity against Citrobacter species, including Citrobacter freundii and Serratia marcescens. Cefodizime inhibits other Gram-negative bacteria, including Haemophilus influenzae, Moraxella catarrhalis, Neisseria gonorrhoeae, and Neisseria meningitidis [1]. Cefodizime is a bactericidal antibiotic with high affinity for penicillin-binding proteins 1A/B, 2 and 3 of Escherichia coli. The in vitro concentrations at which cefodizime is bactericidal against susceptible strains of Gram-positive and Gram-negative bacter

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Cefodizime (HR 221, compound 1a) exhibited broad-spectrum antibacterial activity against Gram-negative and Gram-positive bacteria. Minimal inhibitory concentrations (MICs, μg/ml) determined by agar dilution on Mueller-Hinton agar: Staphylococcus aureus SG 511: 3.13; Staphylococcus aureus 285: 6.25; Streptococcus pyogenes 308A: 0.062; Escherichia coli TEM: 0.313; Escherichia coli 1507E: 0.313; Salmonella typhimurium: 0.156; Klebsiella aerogenes 1522E: 0.313; Enterobacter cloacae 1321: 0.313; Proteus mirabilis ATCC 14273: 0.39. Cefodizime was less active against Klebsiella aerogenes 1082E (MIC 125 μg/ml) and inactive against Enterobacter cloacae P99 (MIC >500 μg/ml). The compound demonstrated stability against TEM-type β-lactamases. The 5-chloroaminothiazolyl derivative (1g) showed high stability against chromosomally mediated K1 β-lactamase. [1]
- The interaction of Cefodizime with human serum albumin (HSA) was investigated using multi-spectroscopic techniques at pH 7.40. Steady-state fluorescence quenching experiments (excitation 280 nm, emission 200-500 nm) revealed that cefodizime quenched the intrinsic fluorescence of HSA (peak at 351 nm) in a concentration-dependent manner. The Stern-Volmer quenching constants (K_SV) at 298K and 310K were 3.35 × 10⁴ L·mol⁻¹ and 2.99 × 10⁴ L·mol⁻¹, respectively, with bimolecular quenching rate constants (k_q) of 3.35 × 10¹² L·mol⁻¹·s⁻¹ and 2.99 × 10¹² L·mol⁻¹·s⁻¹, indicating a static quenching mechanism. The binding constants (K_a) were 1.12 × 10⁵ L·mol⁻¹ at 298K and 0.50 × 10⁵ L·mol⁻¹ at 310K, with approximately one binding site (n ≈ 1). Thermodynamic parameters: ΔH = -6.20 kJ·mol⁻¹, ΔS = -75.83 J·mol⁻¹·K⁻¹, ΔG = -28.80 kJ·mol⁻¹ (298K) and -27.89 kJ·mol⁻¹ (310K), indicating that hydrogen bonds and van der Waals forces were the main driving forces. The binding distance (r) between the donor (Trp-214) and acceptor (cefodizime) was calculated as 3.30 nm (R₀ = 2.31 nm, energy transfer efficiency E = 0.11), suggesting non-radiative energy transfer could occur. Site marker competitive experiments showed that phenylbutazone (site I marker) displaced cefodizime, while ibuprofen (site II marker) had little effect, indicating that cefodizime binds to site I (subdomain IIA) of HSA. Circular dichroism (CD) spectroscopy revealed that upon binding, the α-helix content of HSA increased from 44.5% (control) to 47.6% (at n_CEF/n_HSA = 20:1). Three-dimensional fluorescence showed a red shift of peak 2 from 347.0 nm to 350.0 nm and decreased fluorescence intensity, confirming conformational changes. [2]

Following a single subcutaneous dose of 50 mg/kg of cephalosporins, cefuroxime, or cefazolin, cefodizime's activity in mice with an experimentally induced respiratory tract infection caused by Klebsiella pneumoniae was higher than that of cefoperazone, ceftazidime, and ceftazidime for eight hours. Cefodizime, on the other hand, has far greater bactericidal activity lasting at least 48 hours following a single injection, in contrast to these cephalosporins. 50% of the mice obtained total bacterial clearance from the lungs in 48 hours, despite the fact that cefodizime was no longer visible in the serum [1].

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Pharmacokinetic study in mice: Cefodizime (1a) was administered subcutaneously at a dose of 10 mg/kg. Blood samples were collected at various time points to determine drug concentrations. The elimination half-life and area under the curve (AUC) were calculated. [1]
- Pharmacokinetic study in dogs: Cefodizime (1a) was administered intravenously at a dose of 10 mg/kg. Pharmacokinetic parameters including elimination half-life and AUC were determined. [1]

In mice following subcutaneous administration at 10 mg/kg, Cefodizime (compound 1a) had an elimination half-life (T₁/₂) of 1.28 hours and an area under the curve (AUC) of 40.7 mg·h/L. [1]
- In dogs following intravenous administration at 10 mg/kg, Cefodizime (1a) had an elimination half-life (T₁/₂) of 1.25 hours and an AUC of 59.8 mg·h/L. [1]

[1]. Barradell LB, et al. Cefodizime. A review of its antibacterial activity, pharmacokinetic properties and therapeutic use. Drugs. 1992 Nov;44(5):800-34.
[2]. Hu T, et al. Probing the interaction of cefodizime with human serum albumin using multi-spectroscopic and molecular docking techniques. J Pharm Biomed Anal. 2015 Mar 25;107:325-32.

Cefodizime is a cephalosporin compound with 5-(carboxymethyl)-4-methyl-1,3-thiazolyl]thio}methyl and 2-(2-amino-1,3-thiazolyl)-2-(methoxyimino)acetyl]amino side groups at positions 3 and 7, respectively. It is an antibacterial drug and a tyrosinase (EC 1.14.18.1) inhibitor. It belongs to the cephalosporin, 1,3-thiazole, and oxime ether classes. Cefodizime is a third-generation aminothiazole cephalosporin used for parenteral administration. Cefodizime has broad-spectrum antibacterial activity and is stable against most β-lactamases.

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Cefodizime is a third-generation cephalosporin antibiotic with an aminothiazolyl side chain and a methoximino group in the 7-position. It contains a mercaptothiazolyl side chain at the 3'-position with an additional acid group. This specific substitution confers both high antibacterial activity and prolonged half-life in laboratory animals. Cefodizime has been reported to markedly stimulate the immune system in laboratory animals. It has no renal toxic effect, good tolerance, and immune-regulatory activity, which distinguishes it from other third-generation cephalosporins. [1][2]
- Molecular docking studies using the HSA crystal structure (PDB code 2BXM) showed that Cefodizime binds within the subdomain IIA hydrophobic cavity (site I). Active site residues within 5 Å of cefodizime included Phe206, Arg484, Trp214, Leu481, Leu198, and Val344. Hydrogen bonds, hydrophobic interactions, and polar forces were involved in the binding. The calculated binding distance between Trp-214 and cefodizime from docking was consistent with the distance (3.30 nm) obtained from Förster’s non-radiative energy transfer analysis. [2]

C20H20N6O7S4

584.65

584.027

69739-16-8

Cefodizime sodium;86329-79-5

5361871

White to off-white solid powder

1.9±0.1 g/cm3

1.852

2.55

4

15

10

37

1030

2

CC1=C(SC(SCC2=C(N3C([C@@H](NC(/C(/C4=CSC(N4)=N)=N\OC)=O)[C@H]3SC2)=O)C(O)=O)=N1)CC(O)=O

XDZKBRJLTGRPSS-BGZQYGJUSA-N

InChI=1S/C20H20N6O7S4/c1-7-10(3-11(27)28)37-20(22-7)36-5-8-4-34-17-13(16(30)26(17)14(8)18(31)32)24-15(29)12(25-33-2)9-6-35-19(21)23-9/h6,13,17H,3-5H2,1-2H3,(H2,21,23)(H,24,29)(H,27,28)(H,31,32)/b25-12-/t13-,17-/m1/s1

(6R,7R)-7-((Z)-2-(2-aminothiazol-4-yl)-2-(methoxyimino)acetamido)-3-(((5-(carboxymethyl)-4-methylthiazol-2-yl)thio)methyl)-8-oxo-5-thia-1-azabicyclo[4.2.0]oct-2-ene-2-carboxylic acid

S-771221 S771221S 771221Cefodizime HR 221 HR221HR-221

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~20.83 mg/mL (~35.63 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (3.56 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (3.56 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (3.56 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)