Chloramphenicol Sodium Succinate

Inquiry

Cat Number

API982570

CAS Number

982-57-0

For research use only. We do not supply to patients.

For pharmaceutical-grade products or other inquiries, please contact our experts.

Product Detail Description Scientific Support Customer Q&A

CAS Number

982-57-0

EINECS

213-568-1

Storage

Under -20℃

Molecular Formula

C15H15Cl2N2NaO8

Molecular Weight

445.2

Smiles

C1=CC(=CC=C1[C@H]([C@@H](COC(=O)CCC(=O)[O-])NC(=O)C(Cl)Cl)O)[N+](=O)[O-].[Na+]

Appearance

White to off-white solid

General Description

Chloramphenicol Sodium Succinate is the water-soluble sodium succinate ester prodrug of chloramphenicol, an amphenicol-class broad-spectrum antibiotic. It is hydrolyzed in vivo by esterases to release active chloramphenicol.

Mechanism of Action

Chloramphenicol binds reversibly to the 50S ribosomal subunit at the peptidyl transferase center, inhibiting peptidyl transferase and blocking peptide bond formation during protein synthesis, producing bacteriostatic activity.

Application

Used in the treatment of serious infections. Chloramphenicol Sodium Succinate is indicated for typhoid fever, bacterial meningitis, rickettsial infections, and serious infections caused by multidrug-resistant organisms.

Chloramphenicol succinate (CAPS), a prodrug of the antibiotic chloramphenicol, exerts a profound cardioprotective effect in a clinically relevant porcine model of acute myocardial infarction. In anesthetized pigs subjected to 45 minutes of coronary occlusion and 3 hours of reperfusion, administration of CAPS significantly reduced infarct size. Pretreatment with CAPS 10 minutes before ischemia reduced infarct size to 25±5% of the area at risk, compared to 56±5% in the saline control group. A delayed treatment, administered 30 minutes after occlusion, still provided significant cardioprotection, reducing infarct size to 41±4%.
Mechanistically, this protective effect was associated with the induction of autophagy, evidenced by a rapid upregulation of Beclin-1 and LC3-II, two key proteins involved in autophagosome formation. These findings support the concept that pharmacological upregulation of autophagy may be a novel therapeutic strategy to limit ischemia-reperfusion injury.

Fig. 1 Expression of Beclin-1 and LC3-II with Chloramphenicol succinate pretreatment. (Sala-Mercado J A.; et al. 2011)

References

Sala-Mercado J A, et al. Profound cardioprotection with chloramphenicol succinate in the swine model of myocardial ischemia-reperfusion injury. Circulation, 2010, 122(11_suppl_1): S179-S184.