Cefpiramide
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| Category | Antibiotics |
| Catalog number | BBF-00737 |
| CAS | 70797-11-4 |
| Molecular Weight | 612.64 |
| Molecular Formula | C25H24N8O7S2 |
| Purity | 95% |
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Description
It is produced by the strain of Semisynthetic third generation cephalosporin for injection. Its sodium salt is used in preparations. Cefpiramide binds to penicillin-binding proteins (PBPs), transpeptidases that are responsible for crosslinking of peptidoglycan. By preventing crosslinking of peptidoglycan, cell wall integrity is lost and cell wall synthesis is halted.
Specification
| Related CAS | 74849-93-7 (sodium salt) |
| Synonyms | Cefpiramide acid; Cefpiramido; Cefpiramidum; (6R,7R)-7-((R)-2-(4-Hydroxy-6-methylnicotinamido)-2-(4-hydroxyphenyl)acetamido)-3-(((1-methyl-1H-tetrazol-5-yl)thio)methyl)-8-oxo-5-thia-1-azabicyclo[4.2.0]oct-2-ene-2-carboxylic acid |
| Storage | −20 °C under inert atmosphere |
| IUPAC Name | (6R,7R)-7-[[(2R)-2-(4-hydroxyphenyl)-2-[(6-methyl-4-oxo-1H-pyridine-3-carbonyl)amino]acetyl]amino]-3-[(1-methyltetrazol-5-yl)sulfanylmethyl]-8-oxo-5-thia-1-azabicyclo[4.2.0]oct-2-ene-2-carboxylic acid |
| Canonical SMILES | CC1=CC(=O)C(=CN1)C(=O)NC(C2=CC=C(C=C2)O)C(=O)NC3C4N(C3=O)C(=C(CS4)CSC5=NN=NN5C)C(=O)O |
| InChI | InChI=1S/C25H24N8O7S2/c1-11-7-16(35)15(8-26-11)20(36)27-17(12-3-5-14(34)6-4-12)21(37)28-18-22(38)33-19(24(39)40)13(9-41-23(18)33)10-42-25-29-30-31-32(25)2/h3-8,17-18,23,34H,9-10H2,1-2H3,(H,26,35)(H,27,36)(H,28,37)(H,39,40)/t17-,18-,23-/m1/s1 |
| InChI Key | PWAUCHMQEXVFJR-PMAPCBKXSA-N |
Properties
| Appearance | White to Yellowish Crystalline Powder |
| Melting Point | 212-215 °C (dec.) |
| Density | 1.75±0.1 g/cm3 (Predicted) |
| Solubility | Highly soluble in DMF; Soluble in Water; Slightly soluble in Methanol, DMSO |
Reference Reading
1.Antibiotic and synergistic effect of Leu-Lys rich peptide against antibiotic resistant microorganisms isolated from patients with cholelithiasis.
Jeong N1, Kim JY, Park SC, Lee JK, Gopal R, Yoo S, Son BK, Hahm JS, Park Y, Hahm KS. Biochem Biophys Res Commun. 2010 Sep 3;399(4):581-6. doi: 10.1016/j.bbrc.2010.07.118. Epub 2010 Aug 2.
Pseudomonas aeruginosa has eventually developed resistance against flomoxef sodium, isepamicin and cefpiramide. Therefore, in this study, the antibacterial activity and synergistic effects of the amphipathic-derived P5-18mer antimicrobial peptide were tested against pathogens associated with cholelithiasis that have developed resistance against commonly used antibiotics. The results were then compared with the activities of the amphipathic-derived peptide, P5-18mer, melittin and common antibiotics. Growth inhibition of planktonic bacteria was tested using the National Committee for Clinical Laboratory Standards (NCCLS). The bactericidal activity of the antimicrobial peptides was measured using time-kill curves. Synergistic effects were evaluated by testing the effects of P5-18mer alone and in combination with flomoxef sodium, isepamicin or cefpiramide at 0.5xMIC. P5-18mer peptide displayed strong activity against pathogens and flomoxef sodium, isepamicin and cefpiramide-resistant bacteria cell lines obtained from a patient with gallstones; however, it did not exert cytotoxicity against the human keratinocyte HaCat cell line.
2.Biliary excretion of olmesartan, an anigotensin II receptor antagonist, in the rat.
Takayanagi M1, Sano N, Takikawa H. J Gastroenterol Hepatol. 2005 May;20(5):784-8.
BACKGROUND AND AIM: Olmesartan (RNH-6270) is a newly developed anigotensin II receptor antagonist, and has been reported to be excreted into feces. To examine the mechanism of the biliary excretion of olmesartan, we studied its biliary excretion in rats.
3.Effects of organic anions and vinblastine on biliary excretion of erythromycin in rats.
Sato A1, Takikawa H, Yamanaka M. Pharmacology. 1999 Nov;59(5):249-56.
Since little is known about the mechanism of biliary excretion of cationic drugs, biliary excretion of erythromycin was studied in rats. Infusion of sulfobromophthalein and taurocholate significantly decreased biliary erythromycin excretion, whereas infusion of dibromosulfophthalein, cefpiramide, ursodeoxycholate-3-O-glucuronide and taurolithocholate-3-sulfate had no effect on biliary excretion of erythromycin. Vinblastine significantly inhibited biliary erythromycin excretion. Phenothiazine treatment significantly increased biliary erythromycin excretion. However, erythromycin infusion did not affect biliary vinblastine excretion. These findings indicate a multiplicity of biliary excretory pathways for organic cations; at least one additonal pathway may exist for organic cations apart from P-glycoprotein.
4.Biliary excretion of phenolphthalein glucuronide in the rat.
Ogasawara T1, Takikawa H. Hepatol Res. 2001 Jun;20(2):221-231.
To examine the substrate specificity of an ATP-dependent organic anion transporter, the multidrug resistance protein 2, we examined the effects of various bile acid conjugates and organic anions on the biliary excretion of phenolphthalein glucuronide, a hydrophilic glucuronide conjugate, in rats. Biliary phenolphthalein glucuronide excretion was markedly inhibited by taurolithocholate-3-sulfate and ursodeoxycholate-3-O-glucuronide. In contrast, ursodeoxycholate-3,7-disulfate and pravastatin only slightly inhibited and cefpiramide did not inhibit biliary phenolphthalein glucuronide excretion. Biliary excretion of sulfobromophthalein, leukotriene C(4) and pravastatin was inhibited by phenolphthalein glucuronide infusion to some extent. These findings suggest that phenolphthalein glucuronide is a relatively low affinity substrate for the multidrug resistance protein 2.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
