Sulbenicillin
- J01CA16 (WHO)
- (2S,5R,6R)-3,3-dimethyl-7-oxo-6-[(2-phenyl-2-sulfoacetyl)amino]-4-thia-1-azabicyclo[3.2.0]heptane-2-carboxylic acid
- 41744-40-5 Y 28002-18-8
- 39031
- 16736045 N
- Q2VYF0562D
- D08534 Y
- ChEMBL564107 N
- DTXSID20873379 DTXSID90873381, DTXSID20873379
- Interactive image
- CC1([C@@H](N2[C@H](S1)[C@@H](C2=O)NC(=O)[C@@H](c3ccccc3)S(=O)(=O)O)C(=O)O)C
- InChI=1S/C16H18N2O7S2/c1-16(2)11(15(21)22)18-13(20)9(14(18)26-16)17-12(19)10(27(23,24)25)8-6-4-3-5-7-8/h3-7,9-11,14H,1-2H3,(H,17,19)(H,21,22)(H,23,24,25)/t9-,10-,11+,14-/m1/s1 N
- Key:JETQIUPBHQNHNZ-NJBDSQKTSA-N N
Sulbenicillin (INN) is a penicillin antibiotic, notable for its combination use with dibekacin. [1] Penicillins, crucial in primary healthcare for potent bactericidal properties and wide distribution, include oral options for enhanced accessibility. Post-World War II, synthetic penicillins like sulbenicillin broadened efficacy, leading to new groups that diversified treatment. This evolution reflects a dynamic interplay between science and clinical needs, emphasizing enduring value in managing infectious diseases in primary care.
Structure and mechanism of action
Characterized by a distinctive beta-lactam ring, penicillins inhibit bacterial cell wall synthesis, leading to cell destruction. This mechanism is effective against a broad spectrum of bacteria.[2]
References
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(inhibit synthesis
of peptidoglycan
layer of bacterial
cell wall by binding
to and inhibiting
PBPs, a group of
D-alanyl-D-alanine
transpeptidases)
Glycopeptides Lipoglycopeptides |
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Lipopeptides |
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Polymyxins |
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Other |
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- Inhibit PG subunit synthesis and transport: NAM synthesis inhibition (Fosfomycin)
- DADAL/AR inhibitors (Cycloserine)
- bactoprenol inhibitors (Bacitracin)
- Hydrolyze NAM-NAG
- Tyrothricin
- Isoniazid#
- Teixobactin
- #WHO-EM
- ‡Withdrawn from market
- Clinical trials:
- †Phase III
- §Never to phase III
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