AvibactaM
AvibactaM Basic information
- Product Name:
- AvibactaM
- Synonyms:
-
- AvibactaM
- Sulfuric acid mono[(1R,2S,5R)-2-(aminocarbonyl)-7-oxo-1,6-diazabicyclo[3.2.1]oct-6-yl] ester
- (E)-7-fluoro-3-methylhept-4-en-2-one
- Avibactam free acid
- AVIBACTAM FREE ACID (NXL-104 FREE ACID)
- Avibactam Impurity 37
- Avibactam,(2S,5R)-7-Oxo-6-(sulfooxy)-1,6-diazabicyclo[3.2.1]octane-2-carbox amide
- (2S,5R)-2-carbamoyl-7-oxo-1,6-diazabicyclo[3.2.1]octan-6-ylhydrogensulfate
- CAS:
- 1192500-31-4
- MF:
- C7H11N3O6S
- MW:
- 265.24
- EINECS:
- 685-962-2
- Mol File:
- 1192500-31-4.mol
AvibactaM Chemical Properties
- Density
- 1.85
- storage temp.
- Store at -20°C
- solubility
- DMSO
- form
- Powder
- pka
- -4.59±0.18(Predicted)
- color
- White to off-white
- InChI
- InChI=1S/C7H11N3O6S/c8-6(11)5-2-1-4-3-9(5)7(12)10(4)16-17(13,14)15/h4-5H,1-3H2,(H2,8,11)(H,13,14,15)/t4-,5+/m1/s1
- InChIKey
- NDCUAPJVLWFHHB-UHNVWZDZSA-N
- SMILES
- S(O)(ON1C(=O)[N@@]2C[C@@]1([H])CC[C@H]2C(N)=O)(=O)=O
AvibactaM Usage And Synthesis
Uses
Avibactam Butylammonium Salt is a novel β-lactamase inhibitor with a non-lactam structural scaffold. Avibactam irreversibly inhibits lactamase from Mycobacterium tuberculosis.
Definition
ChEBI: A member of the class of azabicycloalkanes that is (2S,5R)-7-oxo-1,6-diazabicyclo[3.2.1]octane-2-carboxamide in which the amino hydrogen at position 6 is replaced by a sulfooxy group. Used (in the form of its sodium salt) n combination with ceftazidime pentahydrate for the treatment of complicated urinary tract infections including pyelonephritis.
Enzyme inhibitor
This non-β-lactam inhibitor of β-lactamase (FW = 261.27 g/mol; CAS 1192500-31-4), also known as NLX104 and AVE1330A, shows a spectrum of action against Classes A and C β-lactamase as well as selected Class D β-lactamase, enzymes that often confer resistance to β-lactam antibiotics. By forming a high-affinity complex with its target enzymes, avibactam enhances the antibacterial activity of certain β-lactam drugs, such as ceftaroline. With over 1000 known β-lactamase, the action of avibactam is apt to depend on the invidual active-site interactions. Mode of Action: Acylation and deacylation rates have been measured for the clinically important enzymes CTX-M-15, KPC-2, E. cloacae AmpC, P. aeruginosa AmpC, OXA-10, and OXA-48. The efficiency of acylation (kon/Ki) varies across the enzyme spectrum, from 1.1 x 101 M–1 s –1 for OXA-10 to 1.0 x 105 M–1 s –1 for CTX-M-15. Inhibition of OXA-10 was shown to follow a reversible covalent mechanism (see below), and the acylated OXA-10 displayed the longest residence time for deacylation, with a half-life of greater than 5 days. The inhibited enzyme forms are stable to hydrolysis for all enzymes with the exception of KPC-2, which displays slow hydrolytic route that involved fragmentation of the acyl-avibactam complex. In the case of TEM-1 lactamase, avibactam slowly covalently acylates its target, and the acylated enzyme subsequently undergoes slow deacylation (koff = 0.045 min?1 ) regenerating avibactam intact. Use as a Combined Drug: Combination of avibactim with extended-spectrum cephalosporins or aztreonam shows promise in inhibiting Klebsiella pneumoniae (KP) isolates harboring carbapenemases, or KPCs. Given abundant experience with ceftazidime and the significant improvement avibactam provides against contemporary β-lactamase-producing Gram-negative pathogens, this combination will likely play a role in the treatment of complicated urinary tract infections (as monotherapy) and complicated intra-abdominal infections (in combination with metronidazole) caused (or suspected to be caused) by otherwise resistant pathogens, such as extended spectrum β-lactamase-, AmpC-, or Klebsiella pneumoniae carbapenemase producing Enterobacteriaceae and multidrug-resistant P. aeruginosa.
in vivo
Ceftazidime-Avibactam (0.375?mg/g; s.c.; q8h for 10 days) has a significant effect on the bacteria and led to a certain therapeutic efficacy in K. pneumoniae strain Y8 infected mouse model[3].
Avibactam (64 mg/kg; s.c.; once) shows mean estimated half-life in plasma in the terminal phase of 0.24 h in Pseudomonas aeruginosa infected neutropenic mice with lung infection[3].
| Animal Model: | Six-week-old BALB/c mice (female), K. pneumoniae strain Y8 infection model[4] |
| Dosage: | 0.375?mg/g in combination with Ceftazidime |
| Administration: | Subcutaneous injection, 4?h post infection and given every 8?h for 10?days |
| Result: | 70% of infection group mice died within 4?days, and all mice in the PBS group died within 13?days. All treatment group mice survived at 10 days post infection with the antibiotic applied every 8?h, whereas 100% of mice in this group died within 4?days after the antibiotic treatment stopped. The spleen and liver of treatment group mice showed lower CFU counts, as compare with that of infected group. |
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