Cilastatin - CAS 82009-34-5
Catalog number:
82009-34-5
Category:
Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C16H26N2O5S
Molecular Weight:
358.45
COA:
Inquire
Targets:
Antibacterial
Description:
Cilastatin can prevent renal metabolism of penem and carbapenem antibiotics by specific and reversible dehydropeptidase I inhibition. It can be used as antibacterial adjunct.
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Purity:
>95%
Appearance:
White to Light-Yellow Solid
Synonyms:
(2Z)-7-[[(2R)-2-amino-2-carboxyethyl]thio]-2-[[[(1S)-2,2-dimethylcyclopropyl]carbonyl]amino]-2-heptenoic Acid;MK-791
Solubility:
Soluble in DMSO
Storage:
-20℃ Freezer
MSDS:
Inquire
Application:
Antibacterial adjunct.
Quality Standard:
In-house standard
Shelf Life:
2 month in rt, long time
Quantity:
Milligrams-Grams
Melting Point:
156-158℃ (dec.)
1.Successful Additional Corticosteroid Treatment in a Patient with Mycoplasma pneumoniae Pneumonia in whom a Monobacterial Infection was Confirmed by a Molecular Method Using Bronchoalveolar Lavage Fluid.
Yamasaki K1, Yatera K, Kato K, Noguchi S, Kawanami T, Fukuda K, Naito K, Akata K, Ishimoto H, Taniguchi H, Mukae H. Intern Med. 2016;55(6):703-7. doi: 10.2169/internalmedicine.55.5124. Epub 2016 Mar 15.
A 23-year-old Japanese woman was admitted to A hospital due to pneumonia. IgM for Mycoplasma pneumoniae was positive, and the patient was treated with imipenem/cilastatin, clindamycin, pazufloxacin and minocycline. However, both the chest radiological findings and the symptoms became exacerbated, and she was therefore transferred to our hospital. The bronchoalveolar lavage fluid was obtained, and a 16S rRNA gene sequencing analysis revealed a monobacterial infection of Mycoplasma pneumoniae. Therefore, corticosteroid treatment in addition to minocycline was administered, and the patients symptoms, laboratory data and chest radiographs improved. Corticosteroid therapy may therefore be considered for patients with refractory M. pneumoniae pneumonia.
2.Analysis of drug resistance in 1,861 strains of Acinetobacter baumannii.
Jin H1, Qiu F2, Ji HJ1, Lu Q1. Biomed Rep. 2016 Apr;4(4):463-466. Epub 2016 Feb 15.
Acinetobacter baumannii is an emerging human pathogen that causes hospital-acquired infections. The trend in increased antimicrobial resistance limits the choice of effective antimicrobial agents. The present study reports the resistance to Acinetobacter baumannii and analyzes the associations between antibiotic use and resistance rates at a general hospital between 2010 and 2014. A total of 1,861 isolates were obtained from clinical cultures, accounting for 10.33% of all detected bacteria (1,861/18,016). The strains were mainly from respiratory samples (1,628 isolates, 87.5%) and the intensive care unit (696 isolates, 37.4%). The resistance rates of Acinetobacter baumannii to the majority of antibiotics were >50%, particularly the resistance rate to cefoperazone/sulbactam increased from 47.37 in 2011 to 89.25% in 2014. However, the rates of imipenem and cilastatin sodium decreased from 81.03 to 69.44% due to the antibiotic policy. There were Pearson significant associations between the use of three antibiotics and resistance in Acinetobacter baumannii to this drug, piperacillin/tazobactam (r=0.
3.Imipenem/cilastatin-induced acute eosinophilic pneumonia.
Foong KS1, Lee A2, Pekez M2, Bin W3. BMJ Case Rep. 2016 Mar 4;2016. pii: bcr2016214804. doi: 10.1136/bcr-2016-214804.
Drugs, toxins, and infections are known to cause acute eosinophilic pneumonia. Daptomycin and minocycline are the commonly reported antibiotics associated with acute eosinophilic pneumonia. In this study, we present a case of imipenem/cilastatin-induced acute eosinophilic pneumonia. The patient presented with fever, acute hypoxic respiratory distress, and diffuse ground-glass opacities on the chest CT a day after the initiation of imipenem/cilastatin. Patient also developed peripheral eosinophilia. A reinstitution of imipenem/cilastatin resulted in recurrence of the signs and symptoms. A bronchoscopy with bronchoalveolar lavage showed 780 nucleated cells/mm(3) with 15% eosinophil. The patient's clinical condition improved significantly after the discontinuation of imipenem/cilastatin therapy and the treatment with corticosteroid.
4.Delayed Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase Inhibition by Trametinib Attenuates Systemic Inflammatory Responses and Multiple Organ Injury in Murine Sepsis.
Smith JA1, Mayeux PR, Schnellmann RG. Crit Care Med. 2016 Mar 30. [Epub ahead of print]
OBJECTIVE: The mitogen-activated protein kinase/extracellular signal-regulated kinase signaling pathway is an essential component of innate immunity necessary for mediating proinflammatory responses in the setting of sepsis. We previously demonstrated that the mitogen-activated protein kinase 1/2 inhibitor trametinib prevents endotoxin-induced renal injury in mice. We therefore assessed efficacy of trametinib in a more clinically relevant experimental model of sepsis.
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CAS 82009-34-5 Cilastatin

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