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Merck

30020

D-Cycloserine

Synonyme(s) :

R-4-Amino-3-isoxazolidinone, (R)-4-Amino-3-isoxazolidone, 4-Amino-3-isoxazolidinone

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A propos de cet article

Formule empirique (notation de Hill) :
C3H6N2O2
Numéro CAS:
Poids moléculaire :
102.09
UNSPSC Code:
51102829
NACRES:
NA.85
PubChem Substance ID:
EC Number:
200-688-4
Beilstein/REAXYS Number:
80798
MDL number:
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InChI key

DYDCUQKUCUHJBH-UWTATZPHSA-N

InChI

1S/C3H6N2O2/c4-2-1-7-5-3(2)6/h2H,1,4H2,(H,5,6)/t2-/m1/s1

SMILES string

N[C@@H]1CONC1=O

biological source

synthetic

form

powder

potency

≥900 μg per mg

color

white to off-white

mp

147 °C (dec.) (lit.)

antibiotic activity spectrum

Gram-negative bacteria
Gram-positive bacteria
mycobacteria

mode of action

cell wall synthesis | interferes

storage temp.

−20°C

Quality Level

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Application

D-Cycloserine acts as inhibitor of various enzymes.

Biochem/physiol Actions

Mode of Action: Inhibits cell wall biosynthesis (D-Ala peptide bond formation). Also prevents conversion of D-Ala to L-Ala. Bacteriostatic.
Partial agonist at the glycine modulatory site of NMDA glutamatergic receptors; antibiotic against Gram-negative bacteria.
Mode of Resistance: D-Ala transport interference.
Mode of Action: Inhibits cell wall biosynthesis (D-Ala peptide bond formation). Also prevents conversion of D-Ala to L-Ala. Bacteriostatic. Mode of Resistance: D-Ala transport interference.

General description

Chemical structure: amino acid derivatives

Other Notes

Keep container tightly closed in a dry and well-ventilated place. Store under inert gas. Air sensitive. Keep in a dry place.

Packaging

1g, 5g, 25g

Classe de stockage

11 - Combustible Solids

wgk

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)


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Consulter la Bibliothèque de documents

Michael L Sulkowski et al.
Current psychiatry reviews, 10(4), 317-324 (2014-11-11)
Variants of exposure therapy are effective for treating obsessive-compulsive and related disorders (OCRDs). However, significant numbers of patients do not respond adequately to exposure therapy resulting in continued distress and functional impairment. Therefore, novel approaches to augmenting exposure therapy are
M.K. Jain
Handbook of Enzyme Inhibitors, 112-112 (1982)
Mary M Torregrossa et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 30(31), 10526-10533 (2010-08-06)
Extinction therapy has been proposed as a method to reduce the motivational impact of drug-associated cues to prevent relapse. Cue extinction therapy, however, takes place in a novel context (e.g., treatment facility), and is unlikely to be effective due to
Rami Yaka et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 21(9), 2033-2041 (2007-03-14)
Traumatic brain injury triggers a massive glutamate efflux, activation of NMDA receptor channels, and cell death. Recently, we reported that NMDA receptors in mice are down-regulated from hours to days following closed head injury (CHI), and treatment with NMDA improved
Simon P Byrne et al.
Depression and anxiety, 32(6), 408-414 (2015-03-17)
For exposure therapy to be successful, it is essential that fear extinction learning extends beyond the treatment setting. D-cycloserine (DCS) may facilitate treatment gains by increasing generalization of extinction learning, however, its effects have not been tested in children. We

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