C8630
DL-Cystine
Sinônimo(s):
(±)-3,3′-Dithiobis(2-aminopropionicacid)
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About This Item
Produtos recomendados
Ensaio
≥98% (TLC)
Formulário
powder
cor
white to off-white
pf
227 °C (dec.) (lit.)
solubilidade
1 M HCl: soluble
cadeia de caracteres SMILES
NC(CSSCC(N)C(O)=O)C(O)=O
InChI
1S/C6H12N2O4S2/c7-3(5(9)10)1-13-14-2-4(8)6(11)12/h3-4H,1-2,7-8H2,(H,9,10)(H,11,12)
chave InChI
LEVWYRKDKASIDU-UHFFFAOYSA-N
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Ações bioquímicas/fisiológicas
DL-Cystine is a racemic mixture of the proteinogenic amino acids L-cystine and the non-proteinogenic D-cystine. DL-cystine is used in the preparation of sulfur-containing dimeric and monomeric surfactants.
Código de classe de armazenamento
11 - Combustible Solids
Classe de risco de água (WGK)
WGK 3
Ponto de fulgor (°F)
Not applicable
Ponto de fulgor (°C)
Not applicable
Equipamento de proteção individual
Eyeshields, Gloves, type N95 (US)
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Journal of colloid and interface science, 351(2), 472-477 (2010-08-31)
Anionic urea-based dimeric (gemini) surfactants derived from the amino acids L-cystine, D-cystine and DL-cystine, as well as monomeric surfactants derived from L-cysteine, L-methionine and L-cysteic acid were synthesized and their solution properties characterized by electrical conductivity, equilibrium surface tension, and
Journal of medical microbiology, 63(Pt 3), 471-477 (2014-01-17)
A group of biofilm-producing bacteria isolated from patients with urinary tract infections was evaluated, identifying the main factors contributing to biofilm formation. Among the 156 isolates, 58 (37.2%) were biofilm producers. The bacterial species (P<0.001), together with patient's gender (P
Pediatric nephrology (Berlin, Germany), 30(4), 595-601 (2014-10-19)
The mutations responsible for cystinosis in South African patients are currently unknown. A pertinent question is whether they are similar to those described elsewhere in the world. Children who were being managed for cystinosis in the Western Cape Province of
Extrasynaptic glutamate release through cystine/glutamate antiporter contributes to ischemic damage.
The Journal of clinical investigation, 124(8), 3645-3655 (2014-07-19)
During brain ischemia, an excessive release of glutamate triggers neuronal death through the overactivation of NMDA receptors (NMDARs); however, the underlying pathways that alter glutamate homeostasis and whether synaptic or extrasynaptic sites are responsible for excess glutamate remain controversial. Here
Journal of physiology and pharmacology : an official journal of the Polish Physiological Society, 65(5), 623-631 (2014-11-06)
The use of glutathione (GSH) and sulfate for the detoxification of paracetamol (acetaminophen, APAP) could occur at the expense of the physiological uses of cysteine (Cys). Indeed GSH and sulfate both originate from Cys. Significant APAP-induced Cys loss could generate
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