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SML0146

Sigma-Aldrich

ZL006

≥98% (HPLC)

Sinônimo(s):

4-((3,5-Dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid

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About This Item

Fórmula empírica (Notação de Hill):
C14H11Cl2NO4
Número CAS:
1181226-02-7
Peso molecular:
328.15
Número MDL:
MFCD20527326
Código UNSPSC:
12352200
ID de substância PubChem:
329825194
NACRES:
NA.25

Nível de qualidade

100

Ensaio

≥98% (HPLC)

Formulário

powder

cor

white to tan

solubilidade

DMSO: ≥5 mg/mL (warmed to 60° C)

temperatura de armazenamento

2-8°C

cadeia de caracteres SMILES

OC1=C(Cl)C=C(Cl)C=C1CNC(C=C2)=CC(O)=C2C(O)=O

InChI

1S/C14H11Cl2NO4/c15-8-3-7(13(19)11(16)4-8)6-17-9-1-2-10(14(20)21)12(18)5-9/h1-5,17-19H,6H2,(H,20,21)

chave InChI

RTEYSQSXRFVKTJ-UHFFFAOYSA-N

Ações bioquímicas/fisiológicas

Inhibitor of nNOS-PSD-95 interaction
ZL006 inhibits the ischemia-induced interaction of nNOS with postsynaptic density protein-95 (PSD-95), preventing glutamate-induced excitotoxicity and cerebral ischemic damage. It does not inhibit nNOS itself. ZL006 is brain penetrant, and has been tested in both rat and mouse models of stroke.
ZL006, a novel neuroprotectant, is also called as 5-(3, 5-dichloro-2-hydroxybenzylamino)-2-hydroxybenzoic acid. It has the ability to block the interaction of neuronal nitric oxide synthase (nNOS)/postsynaptic density protein-95 (PSD-95) in co-immunoprecipitation assays of extracts from glutamate or cultured neurons and cortical brain, stimulated by ischemia.

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

WGK 3

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Certificados de análise (COA)

Lot/Batch Number
125M4605V
091M4618V

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Sandra Tillmann et al.
PloS one, 12(8), e0182698-e0182698 (2017-08-05)
N-methyl-D-aspartate receptor (NMDA-R) antagonists and nitric oxide inhibitors have shown promising efficacy in depression but commonly induce adverse events. To circumvent these, a more indirect disruption of the nitric oxide synthase/postsynaptic density protein 95 kDa complex at the NMDA-R has
Wenrui Qu et al.
Cerebral cortex (New York, N.Y. : 1991), 30(7), 3859-3871 (2020-01-29)
Excessive activation of N-methyl-D-aspartate receptors (NMDARs) and the resulting neuronal nitric oxide synthase (nNOS) activation plays a crucial role in the pathogenesis of traumatic brain injury (TBI). However, directly inhibiting NMDARs or nNOS produces adverse side effects because they play
Xiaoli Gu et al.
Journal of separation science, 40(17), 3522-3534 (2017-07-14)
In the scope of stroke treatment, new neuronal nitric oxide synthase-postsynaptic density protein-95 uncouplers from herbal medicines were discovered and captured. To do so, highly selective magnetic molecularly imprinted polymers with a core-shell structure were prepared as artificial antibodies. According
Peng Luo et al.
Cell death & disease, 10(7), 496-496 (2019-06-27)
Traumatic brain injury (TBI) has become a major health concern worldwide, and the poor outcome of TBI increases the need for therapeutic improvement. Secondary injuries following TBI, including excitotoxicity, lead to synaptic dysfunction and provide potential targets for intervention. Postsynaptic
Satoshi Deyama et al.
Neuropharmacology, 118, 59-68 (2017-03-13)
Pain consists of sensory and affective components. Although the neuronal mechanisms underlying the sensory component of pain have been studied extensively, those underlying its affective component are only beginning to be elucidated. Previously, we showed the pivotal role of the
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