SML1949
Synta66
≥98% (HPLC)
Sinônimo(s):
4-Pyridinecarboxamide, N-(2′,5′-dimethoxy[1,1′-biphenyl]-4-yl)-3-fluoro-, GSK1349571A, N-(2′,5′-Dimethoxy[1,1′-biphenyl]-4-yl)-3-fluoro-4-pyridinecarboxamide, S66, Synta 66, Synta-66
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5 MG
R$ 651,00
25 MG
R$ 2.620,00
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5 MG
R$ 651,00
25 MG
R$ 2.620,00
About This Item
Fórmula empírica (Notação de Hill):
C20H17FN2O3
Número CAS:
Peso molecular:
352.36
Código UNSPSC:
12352200
NACRES:
NA.77
Produtos recomendados
Nível de qualidade
Ensaio
≥98% (HPLC)
Formulário
powder
cor
white to beige
solubilidade
DMSO: 20 mg/mL, clear
temperatura de armazenamento
2-8°C
cadeia de caracteres SMILES
O=C(NC1=CC=C(C2=C(OC)C=CC(OC)=C2)C=C1)C3=CC=NC=C3F
chave InChI
GFEIWXNLDKUWIK-UHFFFAOYSA-N
Aplicação
Synta66 has been used:
- as a Ca2+ release-activated calcium (CRAC) channel inhibitor to study its effects on ORAI isoforms[1]
- as an ORAI1 blocker to study its effects on the entry of Ca2+ in chronic lymphocytic leukemia (CLL) B cells[2]
- as a CRAC blocker to study its effects on the influx of Ca2+ by store-operated Ca2+ entry (SOCE) in enamel cells[3]
Ações bioquímicas/fisiológicas
A selective SOCE inhibitor that blocks CRAC current (ICRAC) without significant off-target potency or affinity.
Synta66 (S66) is a CRAC (Ca2+ release-activated Ca2+) channel inhibitor that blocks SOCE (store-operated Ca2+ entry) upon Ca2+ depletion from intracellular stores by thapsigargin in human vascular smooth muscle cells (VSMCs) with high potency (IC50 = 26 nM & 43 nM based on maximum Ca2+ level & rate of increase, respectly). Synta66 exhibits no affinity toward a range of receptors and ion channels (e.g. L-type Ca2+ channel) and does not affect TRPC1/5-mediated SOCE or store-operated non-selective cationic current. Leukocytes are reported to be less sensitive to CRAC inhibition by Synta66 (IC50 = 1.76 μM/HL-60, 1 ?M/Jurkat, 1.4 μM/rat RBL).
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
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Antonio Di Sabatino et al.
Journal of immunology (Baltimore, Md. : 1950), 183(5), 3454-3462 (2009-08-04)
Prolonged Ca(2+) entry through Ca(2+) release-activated Ca(2+) (CRAC) channels is crucial in activating the Ca(2+)-sensitive transcription factor NFAT, which is responsible for directing T cell proliferation and cytokine gene expression. To establish whether targeting CRAC might counteract intestinal inflammation, we
Jing Li et al.
British journal of pharmacology, 164(2), 382-393 (2011-05-07)
The aim was to advance the understanding of Orai proteins and identify a specific inhibitor of the associated calcium entry mechanism in vascular smooth muscle cells (VSMCs). Proliferating VSMCs were cultured from human saphenous veins. Intracellular calcium was measured using
Siaw Wei Ng et al.
The Journal of biological chemistry, 283(46), 31348-31355 (2008-09-23)
Mast cell activation involves cross-linking of IgE receptors followed by phosphorylation of the non-receptor tyrosine kinase Syk. This results in activation of the plasma membrane-bound enzyme phospholipase Cgamma1, which hydrolyzes the minor membrane phospholipid phosphatidylinositol 4,5-bisphosphate to generate diacylglycerol and
Marjolaine Debant et al.
Journal for immunotherapy of cancer, 7(1), 111-111 (2019-04-25)
Dysregulation in calcium (Ca2+) signaling is a hallmark of chronic lymphocytic leukemia (CLL). While the role of the B cell receptor (BCR) Ca2+ pathway has been associated with disease progression, the importance of the newly described constitutive Ca2+ entry (CE)
Xuexin Zhang et al.
Cell calcium, 91, 102281-102281 (2020-09-09)
The ubiquitous Ca2+ release-activated Ca2+ (CRAC) channel is crucial to many physiological functions. Both gain and loss of CRAC function is linked to disease. While ORAI1 is a crucial subunit of CRAC channels, recent evidence suggests that ORAI2 and ORAI3
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