SML2382
SC75741
≥97% (HPLC)
别名:
4SC-301, N-(5-Benzoyl-1H-benzimidazol-2-yl)-2-(1-thieno[3,2-d]pyrimidin-4-yl-4-piperidinyl)-4-thiazolecarboxamide, N-(6-Benzoyl-1H-benzimidazol-2-yl)-2-(1-thieno[3,2-d]pyrimidin-4-yl-4-piperidinyl)-4-thiazolecarboxamide, SC 75741, V1810
产品名称
SC75741, ≥97% (HPLC)
InChI
1S/C29H23N7O2S2/c37-24(17-4-2-1-3-5-17)19-6-7-20-22(14-19)34-29(33-20)35-27(38)23-15-40-28(32-23)18-8-11-36(12-9-18)26-25-21(10-13-39-25)30-16-31-26/h1-7,10,13-16,18H,8-9,11-12H2,(H2,33,34,35,38)
InChI key
QNZVBFMXWNWVKG-UHFFFAOYSA-N
SMILES string
O=C(C1=CSC(C2CCN(C3=C4C(C=CS4)=NC=N3)CC2)=N1)NC5=NC6=CC(C(C7=CC=CC=C7)=O)=CC=C6N5
assay
≥97% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
storage temp.
2-8°C
Biochem/physiol Actions
NF-κB p65 subunit (RelA) DNA-binding inhibitor that effectively blocks influenza virus propagation both in cultures and in mice in vivo.
SC75741 (4SC-301; V1810) is a potent NF-kappaB (NF-κB) inhibitor (IC50 = 200 nM against 10 ng/mL TNF-α-induced NF-κB reporter gene expression in A549 cells) that impairs p65 subunit (RelA) DNA-binding activity without affecting p65 phosphorylation or nuclear translocation, nor proteasome-mediated IκBα degradation. SC75741 induces apoptosis in multiple myeloma cultures (IC50 from 5 to 12 μM in 48 hrs; OPM2, U266, NCI-H929, RPMI-8226), but not PBMCs (89% viability post 4-hr 100 μM SC75741 treatment). NF-κB inhibition by SC75741 treatment is reported to effectively block influenza virus propagation both in cultures in vitro (1-5 μM) and in mice in vivo (5 mg/kg daily i.v. or 7.5-15 mg/kg twice a day i.p.).
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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Christina Ehrhardt et al.
Cellular microbiology, 15(7), 1198-1211 (2013-01-17)
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Johann Leban et al.
Bioorganic & medicinal chemistry letters, 17(21), 5858-5862 (2007-09-18)
A novel class of NF-kappaB pathway signaling inhibitors was discovered by virtual screening, medicinal chemistry, and QSAR analysis. An initial set of compounds inhibited NF-kappaB signaling in a whole cell reporter gene assay in the micro-molar range. Activity was improved
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Felix G Meinel et al.
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Evidence is increasing that aberrant NF-kappaB activation is crucial for multiple myeloma pathophysiology and a promising target for new antimyeloma therapies. In this study, we assessed the in vitro antimyeloma activity of the novel NF-kappaB inhibitor V1810. Pharmacokinetics and toxicity
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