SML2625
RCM-1
≥98% (HPLC)
Synonym(s):
2-[[2-Oxo-2-(2-thienyl)ethyl]thio]-4,6-di-2-thienyl-3-pyridinecarbonitrile, 2-{[2-Oxo-2-(thiophen-2-yl)ethyl]sulfanyl}-4,6-di(thiophen-2-yl)pyridine-3-carbonitrile
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About This Item
Empirical Formula (Hill Notation):
C20H12N2OS4
CAS Number:
Molecular Weight:
424.58
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
SMILES string
[s]1c(ccc1)c2nc(c(c(c2)c4[s]ccc4)C#N)SCC(=O)c3[s]ccc3
InChI key
DCCYTKKDAZEVLY-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
powder
color
white to very dark orange
solubility
DMSO: 2 mg/mL, clear
storage temp.
2-8°C
Quality Level
Biochem/physiol Actions
Induces FOXM1 degradation and blocks its nuclear localization, suppresses FOXM1-mediated goblet cell metaplasia and airway hyperresponsiveness in vivo.
RCM-1 is a forkhead box M1 (FOXM1) inhibitor that blocks FOXM1 nuclear localization (IC50 = 720 nM using GFP-FOXM1-expressing U2OS cells) and causes FOXM1 degradation via ubiquitination induction (2.9- and 4.8-fold of basal level in A549 cells with 10 μM or 20 μM RCM-1, respectively) without affecting cellular YAP, FACT140, NF-κB, FOXA2, and FOXJ1 levels. RCM-1 intraperitoneal injection (1.7 mg/kg) in mice downregulates endogenous murine FOXM1 level as well as transgenic human FOXM1 GFP fusion level in vivo, effectively suppressing house dust mite-induced lung inflammation as well as goblet cell metaplasia and airway hyperresponsiveness in response to IL-13.
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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Gaohui Wu et al.
Biochemical and biophysical research communications, 495(1), 1432-1439 (2017-11-22)
Functional abnormal airway epithelial cells, along with activated inflammatory cells, resulting in chronic airway inflammation, are considered as the characteristic of asthma. Fatty Acid Binding Protein 4 (FABP4) takes part in glucose and lipid homeostasis, and also have an important
Lifeng Sun et al.
Science signaling, 10(475) (2017-04-20)
Goblet cell metaplasia and excessive mucus secretion associated with asthma, cystic fibrosis, and chronic obstructive pulmonary disease contribute to morbidity and mortality worldwide. We performed a high-throughput screen to identify small molecules targeting a transcriptional network critical for the differentiation
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