SML1726
MSAB
≥95% (HPLC)
Synonym(s):
3-[[(4-Methylphenyl)sulfonyl]amino]-benzoic acid methyl ester, Methyl 3-{[(4-methylphenyl)sulfonyl]amino}benzoate, WI-21
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About This Item
Quality Level
Assay
≥95% (HPLC)
form
powder
color
off-white to purple
solubility
DMSO: 25 mg/mL, clear
storage temp.
2-8°C
SMILES string
CC1=CC=C(S(NC2=CC(C(OC)=O)=CC=C2)(=O)=O)C=C1
Biochem/physiol Actions
A cell-permeable compound that targets β-catenin via direct affinity interaction within the C-terminal two thirds (a.a. 301-670) of the Armadillo repeat region (a.a. 136–686), inducing β-catenin ubiquitination and proteasomal degradation (Eff. conc. 1.25-5 μM in DLD-1, SW480 and LS174T cultures). MSAB selectively inhibits against Wnt sginaling-dependent proliferation of cancer cells (IC50 <6 μM), while exhibiting little efficacy in Wnt-independent cultures (<10% inhibition at 10 μM). Likewise, daily intraperitoneal injection (10-20 mg/kg/day) is efficacious in suppressing the expansion of established tumors from HCT116, HT115, and H23 xenografts in mice, while exhibiting little efficacy against the Wnt-independent H460 tumor growth.
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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International journal of molecular sciences, 23(16) (2022-08-27)
Zinc finger protein with KRAB and SCAN domains 3 (ZKSCAN3) acts as an oncogenic transcription factor in human malignant tumors, including colon and prostate cancer. However, most of the ZKSCAN3-induced carcinogenic mechanisms remain unknown. In this study, we identified ZKSCAN3
Molecular cancer research : MCR, 17(11), 2154-2168 (2019-08-10)
The incidence of treatment-related neuroendocrine prostate cancer (t-NEPC) is rising as more potent drugs targeting the androgen signaling axis are clinically implemented. Neuroendocrine transdifferentiation (NEtD), an putative initial step in t-NEPC development, is induced by androgen-deprivation therapy (ADT) or anti-androgens
Cell reports, 30(7), 2055-2064 (2020-02-23)
Mechanisms underpinning airway epithelial homeostatic maintenance and ways to prevent its dysregulation remain elusive. Herein, we identify that β-catenin phosphorylated at Y489 (p-β-cateninY489) emerges during human squamous lung cancer progression. This led us to develop a model of airway basal
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