| Identification | Back Directory | [Name]
C188-9 | [CAS]
432001-19-9 | [Synonyms]
C188-9
TTI-101
F0808-0084
C 188-9;C-188-9;C-1889;C1889;C 1889;C-1889;F0808-0084
C188-9; C 188-9; C-188-9; C-1889; C1889; C 1889; C-1889; F0808-0084
N-(1',2-dihydroxy-1.2'-binaphthhalen-4'-yl)-4-methoxybenzene-sulphonamide
Benzenesulfonamide, N-(1',2-dihydroxy[1,2'-binaphthalen]-4'-yl)-4-methoxy- | [Molecular Formula]
C27H21NO5S | [MDL Number]
MFCD03141581 | [MOL File]
432001-19-9.mol | [Molecular Weight]
471.52 |
| Chemical Properties | Back Directory | [Boiling point ]
680.9±65.0 °C(Predicted) | [density ]
1.416±0.06 g/cm3(Predicted) | [storage temp. ]
Inert atmosphere,2-8°C | [solubility ]
DMF: 10 mg/ml; DMSO: 10 mg/ml; DMSO:PBS (pH 7.2) (1:5): 0.16 mg/ml | [form ]
A crystalline solid | [pka]
8.14±0.50(Predicted) | [color ]
Off-white to pink |
| Hazard Information | Back Directory | [Uses]
C188-9 (TTI-101) is a STAT3 inhibitor, with a Kd of 4.7 nM. C188-9 inhibits G-CSF-induced STAT3 activation and STAT3-dependent gene expression. C188-9 induces apoptosis in AML cell lines and primary samples and inhibits colony formation by primary AML blasts[1][2][3][4]. | [Biological Activity]
C188-9 (TTI 101) is a potent STAT3 inhibitor, binds STAT3 with high affinity, Kd=4.7±0.4 nM. It is well tolerated in mice, has good oral bioavailability, and is mainly enriched in tumor tissues. | [in vitro]
C188-9 is a small molecule inhibitor of STAT3, targeting the phosphotyrosine peptide binding site in the SH2 region of STAT3 with a Ki value of 136 nM. It does not inhibit upstream Jak or Src kinases. | [in vivo]
C188-9 inhibited tumor growth in mice bearing UM-SCC-17B xenografts after administration of C188-9. C188-9 was well tolerated in mice, had good oral bioavailability, and was concentrated in tumor tissue after administration. | [target]
| Target | Value | STAT3
(Cell-free) | 4.7 nM(Kd) |
| [IC 50]
STAT3: 4.7 nM (Kd) | [storage]
4°C, protect from light | [References]
[1] Silva KA, et al. Inhibition of Stat3 activation suppresses caspase-3 and the ubiquitin-proteasome system, leading to preservation of muscle mass in cancer cachexia. J Biol Chem. 2015 Apr 24;290(17):11177-87. DOI:10.1074/jbc.M115.641514
[2] Redell MS, et al. Stat3 signaling in acute myeloid leukemia: ligand-dependent and -independent activation and induction of apoptosis by a novel small-molecule Stat3 inhibitor. Blood. 2011 May 26;117(21):5701-9. DOI:10.1182/blood-2010-04-280123
[3] Bharadwaj U, et al. Small-molecule inhibition of STAT3 in radioresistant head and neck squamous cell carcinoma. Oncotarget. 2016 May 3;7(18):26307-30. DOI:10.18632/oncotarget.8368
[4] Redell MS, et al. Stat3 signaling in acute myeloid leukemia: ligand-dependent and -independent activation and induction of apoptosis by a novel small-molecule Stat3 inhibitor. Blood. 2011;117(21):5701-5709. DOI:10.1182/blood-2010-04-280123 |
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