X4753
XCT790
≥98% (HPLC), solid
Sinônimo(s):
3-[4-(2,4-Bis-trifluoromethylbenzyloxy)-3-methoxyphenyl]-2-cyano-N-(5-trifluoromethyl-1,3,4-thiadiazol-2-yl)acrylamide
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About This Item
Fórmula empírica (Notação de Hill):
C23H13F9N4O3S
Número CAS:
Peso molecular:
596.42
Número MDL:
Código UNSPSC:
12352202
ID de substância PubChem:
NACRES:
NA.77
Produtos recomendados
Nível de qualidade
Ensaio
≥98% (HPLC)
Formulário
solid
cor
yellow
solubilidade
DMSO: ≥10 mg/mL
temperatura de armazenamento
2-8°C
cadeia de caracteres SMILES
COc1cc(ccc1OCc2ccc(cc2C(F)(F)F)C(F)(F)F)\C=C(/C#N)C(=O)Nc3nnc(s3)C(F)(F)F
InChI
1S/C23H13F9N4O3S/c1-38-17-7-11(6-13(9-33)18(37)34-20-36-35-19(40-20)23(30,31)32)2-5-16(17)39-10-12-3-4-14(21(24,25)26)8-15(12)22(27,28)29/h2-8H,10H2,1H3,(H,34,36,37)/b13-6+
chave InChI
HQFNFOOGGLSBBT-AWNIVKPZSA-N
Aplicação
XCT790 has been used:
- as an estrogen-related receptor (ERR)α inverse agonist in C2C12 myotubes
- as an estrogen-related receptor (ERR)α inverse agonist to elucidate decidualization functionality of ERRα in endometrial embryonic stem cells
- as an autophagy inducer in human neuroblastoma SH-SY5Y and HeLa cell lines.
Ações bioquímicas/fisiológicas
XCT 790 is a 5′adenosine monophosphate-activated protein kinase (AMPK) activator. It also acts as a proton ionophore and an uncoupler of oxidative phosphorylation in mitochondria. XCT790 impairs vascular endothelial growth factor (VEGF) and angiopoietin 2 (Ang-2) expression and exhibits suppression of endometrial tumor via estrogen-related receptor (ERRα) inhibition. XCT790 mediates cell cycle arrest and favors apoptosis in triple-negative breast cancer (TNBC).
XCT790 is a potent and specific inverse agonist of ERRα. Selective; showing no significant antagonist activity on related nuclear receptors, such as ERRγ or ERα at concentrations below 10 μM.
XCT790 is a potent and specific inverse agonist of ERRα. XCT790 is selective; showing no significant antagonist activity on related nuclear receptors, such as ERRγ or ERα at concentrations below 10 μM. XCT790 inhibits the constitutive activity of ERRα in both biochemical and cell-based assays. The IC50 value is 300-500 nM in transient transfection assays using GAL4-ERR LBD or full-length ERR with the mSHP promoter.
Frases de perigo
Declarações de precaução
Classificações de perigo
Aquatic Chronic 4
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
Equipamento de proteção individual
Eyeshields, Gloves, type N95 (US)
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G Vargas et al.
Oncogene, 38(7), 950-964 (2018-11-28)
Bone is the most common metastatic site for breast cancer. Estrogen-related-receptor alpha (ERRα) has been implicated in cancer cell invasiveness. Here, we established that ERRα promotes spontaneous metastatic dissemination of breast cancer cells from primary mammary tumors to the skeleton.
Banu Eskiocak et al.
Biochemistry, 53(29), 4839-4846 (2014-07-08)
XCT 790 is widely used to inhibit estrogen-related receptor α (ERRα) activity as an inverse agonist. Here, we report that XCT 790 potently activates AMP kinase (AMPK) in a dose-dependent and ERRα-independent manner, with active concentrations more than 25-fold below
Sin-Aye Park et al.
British journal of cancer, 123(6), 988-999 (2020-06-24)
Gremlin-1 (GREM1), one of the bone morphogenetic protein antagonists, is involved in organogenesis, tissue differentiation and kidney development. However, the role of GREM1 in cancer progression and its underlying mechanisms remain poorly understood. The role of GREM1 in breast cancer
LiLi Chen et al.
Aging, 12(17), 16963-16980 (2020-09-14)
PGC-1α and ERRα are closely related to tumor formation and progression. However, the mechanism underlying the involvement of PGC-1α/ERRα in regulating invasion and migration in endometrial cancer remains to be explored. Elevated levels of PGC-1α and ERRα were associated with
Zhenyu Xu et al.
Theranostics, 10(9), 4201-4216 (2020-04-01)
Enhanced intratumoral androgen biosynthesis and persistent androgen receptor (AR) signaling are key factors responsible for the relapse growth of castration-resistant prostate cancer (CRPC). Residual intraprostatic androgens can be produced by de novo synthesis of androgens from cholesterol or conversion from
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