SLC-0111 - CAS 178606-66-1
Catalog number: B0084-007841
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
Molecular Weight:
Carbonic Anhydrase
SLC-0111, also known as U-104, MST-104 and NSC 213841, is a potent carbonic anhydrase (CA) inhibitor (Ki values are 4.5, 45.1, 5080 and 9640 nM for CA XII, CA IX, CA I and CA II respectively in MDA-MB-231 cells). U-104 associates with CAIX/CAXII only under hypoxic conditions in vivo, reducing extracellular acidity and resulting in significant inhibition of tumor growth and metastasis in experimental models.
Ordering Information
Catalog Number Size Price Stock Quantity
B0084-007841 50 mg $178 In stock
Bulk Inquiry
Solid powder
4-(3-(4-fluorophenyl)ureido)benzenesulfonamide; SLC-0111; SLC0111; SLC 0111; MST-104; MST-104; MST-104; NSC-213841; NSC213841; NSC 213841; U-104; U104; U 104.
Store in a cool and dry place (or refer to the Certificate of Analysis).
Melting Point:
242-243 °C
1.523±0.06 g/cm3
Canonical SMILES:
1.Association between SOX9 and CA9 in glioma, and its effects on chemosensitivity to TMZ.
Xu X;Wang Z;Liu N;Cheng Y;Jin W;Zhang P;Wang X;Yang H;Liu H;Zhang Y;Tu Y Int J Oncol. 2018 Jul;53(1):189-202. doi: 10.3892/ijo.2018.4382. Epub 2018 Apr 26.
Temozolomide (TMZ) is a standard chemotherapeutic drug used in the treatment of glioblastoma multiforme (GBM); however, resistance to this drug is common. SRY-Box 9 (SOX9) expression is associated with a poor prognosis of patients with GBM and with resistance to TMZ. Therefore, the aim of this study was to examine the effects of SOX9 inhibition on the sensitivity of glioma cells to TMZ treatment. We knocked down the expression of SOX9 (SOX9KD) via lentiviral infection in two glioblastoma (U87 and U251) cell lines, and the cells were then subjected to gene microarray, Gene Ontology and KEGG analysis pathway, all of which revealed a close association between SOX9 and the carbonic anhydrase 9 (CA9) gene. The TMZ-mediated apoptosis of glioma cells was significantly increased in the cells in the SOX9KD group. The potential underlying mechanism involved the downregulation of SOX9 and CA9 expression, which in turn decreased Akt phosphorylation, downregulated BCL‑2 expression, and upregulated BAX expression, as assessed by western blot analysis and RT-qPCR. The effects were found to be substantially enhanced in the cells in the SOX9KD group treated with TMZ. Subsequently, considering the association between SOX9 and CA9, the effects of CA9 inhibition, using a CA9 inhibitor (U‑104), on the chemosensitivity of glioma cells to TMZ were assessed.
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CAS 178606-66-1 SLC-0111

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