1241832-99-4

Upstream product

• 937798-19-1 benzyl 2-(benzyloxy)-4-nitrobenzoate 
• 100-39-0 benzyl bromide 
• 65-49-6 4-Aminosalicylic acid 

Downstream Products

• 1331747-34-2 benzyl 2-(benzyloxy)-4-((cyclohexylmethyl)amino)benzoate 
• 1361416-82-1 C₃₂H₃₈N₂O₅ 
• 1241833-13-5 C₃₄H₂₉NO₃ 
• 1241833-08-8 C₂₉H₂₄N₂O₃ 
• 1331747-35-3 benzyl 2-(benzyloxy)-4-(naphthalen-2-ylmethylamino)benzoate 
• 1241833-06-6 benzyl 2-(benzyloxy)-4-((4-bromobenzyl)amino)benzoate 
• 1241833-02-2 benzyl 4-(benzylamino)-2-(benzyloxy)benzoate 
• 1241833-19-1 benzyl 2-(benzyloxy)-4-(2-(N,4-dimethylphenylsulfonamido)acetamido)benzoate 
• 1241832-71-2 C₁₇H₁₈N₂O₆S 
• 1241833-04-4 C₂₉H₂₄N₂O₃ 
• 1241833-16-8 benzyl 2-(benzyloxy)-4-((4-cyclohexylbenzyl)amino)benzoate 
• 1241833-10-2 benzyl 2-(benzyloxy)-4-((4-(tert-butyl)benzyl)amino)benzoate 
• 1331747-33-1 C₂₈H₂₄BrNO₃ 
• 1357182-40-1 benzyl 2-(benzyloxy)-4-(N-(4-(1-((4-cyanophenyl)sulfonyl)piperidin-4-yl)benzyl)-2-(N,4-dimethylphenylsulfonamido)acetamido)benzoate 

Relevant academic research and scientific papers

Potent targeting of the STAT3 protein in brain cancer stem cells: A promising route for treating glioblastoma

The STAT3 gene is abnormally active in glioblastoma (GBM) and is a critically important mediator of tumor growth and therapeutic resistance in GBM. Thus, for poorly treated brain cancers such as gliomas, astrocytomas, and glioblastomas, which harbor constitutively activated STAT3, a STAT3-targeting therapeutic will be of significant importance. Herein, we report a most potent, small molecule, nonphosphorylated STAT3 inhibitor, 31 (SH-4-54) that strongly binds to STAT3 protein (KD = 300 nM). Inhibitor 31 potently kills glioblastoma brain cancer stem cells (BTSCs) and effectively suppresses STAT3 phosphorylation and its downstream transcriptional targets at low nM concentrations. Moreover, in vivo, 31 exhibited blood-brain barrier permeability, potently controlled glioma tumor growth, and inhibited pSTAT3 in vivo. This work, for the first time, demonstrates the power of STAT3 inhibitors for the treatment of BTSCs and validates the therapeutic efficacy of a STAT3 inhibitor for GBM clinical application.

ARYL SULFONAMIDES AS SMALL MOLECULE STAT3 INHIBITORS

The present disclosure provides pharmaceutical compositions comprising aryl sulfonamide Stat3 small molecule inhibitors and certain pharmaceutically acceptable salts thereof, and methods of their use for treating cancer.

Design, synthesis, and in?vitro evaluation of BP-1-102 analogs with modified hydrophobic fragments for STAT3 inhibition

Twelve novel analogs of STAT3 inhibitor BP-1-102 were designed and synthesised with the aim to modify hydrophobic fragments of the molecules that are important for interaction with the STAT3 SH2 domain. The cytotoxic activity of the reference and novel co

Substituted 2-hydroxy-4-(2-(phenylsulfonamido)acetamido)benzoic acid analogs as inhibitors of STAT protein

In one aspect, the invention relates to substituted 2-hydroxy-4-(2-(phenylsulfonamido)acetamido)benzoic acid analogs, derivatives thereof, and related compounds, which are useful as inhibitors of STAT protein activity; synthetic methods for making the com

2-ARYLSULFONAMIDO-N-ARYLACETAMIDE DERIVATIZED STAT3 INHIBITORS

The present disclosure provides pharmaceutical compositions comprising 2-arylsulfonamido-N-arylacetamide derivatized Stat3 inhibitors and certain pharmaceutically acceptable salts thereof, and methods of their use.

Detection of Sulfatase Enzyme Activity with a CatalyCEST MRI Contrast Agent

A chemical exchange saturation transfer (CEST) MRI contrast agent has been developed that detects sulfatase enzyme activity. The agent produces a CEST signal at δ=5.0 ppm before enzyme activity, and a second CEST signal appears at δ=9.0 ppm after the enzyme cleaves a sulfate group from the agent. The comparison of the two signals improved detection of sulfatase activity.

Identification of bidentate salicylic acid inhibitors of PTP1B

PTP1B is a master regulator in the insulin and leptin metabolic pathways. Hyper-activated PTP1B results in insulin resistance and is viewed as a key factor in the onset of type II diabetes and obesity. Moreover, inhibition of PTP1B expression in cancer cells dramatically inhibits cell growth in vitro and in vivo. Herein, we report the computationally guided optimization of a salicylic acid-based PTP1B inhibitor 6, identifying new and more potent bidentate PTP1B inhibitors, such as 20h, which exhibited a > 4-fold improvement in activity. In CHO-IR cells, 20f, 20h, and 20j suppressed PTP1B activity and restored insulin receptor phosphorylation levels. Notably, 20f, which displayed a 5-fold selectivity for PTP1B over the closely related PTPσ protein, showed no inhibition of PTP-LAR, PRL2 A/S, MKPX, or papain. Finally, 20i and 20j displayed nanomolar inhibition of PTPσ, representing interesting lead compounds for further investigation.

SULFONAMIDE COMPOUNDS AND THEIR USE AS STAT5 INHIBITORS

The present disclosure relates to compounds having the Formula (Formula (I)) which are inhibitors of STAT5.

Nanomolar-potency small molecule inhibitor of STAT5 protein

We herein report the design and synthesis of the first nanomolar binding inhibitor of STAT5 protein. Lead compound 13a, possessing a phosphotyrosyl-mimicking salicylic acid group, potently and selectively binds to STAT5 over STAT3, inhibits STAT5-SH2 doma

Nanomolar-Potency Small Molecule Inhibitor of STAT5 Protein

We herein report the design and synthesis of the first nanomolar binding inhibitor of STAT5 protein. Lead compound 13a, possessing a phosphotyrosyl-mimicking salicylic acid group, potently and selectively binds to STAT5 over STAT3, inhibits STAT5-SH2 doma