1192-79-6Relevant articles and documents
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Lightner,Park
, p. 463,465,468 (1979)
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Chemical synthesis of a 'GSA-pyrrole' and its reaction with Ehrlich's reagent
Liddell,Forsyth,Senge,Smith
, p. 1343 - 1350 (1993)
A rational chemical synthesis of 4-acetyl-2-(2-carboxyethyl)-5-methylpyrrole (5), the product formed when glutamate-1-semialdehyde (GSA, 2) is reacted with acetylacetone in the first step of the quantitative analysis for GSA in biological media. Rates of reaction of the GSA-pyrrole (5) with Ehrlich's reagent (the second step in GSA quantitation) are compared with the rates of the reactions of well-characterized 'ALA-pyrroles' (3) and (4). Pyrrole (5) reacts more slowly with Ehrlich's reagent, and extinction coefficients for the corresponding Ehrlich's adducts were determined to be 46,000 for (3) and 865 for (5). These observations resolve the discrepancies observed in earlier quantitations of GSA and allow more accurate determinations of it in biological materials.
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Marion et al.
, p. 1509 (1967)
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Discovery of 1-(5-(1H-benzo[d]imidazole-2-yl)-2,4-dimethyl-1H-pyrrol-3-yl)ethan-1-one derivatives as novel and potent bromodomain and extra-terminal (BET) inhibitors with anticancer efficacy
Bian, Yuanyuan,Chen, Yadong,Hong, Qianqian,Jiang, Fei,Kong, Bo,Li, Hongmei,Lu, Tao,Ma, Yu,Ran, Ting,Tang, Weifang,Wang, Cong,Yang, Na,Zhang, Zhimin,Zheng, Wan,Zhu, Jiapeng,Zhu, Zhaohong
, (2021/11/03)
As epigenetic readers, bromodomain and extra-terminal domain (BET) family proteins bind to acetylated-lysine residues in histones and recruit protein complexes to promote transcription initiation and elongation. Inhibition of BET bromodomains by small molecule inhibitors has emerged as a promising therapeutic strategy for cancer. Herein, we describe our efforts toward the discovery of a novel series of 1-(5-(1H-benzo[d]imidazole-2-yl)-2,4-dimethyl-1H-pyrrol-3-yl)ethan-1-one derivatives as BET inhibitors. Intensive structural modifications led to the identification of compound 35f as the most active inhibitor of BET BRD4 with selectivity against BET family proteins. Further biological studies revealed that compound 35f can arrest the cell cycle in G0/G1 phase and induce apoptosis via decreasing the expression of c-Myc and other proteins related to cell cycle and apoptosis. More importantly, compound 35f showed favorable pharmacokinetic properties and antitumor efficacy in MV4-11 mouse xenograft model with acceptable tolerability. These results indicated that BET inhibitors could be potentially used to treat hematologic malignancies and some solid tumors.
PYRROLOTRIAZINONES AND IMIDAZOTRIAZINONES AS UBIQUITIN-SPECIFIC PROTEASE 7 INHIBITORS
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Paragraph 0606, (2016/07/27)
The invention relates to inhibitors of USP7 inhibitors useful in the treatment of cancers, neurodegenerative diseases, immunological disorders, inflammatory disorders, cardiovascular diseases, ischemic diseases, viral infections and diseases, and bacterial infections and diseases, having the Formula: where R1, R2, R3, R4, R5, R5′, R6, X1, X2, m, and n are described herein.
Photoinduced cytotoxicity and thioadduct formation by a prodigiosin analogue
Tomlinson, John T.,Park, Gyungse,Misenheimer, Jacob A.,Kucera, Gregory L.,Hesp, Kevin,Manderville, Richard A.
, p. 4951 - 4954 (2007/10/03)
(Chemical Equation Presented) The prodigiosin alkaloid 1 and the synthetic analogue 2 show photoinduced cytotoxicity against HL-60 cancer cells. Photoirradiation of 1 and 2 causes photofading, photooxidation, and thioadduct formation. These results provide a model for the redox properties of prodigiosins that play a role in their biological activity and provide a new way to functionalize their pyrromethene entity with water-soluble thiol groups.
