Category: 87240-07-1

So far, in addition to halogen atoms, other non-metallic atoms can become part of the aromatic heterocycle, and the target ring system is still aromatic.Li, Yangfeng; Zhao, Jiong; Gutgesell, Lauren M.; Shen, Zhengnan; Ratia, Kiira; Dye, Katherine; Dubrovskyi, Oleksii; Zhao, Huiping; Huang, Fei; Tonetti, Debra A.; Thatcher, Gregory R. J.; Xiong, Rui researched the compound: 7-Bromo-5-nitro-1H-indole( cas:87240-07-1 ).Related Products of 87240-07-1.They published the article 《Novel Pyrrolopyridone Bromodomain and Extra-Terminal Motif (BET) Inhibitors Effective in Endocrine-Resistant ER+ Breast Cancer with Acquired Resistance to Fulvestrant and Palbociclib》 about this compound( cas:87240-07-1 ) in Journal of Medicinal Chemistry. Keywords: pyrrolopyridone bromodomain BET inhibitor preparation resistant breast cancer thrombocytopenia. We’ll tell you more about this compound (cas:87240-07-1).

Acquired resistance to fulvestrant and palbociclib is a new challenge to treatment of estrogen receptor pos. (ER+) breast cancer. ER is expressed in most resistance settings; thus, bromodomain and extra-terminal protein inhibitors (BETi) that target BET-amplified ER-mediated transcription have therapeutic potential. Novel pyrrolopyridone BETi leveraged novel interactions with L92/L94 confirmed by a cocrystal structure of 27 with BRD4. Optimization of BETi using growth inhibition in fulvestrant-resistant (MCF-7:CFR) cells was confirmed in endocrine-resistant, palbociclib-resistant, and ESR1 mutant cell lines. 27 was more potent in MCF-7:CFR cells than six BET inhibitors in clin. trials. Transcriptomic anal. differentiated 27 from the benchmark BETi, JQ-1, showing downregulation of oncogenes and upregulation of tumor suppressors and apoptosis. The therapeutic approach was validated by oral administration of 27 in orthotopic xenografts of endocrine-resistant breast cancer in monotherapy and in combination with fulvestrant. Importantly, at an equivalent dose in rats, thrombocytopenia was mitigated.

This literature about this compound(87240-07-1)Related Products of 87240-07-1has given us a lot of inspiration, and I hope that the research on this compound(7-Bromo-5-nitro-1H-indole) can be further advanced. Maybe we can get more compounds in a similar way.

Reference:
Tetrahydroisoquinoline – Wikipedia,
1,2,3,4-Tetrahydroisoquinoline | C9H11N – PubChem

So far, in addition to halogen atoms, other non-metallic atoms can become part of the aromatic heterocycle, and the target ring system is still aromatic.Li, Yangfeng; Zhao, Jiong; Gutgesell, Lauren M.; Shen, Zhengnan; Ratia, Kiira; Dye, Katherine; Dubrovskyi, Oleksii; Zhao, Huiping; Huang, Fei; Tonetti, Debra A.; Thatcher, Gregory R. J.; Xiong, Rui researched the compound: 7-Bromo-5-nitro-1H-indole( cas:87240-07-1 ).Related Products of 87240-07-1.They published the article 《Novel Pyrrolopyridone Bromodomain and Extra-Terminal Motif (BET) Inhibitors Effective in Endocrine-Resistant ER+ Breast Cancer with Acquired Resistance to Fulvestrant and Palbociclib》 about this compound( cas:87240-07-1 ) in Journal of Medicinal Chemistry. Keywords: pyrrolopyridone bromodomain BET inhibitor preparation resistant breast cancer thrombocytopenia. We’ll tell you more about this compound (cas:87240-07-1).

Acquired resistance to fulvestrant and palbociclib is a new challenge to treatment of estrogen receptor pos. (ER+) breast cancer. ER is expressed in most resistance settings; thus, bromodomain and extra-terminal protein inhibitors (BETi) that target BET-amplified ER-mediated transcription have therapeutic potential. Novel pyrrolopyridone BETi leveraged novel interactions with L92/L94 confirmed by a cocrystal structure of 27 with BRD4. Optimization of BETi using growth inhibition in fulvestrant-resistant (MCF-7:CFR) cells was confirmed in endocrine-resistant, palbociclib-resistant, and ESR1 mutant cell lines. 27 was more potent in MCF-7:CFR cells than six BET inhibitors in clin. trials. Transcriptomic anal. differentiated 27 from the benchmark BETi, JQ-1, showing downregulation of oncogenes and upregulation of tumor suppressors and apoptosis. The therapeutic approach was validated by oral administration of 27 in orthotopic xenografts of endocrine-resistant breast cancer in monotherapy and in combination with fulvestrant. Importantly, at an equivalent dose in rats, thrombocytopenia was mitigated.

This literature about this compound(87240-07-1)Related Products of 87240-07-1has given us a lot of inspiration, and I hope that the research on this compound(7-Bromo-5-nitro-1H-indole) can be further advanced. Maybe we can get more compounds in a similar way.

Reference:
Tetrahydroisoquinoline – Wikipedia,
1,2,3,4-Tetrahydroisoquinoline | C9H11N – PubChem

Application In Synthesis of 7-Bromo-5-nitro-1H-indole. Aromatic compounds can be divided into two categories: single heterocycles and fused heterocycles. Compound: 7-Bromo-5-nitro-1H-indole, is researched, Molecular C8H5BrN2O2, CAS is 87240-07-1, about Novel Pyrrolopyridone Bromodomain and Extra-Terminal Motif (BET) Inhibitors Effective in Endocrine-Resistant ER+ Breast Cancer with Acquired Resistance to Fulvestrant and Palbociclib. Author is Li, Yangfeng; Zhao, Jiong; Gutgesell, Lauren M.; Shen, Zhengnan; Ratia, Kiira; Dye, Katherine; Dubrovskyi, Oleksii; Zhao, Huiping; Huang, Fei; Tonetti, Debra A.; Thatcher, Gregory R. J.; Xiong, Rui.

Acquired resistance to fulvestrant and palbociclib is a new challenge to treatment of estrogen receptor pos. (ER+) breast cancer. ER is expressed in most resistance settings; thus, bromodomain and extra-terminal protein inhibitors (BETi) that target BET-amplified ER-mediated transcription have therapeutic potential. Novel pyrrolopyridone BETi leveraged novel interactions with L92/L94 confirmed by a cocrystal structure of 27 with BRD4. Optimization of BETi using growth inhibition in fulvestrant-resistant (MCF-7:CFR) cells was confirmed in endocrine-resistant, palbociclib-resistant, and ESR1 mutant cell lines. 27 was more potent in MCF-7:CFR cells than six BET inhibitors in clin. trials. Transcriptomic anal. differentiated 27 from the benchmark BETi, JQ-1, showing downregulation of oncogenes and upregulation of tumor suppressors and apoptosis. The therapeutic approach was validated by oral administration of 27 in orthotopic xenografts of endocrine-resistant breast cancer in monotherapy and in combination with fulvestrant. Importantly, at an equivalent dose in rats, thrombocytopenia was mitigated.

From this literature《Novel Pyrrolopyridone Bromodomain and Extra-Terminal Motif (BET) Inhibitors Effective in Endocrine-Resistant ER+ Breast Cancer with Acquired Resistance to Fulvestrant and Palbociclib》,we know some information about this compound(87240-07-1)Application In Synthesis of 7-Bromo-5-nitro-1H-indole, but this is not all information, there are many literatures related to this compound(87240-07-1).

Reference:
Tetrahydroisoquinoline – Wikipedia,
1,2,3,4-Tetrahydroisoquinoline | C9H11N – PubChem

HPLC of Formula: 87240-07-1. The mechanism of aromatic electrophilic substitution of aromatic heterocycles is consistent with that of benzene. Compound: 7-Bromo-5-nitro-1H-indole, is researched, Molecular C8H5BrN2O2, CAS is 87240-07-1, about Novel Pyrrolopyridone Bromodomain and Extra-Terminal Motif (BET) Inhibitors Effective in Endocrine-Resistant ER+ Breast Cancer with Acquired Resistance to Fulvestrant and Palbociclib. Author is Li, Yangfeng; Zhao, Jiong; Gutgesell, Lauren M.; Shen, Zhengnan; Ratia, Kiira; Dye, Katherine; Dubrovskyi, Oleksii; Zhao, Huiping; Huang, Fei; Tonetti, Debra A.; Thatcher, Gregory R. J.; Xiong, Rui.

Acquired resistance to fulvestrant and palbociclib is a new challenge to treatment of estrogen receptor pos. (ER+) breast cancer. ER is expressed in most resistance settings; thus, bromodomain and extra-terminal protein inhibitors (BETi) that target BET-amplified ER-mediated transcription have therapeutic potential. Novel pyrrolopyridone BETi leveraged novel interactions with L92/L94 confirmed by a cocrystal structure of 27 with BRD4. Optimization of BETi using growth inhibition in fulvestrant-resistant (MCF-7:CFR) cells was confirmed in endocrine-resistant, palbociclib-resistant, and ESR1 mutant cell lines. 27 was more potent in MCF-7:CFR cells than six BET inhibitors in clin. trials. Transcriptomic anal. differentiated 27 from the benchmark BETi, JQ-1, showing downregulation of oncogenes and upregulation of tumor suppressors and apoptosis. The therapeutic approach was validated by oral administration of 27 in orthotopic xenografts of endocrine-resistant breast cancer in monotherapy and in combination with fulvestrant. Importantly, at an equivalent dose in rats, thrombocytopenia was mitigated.

I hope my short article helps more people learn about this compound(7-Bromo-5-nitro-1H-indole)HPLC of Formula: 87240-07-1. Apart from the compound(87240-07-1), you can read my other articles to know other related compounds.

Reference:
Tetrahydroisoquinoline – Wikipedia,
1,2,3,4-Tetrahydroisoquinoline | C9H11N – PubChem

Most of the compounds have physiologically active properties, and their biological properties are often attributed to the heteroatoms contained in their molecules, and most of these heteroatoms also appear in cyclic structures. A Journal, Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov’t, Journal of Medicinal Chemistry called Novel Pyrrolopyridone Bromodomain and Extra-Terminal Motif (BET) Inhibitors Effective in Endocrine-Resistant ER+ Breast Cancer with Acquired Resistance to Fulvestrant and Palbociclib, Author is Li, Yangfeng; Zhao, Jiong; Gutgesell, Lauren M.; Shen, Zhengnan; Ratia, Kiira; Dye, Katherine; Dubrovskyi, Oleksii; Zhao, Huiping; Huang, Fei; Tonetti, Debra A.; Thatcher, Gregory R. J.; Xiong, Rui, which mentions a compound: 87240-07-1, SMILESS is O=[N+](C1=CC2=C(NC=C2)C(Br)=C1)[O-], Molecular C8H5BrN2O2, HPLC of Formula: 87240-07-1.

Acquired resistance to fulvestrant and palbociclib is a new challenge to treatment of estrogen receptor pos. (ER+) breast cancer. ER is expressed in most resistance settings; thus, bromodomain and extra-terminal protein inhibitors (BETi) that target BET-amplified ER-mediated transcription have therapeutic potential. Novel pyrrolopyridone BETi leveraged novel interactions with L92/L94 confirmed by a cocrystal structure of 27 with BRD4. Optimization of BETi using growth inhibition in fulvestrant-resistant (MCF-7:CFR) cells was confirmed in endocrine-resistant, palbociclib-resistant, and ESR1 mutant cell lines. 27 was more potent in MCF-7:CFR cells than six BET inhibitors in clin. trials. Transcriptomic anal. differentiated 27 from the benchmark BETi, JQ-1, showing downregulation of oncogenes and upregulation of tumor suppressors and apoptosis. The therapeutic approach was validated by oral administration of 27 in orthotopic xenografts of endocrine-resistant breast cancer in monotherapy and in combination with fulvestrant. Importantly, at an equivalent dose in rats, thrombocytopenia was mitigated.

There is still a lot of research devoted to this compound(SMILES：O=[N+](C1=CC2=C(NC=C2)C(Br)=C1)[O-])HPLC of Formula: 87240-07-1, and with the development of science, more effects of this compound(87240-07-1) can be discovered.

Reference:
Tetrahydroisoquinoline – Wikipedia,
1,2,3,4-Tetrahydroisoquinoline | C9H11N – PubChem