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1578191-46-4

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1578191-46-4 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 1578191-46-4 includes 10 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 7 digits, 1,5,7,8,1,9 and 1 respectively; the second part has 2 digits, 4 and 6 respectively.
Calculate Digit Verification of CAS Registry Number 1578191-46:
(9*1)+(8*5)+(7*7)+(6*8)+(5*1)+(4*9)+(3*1)+(2*4)+(1*6)=204
204 % 10 = 4
So 1578191-46-4 is a valid CAS Registry Number.

1578191-46-4Downstream Products

1578191-46-4Relevant articles and documents

1-Aryl-1H- and 2-aryl-2H-1,2,3-triazole derivatives blockade P2X7 receptor in?vitro and inflammatory response in?vivo

Gonzaga, Daniel Tadeu Gomes,Ferreira, Leonardo Braga Gomes,Moreira Maramaldo Costa, Thadeu Estevam,von Ranke, Natalia Lidmar,Anastácio Furtado Pacheco, Paulo,Sposito Sim?es, Ana Paula,Arruda, Juliana Carvalho,Dantas, Luiza Pereira,de Freitas, Hércules Rezende,de Melo Reis, Ricardo Augusto,Penido, Carmen,Bello, Murilo Lamim,Castro, Helena Carla,Rodrigues, Carlos Rangel,Ferreira, Vitor Francisco,Faria, Robson Xavier,da Silva, Fernando de Carvalho

, p. 698 - 717 (2017/09/01)

Fifty-one 1,2,3-triazole derivatives were synthesized and evaluated with respect to P2X7 receptor (P2X7R) activity and its associated pore. These triazoles were screened in vitro for dye uptake assay and its cytotoxicity against mammalian cell types. Seven 1,2,3-triazole derivatives (5e, 6e, 8h, 9d, 9i, 11, and 12) potently blocked P2X7 receptor pore formation in vitro (J774.G8 cells and peritoneal macrophages). All blockers displayed IC50 value inferior to 500 nM, and they have low toxicity in either cell types. These seven selected triazoles inhibited P2X7R mediated interleukin-1 (IL-1β) release. In particular, compound 9d was the most potent P2X7R blocker. Additionally, in mouse acute models of inflammatory responses induced by ATP or carrageenan administration in the paw, compound 9d promoted a potent blocking response. Similarly, 9d also reduced mouse LPS-induced pleurisy cellularity. In silico predictions indicate this molecule appropriate to develop an anti-inflammatory agent when it was compared to commercial analogs. Electrophysiological studies suggest a competitive mechanism of action of 9d to block P2X7 receptor. Molecular docking was performed on the ATP binding site in order to observe the preferential interaction pose, indicating that binding mode of the 9d is by interacting its 1,2,3-triazole and ether moiety with positively charged residues and with its chlorobenzene moiety orientated toward the apolar end of the ATP binding site which are mainly composed by the Ile170, Trp167 and Leu309 residues from α subunit. These results highlight 9d derivative as a drug candidate with potential therapeutic application based on P2X7 receptor blockade.

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