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1 thesis of the nonsteroidal anti-inflammatory diflunisal.
2 zation by the potential therapeutic compound diflunisal.
3 n applied to a highly efficient synthesis of diflunisal.
4                      However, with the drugs diflunisal (1) or Tafamidis (2), an analogous chaperonin
5 ain III of human serum albumin (HSA-III) and diflunisal, a cyclooxygenase inhibitor with antiinflamma
6                          Among those tested, diflunisal, a salicylate derivative not previously ident
7                                 Analogues of diflunisal, an FDA-approved nonsteroidal antiinflammator
8 -derived binding constants were obtained for diflunisal and closely related analogues to develop a st
9                      TTR protein stabilisers diflunisal and tafamidis can delay the progression of th
10 e pharmaceutical ingredient for sitagliptin, diflunisal, and other pharmaceutically important molecul
11  studies indicate that the aromatic rings of diflunisal are involved in extensive and specific intera
12 50)) values 1 order of magnitude better than diflunisal at 1.32 +/- 0.07 muM (22) and 3.10 +/- 0.11 m
13 50)) values 1 order of magnitude better than diflunisal at 1.32 0.07 uM (22) and 3.10 0.11 uM (20), r
14                     The results suggest that diflunisal derivatives have the potential to modulate NA
15                    Moreover, two synthesized diflunisal derivatives showed half-maximal inhibitory co
16                    Moreover, two synthesized diflunisal derivatives showed half-maximal inhibitory co
17 ceiving the p300/CBP inhibitors salsalate or diflunisal exhibit decreased incidence of AD and clinica
18                       The carboxylic acid of diflunisal forms electrostatic interactions with the pro
19 inity for TTR was unchanged by halogenation, diflunisal gradually improves binding up to 1 order of m
20 ke peptide 1 (GLP-1) was functionalized with diflunisal, indomethacin, or both.
21 armacological chaperones, Tafamidis((R)) and diflunisal, inhibit TTR misfolding by stabilizing native
22                                              Diflunisal itself appears to occupy both orientations ba
23 ave a K(i) of 34 muM, well below peak plasma diflunisal levels reached at typical dosage levels.
24          The complex structure of ACMSD with diflunisal revealed a previously unknown ligand-binding
25 and Drug Administration (FDA)-approved drug, diflunisal, was found to competitively inhibit ACMSD.