n-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide has been researched along with Protein Aggregation, Pathological in 2 studies
N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide: structure given in first source
NS-398 : A C-nitro compound that is N-methylsulfonyl-4-nitroaniline bearing an additional cyclohexyloxy substituent at position 2.
Protein Aggregation, Pathological: A biochemical phenomenon in which misfolded proteins aggregate either intra- or extracellularly. Triggered by factors such as MUTATION; POST-TRANSLATIONAL MODIFICATIONS, and environmental stress, it is generally associated with ALZHEIMER DISEASE; PARKINSON DISEASE; HUNTINGTON DISEASE; and TYPE 2 DIABETES MELLITUS.
Excerpt | Relevance | Reference |
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"To evaluate their potential use against Alzheimer's disease, in vitro evaluation of β-amyloid fibril formation using Aβ(1-40) and Aβ(1-42) peptides was performed." | 1.42 | 1,2-Diaryl-2-hydroxyiminoethanones as dual COX-1 and β-amyloid aggregation inhibitors: biological evaluation and in silico study. ( Ahangar, N; Ahmadnejad, M; Dadashpour, S; Emami, S; Irannejad, H; Ozadali, K; Tuylu Kucukkilinc, T; Unsal Tan, O, 2015) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 0 (0.00) | 18.7374 |
1990's | 0 (0.00) | 18.2507 |
2000's | 0 (0.00) | 29.6817 |
2010's | 2 (100.00) | 24.3611 |
2020's | 0 (0.00) | 2.80 |
Authors | Studies |
---|---|
Irannejad, H | 1 |
Unsal Tan, O | 1 |
Ozadali, K | 1 |
Dadashpour, S | 1 |
Tuylu Kucukkilinc, T | 1 |
Ahangar, N | 1 |
Ahmadnejad, M | 1 |
Emami, S | 1 |
Wang, P | 1 |
Guan, PP | 1 |
Yu, X | 1 |
Zhang, LC | 1 |
Su, YN | 1 |
Wang, ZY | 1 |
2 other studies available for n-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide and Protein Aggregation, Pathological
Article | Year |
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1,2-Diaryl-2-hydroxyiminoethanones as dual COX-1 and β-amyloid aggregation inhibitors: biological evaluation and in silico study.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Anti-Inflammatory Agents; Cyclooxygenase 1; Cyclo | 2015 |
Prostaglandin I₂ Attenuates Prostaglandin E₂-Stimulated Expression of Interferon γ in a β-Amyloid Protein- and NF-κB-Dependent Mechanism.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Astrocytes; Brain; Cell Nucleus; Dinoprostone; Di | 2016 |