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116686-15-8

中文名稱 N-[4-乙?;?2-(2,4-二氟苯氧基)苯基]-甲烷磺酰胺
英文名稱 FK-3311
CAS 116686-15-8
分子式 C15H13F2NO4S
分子量 341.33
MOL 文件 116686-15-8.mol
更新日期 2024/12/24 22:33:51
116686-15-8 結(jié)構(gòu)式 116686-15-8 結(jié)構(gòu)式

基本信息

中文別名
N-[4-乙?;?2-(2,4-二氟苯氧基)苯基]-甲烷磺酰胺
英文別名
FK-3311
CS-1073
FK-3311
FK3311
COX-2 Inhibitor V
COX-2 Inhibitor V, FK3311
N-[4-Acetyl-2-(2,4-difluorophenoxy)phenyl]methanesulfonamide
Methanesulfonamide, N-[4-acetyl-2-(2,4-difluorophenoxy)phenyl]-
N-[4-Acetyl-2-(2,4-difluorophenoxy)phenyl]-methanesulfonamide FK3311
所屬類別
生物化工:激動劑抑制劑

物理化學性質(zhì)

沸點431.3±55.0 °C(Predicted)
密度1.419±0.06 g/cm3(Predicted)
儲存條件Store at RT
溶解度Soluble in DMSO
酸度系數(shù)(pKa)6.82±0.10(Predicted)
形態(tài)白色固體
顏色Light yellow to yellow

常見問題列表

生物活性
FK-3311 (COX-2 Inhibitor V)是選擇性的、細胞可滲透的、口服 cyclooxygenase-2 (COX-2) 抑制劑,具有抗炎作用。FK-3311 可通過顯著抑制 TxA2 來對肝熱性缺血再灌注損傷起到保護作用。
靶點
TargetValue
COX-2
()
TxA2
()
體外研究

Cyclooxygenase (COX) is an intracellular enzyme that converts arachidonic acid into prostaglandin (PG)G2 and PGH2.
The racemic mixtures and the (R)- and (S)-isomers of the 2 metabolites were inactive in the PGE2 test. IC50 values were more than 100 uM for (2 and 5), compared to 1.6 uM for FK 3311 (COX-2 Inhibitor V). Antiinflammatory activity was assessed by inhibition of adjuvant-induced arthritis, and analgesic activity was determined in the acetic acid-induced writhing assay. Following p.o. administration of 10 mg/kg, racemic (2) and its optical isomers showed activity comparable to FK-3311 (76% inhibition) in the adjuvant arthritis test, whereas racemic (5) showed very weak activity, and (R)- and (S)-(5) were not tested. With regard to analgesic effects, FK-3311 and racemic (2) showed 81 and 62% inhibitions, respectively, at a dose of 100 mg/kg p.o. The (R)- and (S)-isomers of (2) and racemic (5) all showed 46% inhibition of writhing syndrome. (R)- and (S)-(5) were less active showing 16 and 20% inhibitions, respectively.

體內(nèi)研究

L-PVR, CO, PaO(2), and WDR were significantly better in the FK group than in the control group. Histological tissue edema was mild, and PMN infiltration was significantly reduced in the FK group compared to the control group. The serum TxB(2) levels were significantly lower in the FK group than in the control group, while 6-keto-PGF(1alpha) levels were not significantly reduced. Two-day survival rate was significantly better in the FK group than in the control group.
Survival rate was significantly better and serum GOT levels 30 min after reperfusion were significantly lower in the FK high-dose group compared to the other two groups. Four hours after reperfusion, GPT levels and liver tissue flow were significantly better in the FK high-dose group compared to the control. Both 30 min and 4 hr after reperfusion, serum TxB(2) levels were significantly lower in the FK high-dose group compared to the control.

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