Flufenamic Acid is aCOX inhibitor and prevents formation of prostaglandins, binds to and reduce the activity of prostaglandin F synthase and activate TRPC6, it is a NSAID drug.
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There will be a HazMat fee per item when shipping a dangerous goods. The HazMat fee will be charged to your UPS/DHL/FedEx collect account or added to the invoice unless the package is shipped via Ground service. Ship by air in Excepted Quantity (each bottle), which is up to 1g/1mL for class 6.1 packing group I or II, and up to 25g/25ml for all other HazMat items.
Type
HazMat fee for 500 gram (Estimated)
Excepted Quantity
USD 0.00
Limited Quantity
USD 15-60
Inaccessible (Haz class 6.1), Domestic
USD 80+
Inaccessible (Haz class 6.1), International
USD 150+
Accessible (Haz class 3, 4, 5 or 8), Domestic
USD 100+
Accessible (Haz class 3, 4, 5 or 8), International
Flufenamic acid is a non-steroidal anti-inflammatory agent, inhibits cyclooxygenase (COX), and also modulates ion channels, blocking chloride channels and L-type Ca2+ channels, modulating non-selective cation channels (NSC), activating K+ channels. Flufenamic acid inhibits a wide spectrum of TRP channels, including: C3, C7, M2, M3, M4, M5, M7, M8, V1, V3, and V4 but activates at least two TRP channels (C6 and A1)[3]. Flufenamic acid (FFA) has previously been demonstrated to be a potent activator of AMP-activated protein kinase (AMPK), which is a negative regulator of NF-κB signaling. In a mouse closed loop model of EL infection, FFA treatment (20mg/kg) significantly abrogated EL-induced intestinal fluid secretion and barrier disruption. In addition, FFA suppressed NF-κB nuclear translocation and expression of proinflammatory mediators and promoted AMPK phosphorylation in the EL-infected mouse intestine. Furthermore, FFA promoted tight junction assembly and prevented interferon gamma (IFN-γ)-induced barrier disruption in an AMPK-dependent manner[4]. FFA inhibited cAMP-dependent Cl- secretion in T84 cell monolayers with IC50 of ∼8 μM. FFA inhibited Ca2+-dependent Cl- secretion with IC50 of ∼10 μM. FFA inhibited activities of Ca2+-activated Cl- channels and KCa3.1, a Ca2+-activated basolateral K+ channels, but had no effect on activities of Na+-K+-Cl- cotransporters and Na+-K+ ATPases[5].
Hong Kong
... 展开 >> Ivan Hung
Recruiting
Hong Kong, Hong Kong
Contact: Ivan FN Hung, MD FRCP 852 22554049 ivanfn@gmail.com
Sub-Investigator: Kelvin To, MD FRCPath
Sub-Investigator: KY Yuen, MD FRCPath 收起 <<
Hong Kong
... 展开 >> Ivan Hung
Recruiting
Hong Kong, Hong Kong
Contact: Ivan FN Hung, MD FRCP 852 22554049 ivanfn@gmail.com
Sub-Investigator: Kelvin To, MD FRCPath
Sub-Investigator: KY Yuen, MD FRCPath 收起 <<
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