Flufenamic acid

Catalog No.S4268 Batch:S426801

Technical Data

Formula

C₁₄H₁₀F₃NO₂

Molecular Weight

281.23

CAS No.

530-78-9

Solubility (25°C)*

In vitro

DMSO

56 mg/mL (199.12 mM)

Ethanol

56 mg/mL (199.12 mM)

Water

Insoluble

In vivo (Add solvents to the product individually and in order)

Clear solution

8%DMSO 1 92%Corn oil

4.0mg/ml

Taking the 1 mL working solution as an example, add 80 μL of 50 mg/ml clear DMSO stock solution to 920 μL of corn oil and mix evenly. The mixed solution should be used immediately for optimal results.

* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description	Flufenamic Acid is an anti-inflammatory agent, and also acts as an ion channel modulator.
In vitro	Flufenamic acids reversibly inhibits ICl(Ca) in Xenopus oocytes with IC50 of 28 mM, elicit in response to depolarizing voltage steps, in a dose-dependent manner, with no effect on the shape of the current-voltage curve. ^[1] Flufenamic acids blocks Ca2(+)-activated non-selective cation channels in inside-out patches from the basolateral membrane of rat exocrine pancreatic cells with IC50 of 10 μM. ^[2] Flufenamic acid binds with high affinity and negative cooperativity (pH 7.6) to wild-type (KD1=30 nM, KD2=255 nM), V30M (KD1=41 nM, KD2=320 nM) and L55P transthyretin (KD1=74 nM, KD2=682 nM), completely inhibiting amyloid fibril formation at a concentration of 10.8 μM, 3× the physiological concentration of transthyretin (3.6 μM), under conditions where transthyretin amyloid fibril formation is maximal (pH 4.4). ^[3] Flufenamic acid (viz 200 μM) produces a near complete collapse of the holding current at −50 mV, mirroring the effect of removal of extracellular Ca2+. Flufenamic acid inhibits recombinant human TRPM2 (hTRPM2) as well as currents activated by intracellular ADP-ribose in the CRI-G1 rat insulinoma cell line. Flufenamic acid antagonises ADP-ribose activated currents in the rat insulinoma cell line CRI-G1 in concentration- and pH-dependent kinetics manner. ^[4] Flufenamic acid reversibly inhibits (IC50 = 13.8 μM) DAPs and phasic firing with a similar time course in rat supraoptic neurones, but has no significant effects (P > 0.05) on membrane potential, spike threshold and input resistance, nor on the frequency and amplitude of spontaneous synaptic potentials. ^[5]

Description

Flufenamic Acid is an anti-inflammatory agent, and also acts as an ion channel modulator.

In vitro

Flufenamic acids reversibly inhibits ICl(Ca) in Xenopus oocytes with IC50 of 28 mM, elicit in response to depolarizing voltage steps, in a dose-dependent manner, with no effect on the shape of the current-voltage curve. ^[1] Flufenamic acids blocks Ca2(+)-activated non-selective cation channels in inside-out patches from the basolateral membrane of rat exocrine pancreatic cells with IC50 of 10 μM. ^[2] Flufenamic acid binds with high affinity and negative cooperativity (pH 7.6) to wild-type (KD1=30 nM, KD2=255 nM), V30M (KD1=41 nM, KD2=320 nM) and L55P transthyretin (KD1=74 nM, KD2=682 nM), completely inhibiting amyloid fibril formation at a concentration of 10.8 μM, 3× the physiological concentration of transthyretin (3.6 μM), under conditions where transthyretin amyloid fibril formation is maximal (pH 4.4). ^[3] Flufenamic acid (viz 200 μM) produces a near complete collapse of the holding current at −50 mV, mirroring the effect of removal of extracellular Ca2+. Flufenamic acid inhibits recombinant human TRPM2 (hTRPM2) as well as currents activated by intracellular ADP-ribose in the CRI-G1 rat insulinoma cell line. Flufenamic acid antagonises ADP-ribose activated currents in the rat insulinoma cell line CRI-G1 in concentration- and pH-dependent kinetics manner. ^[4] Flufenamic acid reversibly inhibits (IC50 = 13.8 μM) DAPs and phasic firing with a similar time course in rat supraoptic neurones, but has no significant effects (P > 0.05) on membrane potential, spike threshold and input resistance, nor on the frequency and amplitude of spontaneous synaptic potentials. ^[5]

Protocol (from reference)

References

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Selleck's Flufenamic acid has been cited by 2 publications

AKR1C3-dependent lipid droplet formation confers hepatocellular carcinoma cell adaptability to targeted therapy [ Theranostics, 2022, 12(18):7681-7698]	PubMed: 36451864
Palmitate induces human glomerular mesangial cells fibrosis through CD36-mediated transient receptor potential canonical channel 6/nuclear factor of activated T cell 2 activation [ Biochim Biophys Acta Mol Cell Biol Lipids, 2020, 1865(12):158793]	PubMed: 32800850

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.