Flufenamic acid-d4

Flufenamic acid-d4 is deuterium labeled Flufenamic acid. Flufenamic acid is a non-steroidal anti-inflammatory agent, inhibits cyclooxygenase (COX), activates AMPK, and also modulates ion channels, blocking chloride channels and L-type Ca2+ channels, modulating non-selective cation channels (NSC), activating K+ channels. Flufenamic acid binds to the central pocket of TEAD2 YBD and inhibits both TEAD function and TEAD-YAP-dependent processes, such as cell migration and proliferation.

Product Specifications

CAS Number

[1185071-99-1]

UNSPSC

12352005

Hazard Statement

H302-H315-H319-H335

Target

AMPK; Calcium Channel; Chloride Channel; COX; Isotope-Labeled Compounds; Parasite; Potassium Channel

Type

Isotope-Labeled Compounds

Related Pathways

Anti-infection; Epigenetics; Immunology/Inflammation; Membrane Transporter/Ion Channel; Neuronal Signaling; Others; PI3K/Akt/mTOR

Applications

COVID-19-immunoregulation

Field of Research

Inflammation/Immunology

Solubility

10 mM in DMSO

Smiles

OC(C(C([2H])=C([2H])C([2H])=C1[2H])=C1NC2=CC(C(F)(F)F)=CC=C2)=O

Molecular Formula

C14H6D4F3NO2

Molecular Weight

285.25

Precautions

P261-P264-P270-P271-P280-P302+P352-P304+P340-P305+P351+P338-P330-P362+P364-P403+P233-P405-P501

References & Citations

[1]Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53 (2) :211-216.|[2]Guinamard R, et al. Flufenamic acid as an ion channel modulator. Pharmacol Ther. 2013 May;138 (2) :272-84.|[3]Pobbati AV, et al. Targeting the Central Pocket in Human Transcription Factor TEAD as a Potential Cancer Therapeutic Strategy. Structure. 2015;23 (11) :2076-2086.|[4]Pongkorpsakol P, et al. Cellular mechanisms underlying the inhibitory effect of flufenamic acid on chloride secretion in human intestinal epithelial cells. J Pharmacol Sci. 2017 Jun;134 (2) :93-100.|[5]Pongkorpsakol P, et al. Flufenamic acid protects against intestinal fluid secretion and barrier leakage in a mouse model of Vibrio cholerae infection through NF-κB inhibition and AMPK activation. Eur J Pharmacol. 2017 Mar 5;798:94-104.