Flufenamic acid-d₄  (Synonyms: 氟芬那酸-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.

Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs^[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

285.25

C₁₄H₆D₄F₃NO₂

1185071-99-1

氟芬那酸-d₄；氟灭酸-d₄

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.  [Content Brief]

  [2]. Guinamard R, et al. Flufenamic acid as an ion channel modulator. Pharmacol Ther. 2013 May;138(2):272-84.  [Content Brief]

  [3]. 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.  [Content Brief]

  [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.  [Content Brief]

  [5]. 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.  [Content Brief]