CAS 13710-19-5 Tolfenamic acid - Analytical Products / Alfa Chemistry

CAT	APS13710195
CAS	13710-19-5
Structure
MDL Number	MFCD00133865
Synonyms	Tolfenamic acid, N-(3-Chlor-o-tolyl)-anthranilsäure, 2-[(3-Chloro-2-methylphenyl)amino]benzoic acid
IUPAC Name	2-(3-chloro-2-methylanilino)benzoic acid
Molecular Weight	261.70
Molecular Formula	C14H12ClNO2
EC Number	237-264-3
Canonical SMILES	Cc1c(Cl)cccc1Nc2ccccc2C(=O)O
InChI	InChI=1S/C14H12ClNO2/c1-9-11(15)6-4-8-12(9)16-13-7-3-2-5-10(13)14(17)18/h2-8,16H,1H3,(H,17,18)
InChI Key	YEZNLOUZAIOMLT-UHFFFAOYSA-N

Accurate Mass	261.0557
Format	Neat

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Case Study

Tolfenamic Acid Inhibits Cytochrome P450 2E1 Expression in Mouse Liver

Shukoor, Mohammed I., et al. Integrative Biology 4.9 (2012): 1122-1129.

Non-steroidal anti-inflammatory drugs (NSAIDs) play an important role in the chemoprevention of cancer. Recently, a specific NSAID, 2-[(3-chloro-2-methylphenyl)amino]benzoic acid, known as tolfenamic acid (TA), demonstrated chemopreventive effects in rat esophageal tumors induced by N-nitrosomethylbenzylamine (NMBA). Preclinical studies indicate that TA inhibits specific protein (Sp) transcription factors and acts as an anticancer agent in several cancer models; however, the relevant mechanisms of its chemopreventive response in esophageal cancer remain unclear.
Given the critical role of cytochrome P450 (CYP) in the bioactivation of carcinogens in cancer induction, the effects of TA on key CYP isoenzymes in mouse liver samples were investigated. Athymic nude mice were treated with either vehicle (corn oil) or TA (50 mg/kg, three times a week) for 4 weeks. Protein extracts (whole-cell lysates and microsomal fractions) were prepared from liver tissue and analyzed by Western blotting to determine the expression of various CYP isoenzymes. Sprague-Dawley rat liver was harvested, and primary hepatocyte cultures were treated with either vehicle (DMSO) or TA (50 μM), with cell viability assessed at 2 and 5 days post-treatment.
TA treatment resulted in a significant decrease in CYP2E1 expression in liver lysates and subcellular fractions, with minimal effects on other tested isoenzymes. TA did not affect the body weight of the animals (mice) or the viability of rat hepatocytes. These results indicate that TA regulates the expression of CYP2E1, which is associated with carcinogen bioactivation, without causing significant toxicity. The data suggest that TA-induced inhibition of CYP2E1 may reduce the bioactivation of carcinogens, potentially contributing to its chemopreventive effects against NMBA-induced esophageal tumors in rats.

Synthesis of Copper(II) Complex with the Non-steroidal Anti-inflammatory Drug Tolfenamic Acid

Tarushi, Alketa, et al. Journal of inorganic biochemistry 149 (2015): 68-79.

The Cu(II) complex formed with deprotonated tolfenamic acid in the presence of nitrogen and/or oxygen donor ligands exhibits significant antioxidant activity and shows considerable binding affinity for serum albumin and calf thymus DNA.
A methanol solution containing tolfenamic acid (0.4 mmol, 104 mg) and KOH (0.4 mmol, 22 mg) was stirred for 1 hour, and then a methanol solution of CuCl₂·2H₂O (0.4 mmol, 68 mg) was slowly added along with a solution of 2,2'-bipyridine (bipy) (0.4 mmol, 62 mg), stirring for an additional 15 minutes. After one week, suitable green crystals [Cu(tolf-O,O')(bipy)Cl] 1 (80 mg, 65%) were collected for X-ray structure determination.

Tolfenamic Acid Regulates TGFβ Signaling to Inhibit Metastasis and Glycolysis in Hepatocellular Carcinoma

Sun, Jingfang, et al. Toxicology and Applied Pharmacology 380 (2019): 114696.

TGFβ signaling plays a critical role in creating a favorable microenvironment for tumor cell growth and promoting epithelial-mesenchymal transition (EMT). As a traditional non-steroidal anti-inflammatory drug, tolfenamic acid (TA) has previously been reported to exhibit anticancer activity.
This study investigates the effects of TA on TGFβ-mediated pro-metastatic activity in hepatocellular carcinoma (HCC) and its potential mechanisms. The results indicate that TA inhibits TGFβ-induced migration and glycolysis in HCC cells, accompanied by reduced Smad phosphorylation and subsequent nuclear transcriptional activity. Mechanistically, TA promotes the lipid raft-caveolae internalization pathway of TGFβ receptors, leading to their rapid turnover. TA consistently suppresses the phosphorylation of Smad induced by the constitutively active TGFβ type I receptor and EMT markers, while the ectopic expression of the TGFβ type II receptor can partially rescue TGFβ-mediated Smad2 phosphorylation and downstream gene expression in the presence of TA. Additionally, TA inhibits the invasion of HCC cells in nude mice, which correlates with changes in characteristics related to cancer cell EMT and glycolysis. Our study suggests that TA can activate the lipid raft pathway and regulate TGFβ-mediated metastasis, indicating its potential application as a modulator of the HCC tumor microenvironment.