| Size | Price | Stock | Qty |
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| 250mg |
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| 500mg |
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| 1g |
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| Targets |
Chloride Channel[1]
Fenamic acid targets chloride channels, including ClC-2 and ClC-7, and also inhibits chloride-bicarbonate exchange. It acts as a potent, non-specific blocker of Cl- channels. It also has been reported to target the cystic fibrosis transmembrane conductance regulator (CFTR). As the basic constituent of NSAIDs, fenamic acid derivatives may also inhibit cyclooxygenase enzymes (COX-1/2). Fenamic acid is an orally active chloride channel blocker. |
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| ln Vitro |
In endothelial cells, fenamic acid (N-Phenylanthranilic acid, NPAA) (2.5 mM; 3 h) inhibits Cl-transport and prevents 36C1-uptake and efflux[1][2]. Fenamic acid suppresses AKR1B10 with IC50s of 0.76 μM for flufenamic acid, 1.6 μM for mefenamic acid, and 9.89 μM for meclofenamic acid, respectively. Fenamic acid shows selectivity to AKR1B10 (the tumor-marker) over human AR[4]. 50% of Neisseria gonorrhoeae with a MIC50 value between 4 and 16 µg/mL (tolfenamic acid, flufenamic acid, and meclofenamic acid) in a low frequency of resistance are inhibited by fenamic acid (4–16 μg/mL; 72 h)[5]. When applied to infected endocervical cells, fenamic acid (2–8 µg/mL; 8 h) decreases the expression of porinflammatory cytokines (IL–8, IL–6, and IL-ß) without inhibiting the cells' ability to bind commensally to Lactobacillus species (>128 µg/mL; 24 h). being a member of a healthy female vaginal microbiota[5].
In vitro, Fenamic acid (N-Phenylanthranilic acid, NPAA) is an orally active chloride channel blocker. It is the basic constituent of non-steroidal anti-inflammatory agents (NSAIA) and derives into mefenamic, tolfenamic, flufenamic, and meclofenamic acids. Fenamic acid also acts as an antibacterial and analgesic agent. It is a potent, non-specific blocker of Cl- channels and inhibits Cl--dependent Glu accumulation into vesicles. It has been used to study the role of chloride channels in various physiological processes. |
| ln Vivo |
RPA-1 is a biomarker used to identify collecting duct damage in male rats with papillary necrosis[3]. In rats, fenamic acid (N-Phenylanthranilic acid, NPAA) (350–700 mg/kg/day; op; 4 d, 8 d, and 15 d) increases urine renal papillary antigen-1 (RPA-1) and promotes renal papillary necrosis[3]. Mice's abdominal constriction caused by acetic acid is inhibited by fenamic acid (20 g/0.2 mL; ip)[6].
In vivo, Fenamic acid is an orally active chloride channel blocker. Its derivatives (mefenamic acid, flufenamic acid, tolfenamic acid, meclofenamic acid) are clinically used as non-steroidal anti-inflammatory drugs (NSAIDs) for the treatment of pain and inflammation. Fenamic acid itself is less potent than its derivatives but serves as a research tool to study chloride channel function and as a scaffold for the development of new therapeutics. It has been used in biomarker studies of collecting duct injury in Han-Wistar and Sprague-Dawley rats. |
| Enzyme Assay |
The specific protocol for assessing chloride channel inhibition uses a membrane vesicle Cl- uptake assay. Membrane vesicles are prepared from rat kidney cortex or from cells expressing ClC-2 or ClC-7. The vesicles (100 ug protein) are incubated in buffer containing 10 uM [3⁶Cl]- (or a chloride-sensitive fluorescent dye such as N-(6-methoxyquinolyl) acetoethyl ester, MQAE) and varying concentrations of Fenamic acid (1-1000 uM). The reaction is initiated by the addition of valinomycin (10 uM) to create a membrane potential. After 1-5 minutes, the uptake is terminated by rapid filtration through nitrocellulose filters. Filters are washed, and the retained [3⁶Cl]- is measured. The IC50 is calculated from the inhibition curve. Alternatively, the patch-clamp technique can be used.
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| Cell Assay |
For in vitro cellular assays, human colonic epithelial cell lines (e.g., T84 cells) are grown on permeable supports to form polarized monolayers. Short-circuit current (Isc) measurements are performed in Ussing chambers. Fenamic acid (10-1000 uM) is added to the apical or basolateral side. The reduction in Isc, which reflects Cl- secretion, is measured. To activate CFTR-mediated Cl- transport, cells are stimulated with 10 uM forskolin and 100 uM IBMX. Fenamic acid should inhibit both CFTR-mediated and Ca2+-activated Cl- currents. The compound also inhibits cAMP-activated Cl- transport pathways. Cell viability is assessed using the MTT assay.
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| Animal Protocol |
Animal/Disease Models: Male Wistar Hannover rats (8-10 weeks old; weighting 220-270 g)[3]
Doses: 50, 350, or up to 700 mg/kg Route of Administration: Oral gavage; one time/day; 7 days or 14 days Experimental Results: Increased absolute paired kidney weights (13.8% at 350 mg/kg and 21.2% at 700/500 mg/kg) and relative to body weight (10.5% at 350 mg/kg/day and 20.3% at 700/500 mg/kg/day). Caused minimal papillary necrosis of tip with necrosis, hemorrhage, and inflammation of collecting ducts. Animal/Disease Models: Male NMRI mice (weighting 20-25 g); abdominal constriction model (writhing test), induced by acetic acid[6] Doses: 100 g/mL, each mice injected with 20 mL Route of Administration: intraperitoneal (ip) injection; once Experimental Results: demonstrated anti-nociceptive activity and inhibited the abdominal constriction with the maximal inhibition of 96.3% (Mefenamic acid). An in vivo protocol for Fenamic acid uses a rat model to study collecting duct injury. Male Han-Wistar rats (6-8 weeks old) are administered Fenamic acid orally by gavage at doses of 50-200 mg/kg (formulated in 0.5% methylcellulose) once daily for 7-14 days. Control animals receive vehicle only. At the end of the study, rats are placed in metabolic cages for 24-hour urine collection. Urine biomarkers of collecting duct injury (e.g., kidney injury molecule-1, clusterin, osteopontin) are measured by ELISA. Rats are euthanized, and the kidneys are harvested for histopathological examination (H&E, PAS staining) and immunohistochemistry for markers of collecting duct injury. Serum creatinine and BUN are measured to assess renal function. |
| ADME/Pharmacokinetics |
Detailed pharmacokinetic data for Fenamic acid is not available. As an orally active compound, it is absorbed from the gastrointestinal tract. Fenamic acid is the basic constituent of NSAIDs and is expected to have similar pharmacokinetic properties to its derivatives: moderate oral bioavailability, high plasma protein binding (>90%), and metabolism primarily via hepatic cytochrome P450 enzymes (CYP2C9). The terminal half-life is likely short (2-4 hours). Excretion occurs primarily in the urine as metabolites.
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| Toxicity/Toxicokinetics |
Specific toxicity data for Fenamic acid is limited. It has been used in biomarker studies of collecting duct injury in rats, indicating potential nephrotoxicity at high doses. In studies of Han-Wistar and Sprague-Dawley rats treated with N-phenylanthranilic acid (Fenamic acid), biomarkers of collecting duct injury were evaluated. Potential adverse effects may include gastrointestinal disturbances (nausea, diarrhea), renal papillary necrosis (as seen with NSAIDs), and hepatic toxicity. Standard safety screening would include acute and repeat-dose toxicity studies in rodents.
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| References |
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| Additional Infomation |
Fenna acid is an aminobenzoic acid, an N-phenyl derivative of anthranilic acid. It serves as the parent skeleton for the synthesis of many nonsteroidal anti-inflammatory drugs (NSAIDs). It acts as a membrane transport regulator. Fenna acid is a secondary amino compound and also an aminobenzoic acid. Functionally, it is related to anthranilic acid.
Fenamic acid is a research-grade chemical and is not approved for clinical use. Its molecular formula is C13H11NO2 with a molecular weight of 213.24 and a purity of ≥98%. It is an orally active chloride channel blocker and is the basic constituent of non-steroidal anti-inflammatory agents (NSAIA), serving as the parent core structure from which fenamates (mefenamic acid, flufenamic acid, tolfenamic acid, meclofenamic acid) are derived. Fenamic acid also acts as an antibacterial and analgesic agent. It is a valuable research tool for studying chloride channel function and as a scaffold for drug discovery. |
| Molecular Formula |
C13H11NO2
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|---|---|
| Molecular Weight |
213.23
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| Exact Mass |
213.078
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| CAS # |
91-40-7
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| PubChem CID |
4386
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| Appearance |
Yellow to khaki solid powder
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| Density |
1.3±0.1 g/cm3
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| Boiling Point |
385.2±25.0 °C at 760 mmHg
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| Melting Point |
182-185 °C(lit.)
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| Flash Point |
186.7±23.2 °C
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| Vapour Pressure |
0.0±0.9 mmHg at 25°C
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| Index of Refraction |
1.667
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| LogP |
4.41
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
3
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| Heavy Atom Count |
16
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| Complexity |
236
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| Defined Atom Stereocenter Count |
0
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| SMILES |
C1=CC=C(C=C1)NC2=CC=CC=C2C(=O)O
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| InChi Key |
ZWJINEZUASEZBH-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C13H11NO2/c15-13(16)11-8-4-5-9-12(11)14-10-6-2-1-3-7-10/h1-9,14H,(H,15,16)
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| Chemical Name |
2-anilinobenzoic acid
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO: 125 mg/mL (586.22 mM)
H2O: < 0.1 mg/mL |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 4.17 mg/mL (19.56 mM) (saturation unknown) in 10% DMSO + 40% PEG300 +5% Tween-80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 41.7 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 + to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 4.6898 mL | 23.4489 mL | 46.8977 mL | |
| 5 mM | 0.9380 mL | 4.6898 mL | 9.3795 mL | |
| 10 mM | 0.4690 mL | 2.3449 mL | 4.6898 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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