| Chemical Properties | White Solid |
| Uses | Tolfenamic acid is a non-steroidal anti-inflammatory agent. It interferes with synthesis of β-amyloid precursor protein, and thus Aβ peptides, by promoting degradation of an essential transcription factor. It inhibits fMLP- and A23187-induced Ca2+ influx in human PMNL with an IC50 value of approximately 20 μM. |
| Uses | A non steroidal anti-inflammatory agent found to inhibit COX-2 isoenzymes |
| Uses | Amidated GRF fragment equipotent to GRF in release of somatotropin from anterior pituitary |
| Uses | Non-steroidal anti-inflammatory drugs (NSAIDs). |
| Uses | antiinflammatory, analgesia |
| Definition | ChEBI: An aminobenzoic acid that is anthranilic acid in which one of the hydrogens attached to the nitrogen is replaced by a 3-chloro-2-methylphenyl group. Tolfenamic acid is used specifically for relieving the pain of migraine. It also shows anticancer activity. |
| General Description | Tolfenamic Acid is an anthranilic acid derivative and a non-steroidal anti-inflammatory drug (NSAID). Its applications in treating pancreatic, esophageal, colorectal and lung cancer is being investigated. |
| Biochem/physiol Actions | Non-steroidal anti-inflammatory agent. Interferes with synthesis of β-amyloid precursor protein, and thus Aβ peptides, by promoting degradation of an essential transcription factor. |
| Clinical Use | NSAID:
Treatment of migraine |
| Veterinary Drugs and Treatments | Tolfenamic acid may be useful for the treatment of acute or chronic
pain and/or inflammation in dogs and acute pain/inflammation in
cats. In Europe, it is also approved for use in cattle. |
| Drug interactions | Potentially hazardous interactions with other drugs
ACE inhibitors and angiotensin-II antagonists:
antagonism of hypotensive effect; increased risk of
nephrotoxicity and hyperkalaemia.
Analgesics: avoid concomitant use of 2 or more
NSAIDs, including aspirin (increased side effects);
avoid with ketorolac (increased risk of side effects
and haemorrhage).
Antibacterials: possibly increased risk of convulsions
with quinolones.
Anticoagulants: effects of coumarins and
phenindione enhanced; possibly increased risk of
bleeding with heparins, dabigatran and edoxaban.
Antidepressants: increased risk of bleeding with
SSRIs and venlafaxine.
Antidiabetic agents: effects of sulphonylureas enhanced.
Antiepileptics: possibly increased phenytoin
concentration.
Antivirals: increased risk of haematological toxicity
with zidovudine; concentration possibly increased by
ritonavir.
Ciclosporin: may potentiate nephrotoxicity.
Cytotoxics: reduced excretion of methotrexate;
increased risk of bleeding with erlotinib.
Diuretics: increased risk of nephrotoxicity;
antagonism of diuretic effect; hyperkalaemia with
potassium-sparing diuretics.
Lithium: excretion decreased.
Pentoxifylline: increased risk of bleeding.
Tacrolimus: increased risk of nephrotoxicity |
| Metabolism | Tolfenamic acid is metabolised in the liver; the metabolites and unchanged drug are conjugated with glucuronic acid. About 90
% of an ingested dose is excreted in the urine and the remainder in the faeces. |
