Fanigan tablets №100


Manufacturer: India

Acute pain (muscle, headache, toothache, with localization in the spine), with extra-articular rheumatism, rheumatoid arthritis, ankylosing spondylitis, osteoarthritis, spondyloarthritis, acute attacks of gout, primary dysmenorrhea, adnexitis, pharyngotonsillitis, otitis. Post-traumatic and post-operative pain syndrome.



Fanigan Storage
active substances: paracetamol, diclofenac sodium;

1 tablet contains paracetamol 500 mg, diclofenac sodium 50 mg;

Excipients: corn starch, povidone K-30, croscarmellose sodium, microcrystalline cellulose, magnesium stearate, yellow FCF (E 110).

Fanigan Dosage form

Main physical and chemical properties: capsule-shaped, orange tablets with white spots.

Fanigan Pharmacotherapeutic group
Nonsteroidal anti-inflammatory and anti-rheumatic drugs.

ATX code M01A B55.

Pharmacological properties


Fanigan is a combined drug that has a pronounced anti-inflammatory, analgesic and antipyretic effect. The pharmacological activity of the drug is due to the properties of diclofenac and paracetamol, which are part of the drug.

Diclofenac sodium has a pronounced anti-inflammatory and analgesic, as well as a moderate antipyretic effect. Paracetamol has a pronounced analgesic, minor antipyretic and anti-inflammatory effect. The mechanism of action is associated with inhibition of prostaglandin synthesis.



Diclofenac sodium is rapidly absorbed into the blood – the maximum concentration in blood plasma is reached in 1-2 hours. Plasma protein binding is greater than 99%. It penetrates well into tissues and synovial fluid, where its concentration grows slowly, after 4 hours reaches higher values ​​than in blood plasma. Food can slow down the rate of absorption without affecting the completeness of absorption. Bioavailability – about 5%.

The half-life from blood plasma is 1-2 hours, from synovial fluid – 3-6 hours. About 35% is excreted as metabolites in the feces; about 65% – is metabolized in the liver and excreted by the kidneys in the form of inactive derivatives, about 1% – unchanged.


Paracetamol is rapidly and almost completely absorbed in the gastrointestinal tract. The maximum concentration in blood plasma is reached in 30-60 minutes. The half-life is 1-4 hours. Evenly distributed in all body fluids. Plasma protein binding is variable. Paracetamol is metabolized in the liver and excreted primarily by the kidneys as conjugated metabolites.
After repeated use of the drug pharmacokinetic parameters of the active substances do not change. Under the conditions of observance of the recommended intervals between reception of tablets accumulation of drug is not noted.


Acute pain (muscle, headache, toothache, localized in the spine), non-articular rheumatism, rheumatoid arthritis, ankylosing spondylitis, osteoarthritis, spondyloarthritis, acute gout attacks, primary dysmenorrhoea, otitiserita, adineorrhea, adnethinorrhea, adnethinorrhea, adine.
Post-traumatic and postoperative pain syndrome.


Hypersensitivity to diclofenac, paracetamol or to any other component of the drug.

Acute gastric or intestinal ulcer; gastrointestinal bleeding or perforation.

History of bleeding or perforation of the gastrointestinal tract associated with previous treatment with nonsteroidal anti-inflammatory drugs (NSAIDs).

Active form of peptic ulcer / bleeding or recurrent peptic ulcer / bleeding history (two or more separate episodes of diagnosed ulcer or bleeding).

High risk of postoperative bleeding, blood clotting, hemostasis disorders, hematopoietic disorders or cerebrovascular bleeding.

Hepatic failure.

Renal failure.

Congestive heart failure (NYHA II – IV).

Ischemic heart disease in patients with angina pectoris who have suffered a myocardial infarction.

Patients who develop bronchial asthma (“aspirin asthma”), angioneurotic edema, urticaria or acute rhinitis, nasal polyps, and others in response to ibuprofen, diclofenac, paracetamol, acetylsalicylic acid, or other NSAIDs.

Blood diseases, hematopoietic disorders of unknown origin, leukopenia, severe anemia.

Congenital hyperbilirubinemia, Gilbert’s syndrome.

Glucose-6-phosphate dehydrogenase deficiency.

Inflammatory bowel disease (Crohn’s disease or ulcerative colitis).


Treatment of postoperative pain during coronary artery bypass grafting (or use of an artificial circulation device).

Diseases of peripheral arteries.

Cerebrovascular disease in patients who have suffered a stroke or have episodes of transient ischemic attacks.