Fanigan Fast

Fanigan Fast Mechanism of Action

Manufacturer:

Kusum

Distributor:

JDS
Full Prescribing Info
Action
Pharmacotherapeutic group: Nonsteroidal anti-inflammatory and anti-rheumatic. ATC Code: M02AA65.
Pharmacology: Pharmacodynamics: Mechanism of Action of each component of Fanigan Fast gel is explained as follows. Diclofenac inhibits the cyclooxygenase, suppresses synthesis of prostaglandins - endogenous substances, which play a significant role in the genesis of the inflammation, pain, and fever. Diclofenac reduces pain, eliminates inflammation.
Menthol acts on the temperature receptors. It gives sensation of coolness, constricts capillaries, and decreases their permeability. It provides local counter-irritation and gentle analgesic actions.
Methyl salicylate is a derivative of salicylic acid, which has local irritation action. Methyl salicylate decreases the pain because of irritation of skin receptors. Methyl salicylate inhibits synthesis of prostaglandins, decreases swelling and infiltration of inflamed tissues.
Linseed oil contains alfalinoleic acid, which has anti-inflammatory, antioxidant actions, improves blood circulation at place of application.
The action of medicine begins within few minutes after application on skin. During 20-30 minutes it achieves maximum activity level. It provides relief from the symptoms from day one of beginning of treatment.
Pharmacokinetics: Absorption: When Diclofenac gel is applied topically, Diclofenac is absorbed into the epidermis. In patients with compromised skin (mainly atopic dermatitis and other dermatitis conditions) of the hands, arms or face, approximately 10% of the applied dose of Diclofenac was absorbed systemically in both normal and compromised epidermis.
After topical application of 2 g Diclofenac gel three times daily for six days, diclofenac could be detected in plasma. Mean bioavailability parameters were AUC0-t 9±19 nghr/mL (mean±SD) with a Cmax of 4±5 ng/mL and a Tmax of 4.5±8 hours. In comparison, a single oral 75 mg dose of diclofenac produced an AUC of 1600 ng.hr/mL. Therefore, the systemic bioavailability after topical application of Diclofenac gel is lower than after oral dosing.
No information is available on the absorption of Diclofenac when Diclofenac gel is used under occlusive bandage.
Distribution: Diclofenac binds tightly to serum albumin. The volume of distribution of diclofenac following oral administration is approximately 550 mL/kg.
Metabolism: Biotransformation of Diclofenac following oral administration involves conjugation at the carboxyl group of the side chain or single or multiple hydroxylation's resulting in several phenolic metabolites, most of which are converted to glucuronide conjugates. Two of these phenolic metabolites are biologically active, however to a much smaller extent than Diclofenac. Metabolism of Diclofenac following topical administration is thought to be similar to that after oral administration. The small amounts of Diclofenac and its metabolites appearing in the plasma following topical administration makes the quantification of specific metabolites imprecise.
Elimination: Diclofenac and its metabolites are excreted mainly in the urine after oral dosing. Systemic clearance of Diclofenac from plasma is 263±56 mL/min (mean±SD). The terminal plasma half-life is 1-2 hours. Four of the metabolites also have short terminal half-lives of 1-3 hours.
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