Dolowin Plus

Dolowin Plus Mechanism of Action

aceclofenac + paracetamol

Manufacturer:

Brown & Burk Phils

Distributor:

Brown & Burk Phils
Full Prescribing Info
Action
Pharmacology: Pharmacodynamics: Aceclofenac relieves pain and inflammation through a variety of mechanisms and in addition exert stimulatory effects on cartilage matrix synthesis.
Anti-inflammatory activity: The anti-inflammatory effects of Aceclofenac have been shown in both acute and chronic inflammation.
It inhibits various mediators of pain and inflammation including: PGE2 via cyclooxygenase inhibition (COX-1 & COX-2) after intracellular metabolism to 4' hydroxy-aceclofenac and diclofenac in human rheumatoid synovial cells and other inflammatory cells.
lL-1 B, lL-6 and tumor necrosis factor in human osteoarthritic synovial cells and human articular chondrocytes.
Reactive oxygen species (which plays a role in joint damage) has also been observed in patients with osteoarthritis of knee.
Expression of cell adhesion molecules (which is implicated in cell migration and inflammation) has also been shown in human neutrophils.
Stimulatory effects on cartilage matrix synthesis: Aceclofenac stimulates glycosaminoglycan synthesis in human osteoarthritic cartilage by inhibition of IL-1B and suppresses cartilage degeneration by inhibiting IL-1B mediated promatrix metalloproteinase production and proteoglycan release. Paracetamol is a clinically proven analgesic and antipyretic agent with weak anti-inflammatory effect.
Analgesic action: The central analgesic action of Paracetamol resembles that of aspirin. It produces analgesia by raising pain threshold.
Antipyretic effect: The antipyretic effect of Paracetamol is attributed to its ability to inhibit COX in the brain where peroxide tone is low. Recent evidence suggests inhibition of COX-3 (believed to be splice variant product of the COX-1 gene) could represent a primary central mechanism by which Paracetamol decreases pain and possibly fever.
Pharmacokinetics: Aceclofenac is well absorbed from gastrointestinal tract and peak plasma concentrations (Cmax) are reached 1-3 hours after an oral dose. The drug is more than 99% bound to plasma proteins and the volume of distribution (Vd) is approximately 25 liters. The presence of food reduced rate of absorption (increased tmax) but not the extent of absorption (Cmax or AUC). In patients with knee pain and synovial fluid effusion, the plasma concentration of Aceclofenac was twice that in synovial fluid after multiple doses of the drug. Aceclofenac is metabolized mainly to 4' hydroxy-aceclofenac. The drug is eliminated primarily through renal excretion with 70-80% of administered dose found in urine as glucoronides and rest being excreted in faeces. The plasma elimination half life of Aceclofenac is approximately 4 hours.
Paracetamol is rapidly and almost completely absorbed from gastrointestinal tract with peak plasma concentration (Cmax) occurring about 10 to 60 minutes after oral administration. Plasma proteins and binding is negligible at usual therapeutic concentration but increases with increasing concentration. Acetaminophen is relatively uniformly distributed throughout most body fluids. The plasma half life (t1/2) is 2-3 hours and the effect after oral dose lasts for 3-5 hours. Paracetamol is metabolized predominantly in liver and excreted in the urine mainly as glucuronide and sulfate conjugate. Less than 5% is excreted unchanged.
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