Brustan Mechanism of Action

Pharmacology: Mechanism of action: Ibuprofen has prominent anti-inflammatory effects in addition to having analgesic and antipyretic actions. The analgesic effects of ibuprofen are due to both peripheral and a central effect, and are distinct from its property as an anti-inflammatory drug. Ibuprofen is a potent inhibitor of the enzyme cyclo-oxygenase which thus results in a marked reduction of prostaglandin synthesis.
Paracetamol may act predominantly by inhibiting prostaglandin synthesis in the central nervous system (CNS) and, to a lesser extent, through a peripheral action by blocking pain-impulse generation. The peripheral action may be due to inhibition of prostaglandin synthesis or to inhibition of the synthesis or actions of other substances that sensitize pain receptors to mechanical or chemical stimulation. Paracetamol probably produces anti-pyresis by acting centrally on the hypothalamus heat-regulating center to produce peripheral vasodilatation resulting in increased blood flow through the skin, sweating and heat loss. The central action probably involves inhibition of prostaglandin synthesis in the hypothalamus.
Some 2 to 5% of a therapeutic dose of paracetamol is excreted unchanged in the urine. Its renal clearance is about 10 ml/min and is weakly dependent on urine flow rate but not on pH.
Pharmacokinetics: Pharmacokinetics of Ibuprofen and Paracetamol when given in combination: Ibuprofen and paracetamol do not seem to affect each other's pharmacokinetics when taken concurrently. This has been established in a study where ibuprofen and paracetamol were given concurrently to 20 healthy volunteers in a randomized crossover design.
Pharmacokinetics in Special Populations: Ibuprofen: Elderly: Old age has no effect on the elimination of ibuprofen.
Renal Impairment: Impairment has no effect on the kinetics of the drug, rapid metabolism still occurs as a consequence of metabolism.
Paracetamol: Renal Impairment: The kinetics of paracetamol elimination has been investigated in patients with renal diseases. No significant changes were observed.
Hepatic Impairment: The kinetics of paracetamol elimination has been investigated in patients with hepatic diseases. No significant changes were observed except in the patients with severe acute and decompensated chronic liver disease in whom the half-life was considerably prolonged.
Toxicology: Carcinogenicity/Mutagenicity/Impairment of Fertility: No evidence of carcinogenicity has been seen in rats. Reproduction studies on white rabbits in the early part of pregnancy showed no treatment related abnormalities; similar satisfactory results were obtained with mice and rats.
Paracetamol demonstrated no carcinogenic potential in F344 rats of either sex. No pathologic or statistical evidence of induction of tumors by acetaminophen was found.
Paracetamol inhibits both replicative DNA synthesis and DNA repair synthesis in vitro and in experimental animals. Paracetamol does not cause gene mutation, either in bacteria or in mammalian cells. A co-mutagenic effect of Paracetamol has however been reported. Furthermore, Paracetamol increases the frequency of chromosomal damage in mammalian cell lines, isolated human lymphocytes and experimental animals.
Chronic toxicity studies in animals have shown that high doses of paracetamol cause testicular atrophy and inhibition of spermatogenesis.