Description
PHARMACOLOGY
PHARMACODYNAMICS
Diclofenac exerts potent anti-inflammatory, anti-pyretic and analgesic activity by inhibition of cyclo-oxygenase pathway (COX) and thus inhibits biosynthesis of prostaglandin and other pro-inflammatory mediators of pain pathway.
Serratiopeptidase, a bacterial peptide-cleaving enzyme obtained from Serratia marcescens. Serratiopeptidase is also a potent anti-inflammatory agent that exerts fibrinolytic and anti-edematic property. The therapeutic enzyme reduce inflammation and swelling in the affected area.
PHARMACOKINETICS:
ABSORPTION:
Diclofenac sodium + Serratiopeptidase is rapidly absorbed in the GIT. However, the absorption rate is very slow in enteric-coated formulations.
DISTRIBUTION:
The drug can enter breast milk and synovial fluid after distribution. The plasma protein binding capability of Diclofenac sodium + Serratiopeptidase is about 99%.
METABOLISM:
Diclofenac sodium + Serratiopeptidase is extensively metabolized in the liver and converted into active metabolites.
EXCRETION:
The drug is extensively excreted in urine as glucuronide and sulfate conjugates. The rest of the elimination is via the bile. The terminal half-life of Diclofenac sodium + Serratiopeptidase is about 1-2 hours.
