Aceclofenac 100 mg + Thicolchicoside 4 mg


Aceclofenac is a novel NSAID known to exhibit multifactor mechanism of action. Aceclofenac was developed
in order to provide a highly effective pain relieving therapy with a reduced side effect profile.

1. Aceclofenac directly blocks PGE 2 secretion at the site of inflammation by inhibiting IL-Beta & TNF in the
inflammatory cells (Intracellular Action). Aceclofenac has been demonstrated to inhibit cyclo-oxygenase
(COX) activity and to suppress the PGE 2 production by inflammatory cells, which are likely to be a primary
source of PGE 2 . Inflammatory cells release IL-1 and TNF, which produce PGE 2 by induction of COX-2.
Aceclofenac and 4′-hydroxyaceclofenac penetrate the inflammatory cells like polymorphonuclears,
monocytes and rheumatoid synovial cells and get hydrolyzed to the active metabolites diclofenac and 4′-
hydroxydiclofenac which inhibit IL-1 and TNF released by the inflammatory cells and therefore suppress
production of PGE 2 at the site of inflammation.

2. Aceclofenac stimulates the synthesis of the extracellular matrix of , the Human Articular Cartilages.
Aceclofenac blocks degeneration and stimulates synthesis of extracellular matrix of cartilages by inhibiting
the action of different cytokines. Aceclofenac and the metabolites inhibit IL-6 production by human
chondrocytes. This leads to inhibition of increase of inflammatory cells in synovial tissue, inhibition of IL-1
amplification, inhibition of increased MMP synthesis and thus ensuring proteoglycan production.
Aceclofenac also inhibits IL-1 and TNF production by human chondrocytes, inflammatory cells and synovial
cells and therefore blocks suppression of GAG and collagen synthesis and stimulates growth factor mediated
synthesis of GAG and collagen. 4′- hydroxyaceclofenac, a metabolite of aceclofenac inhibits pro MMP1 and
pro MMP3 produced by synovial cells (Rheumatoid Synovial Cells) in serum and in synovial fluid and thus
inhibits progressive joint destruction by MMPs.

3. Aceclofenac inhibits Neutrophil Adhesion & Accumulation at the inflammatory site in the early phase and
thus blocks the pro-inflammatory actions of Neutrophils.

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