Zobid Injection

Zobid Injection Mechanism of Action



SM Pharmaceuticals


SM Pharmaceuticals
Full Prescribing Info
Pharmacology: Pharmacodynamics: Mode or Mechanisms of Action: Diclofenac is a potent non-steroidal anti-inflammatory drug (NSAID) with analgesic property. NSAIDs inhibit the activity of the enzyme cyclo-oxygenase, resulting in decreased formation of precursors of prostaglandins and thromboxanes from arachidonic acid. Although the resultant decrease in prostaglandin synthesis and activity in various tissues may be responsible for many of the therapeutic (and adverse) effects of NSAIDs, other actions may also contribute significantly to the therapeutic effects of these medications.
Anti-rheumatic (non-steroidal anti-inflammatory): Act via analgesic and anti-inflammatory mechanisms; the therapeutic effects are not due to pituitary-adrenal stimulation. These medications do not affect progressive course of rheumatoid arthritis.
In rheumatic diseases, the anti-inflammatory and analgesic properties of Zobid Injection elicit a clinical response characterised by marked relief from signs and symptoms, e.g pain at rest, pain on movement, morning stiffness and swelling of the joints as well as by an improvement in function.
In post-traumatic and post-operative inflammatory conditions, Zobid Injection rapidly relieves both spontaneous pain and pain on movement and reduces inflammatory swelling and wound oedema.
Analgesic: May block pain impulse generation via a peripheral action that may involve reduction of the activity of prostaglandins, and possibly inhibition of the synthesis or actions of other substances that sensitise pain receptors to mechanical or chemical stimulation.
In clinical trials, Zobid Injection has been found to exert a pronounced analgesic effect in moderate and severe pain of non-rheumatic origin, its onset of effect taking place within 15-30 min.
Antigout agent: Act via analgesic and anti-inflammatory mechanisms; do not correct hyperuricemia.
Pharmacokinetics: Absorption: Diclofenac is rapidly absorbed when given by intramuscular injection. Mean peak plasma concentrations of 2.5 μg/mL (8 μmol/L) are reached approximately 20 min after IM injection of 75mg diclofenac. The plasma concentration is in linear proportion to the size of the dose, over the range 25 - 150 mg.
Distribution: The area under the concentration curve (AUC) is about twice as large after parenteral administration as after oral or rectal doses, because the oral or rectal routes lead to about half of the active substance being metabolised during its first passage through the liver.
99.7% of diclofenac is bound to serum proteins, mainly to albumin (99.4%). No accumulation occurs if the recommended dosage intervals are observed. Diclofenac enters the synovial fluid, where peak concentrations are measured 2-4 hrs after the peak plasma values have been reached.
Metabolism: Biotransformation takes place by glucuronidation partly of the intact molecule, but mainly after single and multiple hydroxylation.
Elimination: The active substance is eliminated from the plasma with a systemic clearance of 263 mL/min (x ± SD). The terminal half-life is 1-2 hrs. Approximately 60% of the dose administered is excreted via the kidneys in the form of metabolites (glucuronide and sulphate conjugates); <1 % is excreted as unchanged substance. The rest of the dose is eliminated in the form of metabolites through the bile in the faeces. The apparent elimination half-life from the synovial fluid is 3-6 hours. This means that concentrations of active substance in the synovial fluid are already higher than plasma concentrations 4-6 hrs after administration and they remain higher up to 12 hours after administration.
Kinetics in Special Clinical Situations: No relevant age-dependent differences in absorption, metabolism and excretion have been observed. In patients with impaired renal function, no accumulation of the unchanged active substance can be inferred from the single-dose kinetics under the usual dosage schedule. At a creatinine clearance of <10 mL/min, the theoretical steady-state plasma levels of metabolites are about 4 times higher than in normal subjects. The metabolites are nevertheless ultimately cleared through the bile. In patients with impaired hepatic function (chronic hepatitis, non-decompensated cirrhosis), the kinetics and metabolism of diclofenac are the same as in patients without liver disease.
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