Etoricoxib (Etorelex) 90 mg – [7 tablets]

Description

Etorelex Pharmacodynamics
When administered orally at therapeutic concentrations, etoricoxib is a selective inhibitor of cyclooxygenase-2 (COX-2). In clinical pharmacological studies, etoricoxib inhibited COX-2 in a dose-dependent manner, with no effect on COX-1 at a daily dose up to 150 mg. The drug Etorelex does not inhibit the synthesis of prostaglandins in the gastric mucosa and does not affect platelet function.
Cyclooxygenase is responsible for formation of prostaglandins. Two isoforms of cyclooxygenase, COX-1 and COX-2, have been isolated. COX-2 is an isoenzyme that is induced by various proinflammatory mediators and is considered the main enzyme responsible for the synthesis of prostanoid mediators of pain, inflammation and fever. COX-2 is involved in the processes of ovulation, implantation and closure of the arterial duct, renal and CNS function (fever induction, pain sensation, cognitive function), and may also play a role in the healing of ulcers. COX-2 has been detected in the tissues surrounding gastric ulcers in humans, but its importance in ulcer healing has not been established.

Efficacy

In patients with osteoarthritis (OA), Etorelex, when administered at a dose of 60 mg once daily, provided a significant reduction in pain and improvement in patients’ assessment of their condition. These favorable effects were observed on the second day of treatment and persisted for 52 weeks. Studies of etoricoxib at a dose of 30 mg once daily (using similar evaluation methods) demonstrated efficacy compared to placebo during the treatment period of 12 weeks. In a study conducted to determine the optimal dose, etoricoxib, when used at a dose of 60 mg, demonstrated significantly greater improvement than the 30 mg dose for all three primary endpoints after 6 weeks of treatment. The 30 mg dose has not been studied in osteoarthritis of the hand joints.

In patients with rheumatoid arthritis (RA), Etorelex at a dose of 90 mg once daily provided a significant reduction in pain and inflammation and improved mobility. These favorable effects were maintained during the treatment period of 12 weeks.
In patients with acute gouty arthritis, etoricoxib at a dose of 120 mg once daily for the entire treatment period of 8 days reduced moderate to severe joint pain and inflammation. The efficacy was comparable to that of indomethacin when used in a dose of 50 mg 3 times/day. Pain reduction was noted as early as 4 hours after the start of treatment.
In patients with ankylosing spondylitis, etoricoxib at a dose of 90 mg once daily provided a significant reduction in back pain, inflammation, stiffness, as well as improved function. The clinical efficacy of etoricoxib was observed as early as the second day of treatment and was maintained throughout the entire treatment period of 52 weeks.

In a clinical study of pain after dental surgery, Etorelex at a dose of 90 mg was administered once daily for 3 days. In a subgroup of patients with moderate pain (at baseline), etoricoxib had the same analgesic effect as ibuprofen at a dose of 90 mg (16.11 versus 16.39; P=0.722) and was superior to the paracetamol/codein combination at 600 mg/60 mg (11.00; and placebo (6.84; according to the overall pain reduction score, within the first 6 h (THORAM). The proportion of patients who required rapid-acting pain medication within the first 24 h after administration of the study drugs was 40.894 with etoricoxib at 90 mg, 25.594 with ibuprofen at 600 mg every 6 h, and 46.70/0 with the paracetamol/codeine combination at 600 mg/60 mg every 6 h, compared with 76.20/0 in the placebo group. In this study, the median onset of action (perceptible pain reduction) with etoricoxib at a dose of 90 mg was 28 min after drug administration.

• Hypersensitivity to any component of the drug;
• Gastric and duodenal ulcer in the acute stage, active gastrointestinal bleeding;
• Complete or incomplete combination of bronchial asthma, recurrent polyposis of the nose and sinuses, and intolerance to acetylsalicylic acid or other NSAIDs (including history).
• Pregnancy, breastfeeding period.
• Severe hepatic impairment (serum albumin <25 g/l or Child-Pugh score);
• Severe renal insufficiency (creatinine clearance less than 30 ml/minute);
• Childhood under 16 years of age;
• Inflammatory bowel disease;
• Chronic heart failure (NYHA functional class II-W);
• Uncontrolled arterial hypertension in which BP values persistently exceed 140/90 mmHg;
• Confirmed coronary heart disease, peripheral arterial disease or cerebrovascular disease;
• Lactase deficiency, lactose intolerance, glucose-galactose malabsorption;
• Confirmed hyperkalemia;
• Progressive renal disease.