Risedronate Sodium — Active Pharmaceutical Ingredient

Risedronate Sodium is an active pharmaceutical ingredient found in 4 FDA-approved drug products. Forms: TABLET, TABLET, DELAYED RELEASE. Routes: ORAL.

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Risedronate Sodium (4 brand names, 2 dosage forms, 1 route)

Available dosage forms: TABLET, TABLET, DELAYED RELEASE.

Routes of administration: ORAL.

Brand Names

  • ACTONEL
  • ACTONEL WITH CALCIUM (COPACKAGED)
  • ATELVIA
  • RISEDRONATE SODIUM

Contraindications

Risedronate sodium delayed-release is contraindicated in patients with the following conditions: Abnormalities of the esophagus which delay esophageal emptying such as stricture or achalasia [ see Warnings and Precautions (5.2) ] Inability to stand or sit upright for at least 30 minutes [ see Dosage and Administration (2) , Warnings and Precautions (5.2) ] Hypocalcemia [ see Warnings and Precautions (5.3) ] Known hypersensitivity to any component of this product. Angioedema, generalized rash, bullous skin reactions, Stevens-Johnson syndrome and toxic epidermal necrolysis have been reported [ see Adverse Reactions (6.2) ]

Adverse Reactions

The following clinically significant adverse drug reactions are described elsewhere in the labeling: Drug Products with the Same Active Ingredient [see Warnings and Precautions (5.1) ] Upper Gastrointestinal Adverse Reactions [see Warnings and Precautions (5.2) ] Mineral Metabolism [see Warnings and Precautions (5.3) ] Jaw Osteonecrosis [see Warnings and Precautions (5.4) ] Musculoskeletal Pain [see Warnings and Precautions (5.5) ] Atypical Fractures Including Femoral Fractures [see Warnings and Precautions (5.6) ] Renal Impairment [see Warnings and Precautions (5.7) ] Laboratory Test Interactions [see Warnings and Precautions (5.8) ]

Drug Interactions

Risedronate is not metabolized and does not induce or inhibit hepatic microsomal drug-metabolizing enzymes (for example, Cytochrome P450).

Mechanism of Action

Risedronate has an affinity for hydroxyapatite crystals in bone and acts as an antiresorptive agent. At the cellular level, risedronate inhibits osteoclasts. The osteoclasts adhere normally to the bone surface, but show evidence of reduced active resorption (for example, lack of ruffled border). Histomorphometry in rats, dogs, and minipigs showed that risedronate treatment reduces bone turnover (activation frequency, that is, the rate at which bone remodeling sites are activated) and bone resorption at remodeling sites.

Overdosage

Decreases in serum calcium and phosphorus following substantial overdose may be expected in some patients. Signs and symptoms of hypocalcemia may also occur in some of these patients. While milk or antacids containing calcium may be given to bind risedronate sodium immediate- release and reduce absorption of the drug, the impact of this intervention for Risedronate sodium delayed-release tablets has not been evaluated. In cases of substantial overdose, gastric lavage may be considered to remove unabsorbed drug. Standard procedures that are effective for treating hypocalcemia, including the administration of calcium intravenously, would be expected to restore physiologic amounts of ionized calcium and to relieve signs and symptoms of hypocalcemia. Lethality after single oral doses of risedronate was seen in female rats at 903 mg/kg and male rats at 1703 mg/kg. The minimum lethal dose in mice and rabbits was 4000 mg/kg and 1000 mg/kg, respectively. These values represent 320 to 620 times the human Paget’s disease dose of 30 mg/day based on surface area (mg/m2).

⚠ Caution
Medical Disclaimer: This information is for educational purposes only. Always consult a healthcare professional before taking any medication.