Risedronate Sodium 150 mg Tablet, Film Coated, 1 tablet — NDC 65862-870-11 (Billing 65862-0870-11)
This is a package of 1 tablet of Risedronate Sodium 150 mg Tablet, Film Coated from Aurobindo Pharma Limited, marketed since Oct 2016 and currently FDA-listed; retail pharmacies pay about $12.91 per tablet (NADAC).
Identity & classification
Regulatory identifiers FDA, NLM and CMS codes for this package
Drug-database identifiers Medi-Span GPI and First Databank GCN / HICL / AHFS classification
- GSN (GCN sequence number): 063925
- GCN: 99637
- GPI-14 (Medi-Span): 30042065100380
- HICL (First Databank): 018565
- AHFS class code: 92:24.00.00
- RxCUI (RxNorm): 905028
Where does this data come from?
- FDA openFDA NDC Directory · synced Oct 1, 2026
- FDA label on DailyMed · label index refreshed Oct 1, 2026
- RxNorm (NLM RxNav) · catalog refreshed Oct 1, 2026
- Medi-Span GPI (licensed)
- First Databank (licensed) · refreshed Oct 1, 2026
Clinical
- It helps strengthen bones. Depending on the product, it treats or prevents osteoporosis in postmenopausal women, treats osteoporosis in men, treats or prevents steroid-related oste...
- Regular tablets go down whole with a full glass of plain water at least 30 minutes before food, drink or other medicines. Delayed-release tablets are taken right after breakfast wi...
- Back pain, joint pain, belly pain and indigestion are the most common. Call your doctor if you have painful swallowing, chest pain, new heartburn, severe bone or muscle pain, or ne...
- Not at the same time. Calcium, antacids, magnesium products and iron can block absorption, so take them at a different time of day. Do get enough calcium and vitamin D, as your doc...
Patient education
Supplement & herbal interactions
Some supplements/herbs that may interact with Risedronate Sodium — tap one for details:
Where does this data come from?
- MedlinePlus (NLM) · refreshed Oct 1, 2026
- FDA label on DailyMed · label index refreshed Oct 1, 2026
Ask a licensed pharmacist directly — free, answered by our team.
Pricing
A drug doesn't have one price. Each row is a different public payment system, and none is what you'd pay at the counter — that depends on your insurance. The ⓘ on each row explains what it measures.
| Price system | Per ea | Per package |
|---|---|---|
| Retail pharmacies payNADAC · weekly | $12.907 | $12.91 / 1 tablet |
| Medicaid paysCMS SDUD · 12 mo | $23.49 | $23.49 / 1 tablet |
| Medicare drug plans payPart D · Q2 2026 | $23.52 | $23.52 / 1 tablet |
Where does this data come from?
- CMS NADAC weekly file · file of Sep 30, 2026
- CMS ASP pricing files · refreshed Sep 20, 2026
- CMS Medicaid State Drug Utilization Data · through Q1 2026
- CMS Part D plan pricing files · refreshed Sep 24, 2026
- VA National Acquisition Center price file
Packaging — all sizes for this product
| Package NDC | Description | Per unit | Per pack | Marketing start | Marketing end | Status |
|---|---|---|---|---|---|---|
| 65862-0870-03 65862-870-03 Main listing | 1 BLISTER PACK in 1 CARTON / 3 TABLET, FILM COATED in 1 BLISTER PACK | $12.91 / ea | $38.72 | 2016-10-21 | — | Active |
| 65862-0870-11 You're viewing this | 1 BLISTER PACK in 1 CARTON / 1 TABLET, FILM COATED in 1 BLISTER PACK | $12.91 / ea | $12.91 | 2016-10-21 | — | Active |
This pack effectively ties for the lowest per-ea cost of the 2 priced pack sizes ($12.91 NADAC).
Pack size FAQ
What quantity is in this package?
How does this package differ from NDC 65862-0870-03?
What NDC number is used to bill for this package of Risedronate Sodium 150 mg Tablet, Film Coated?
Prices are the latest CMS NADAC pharmacy acquisition cost per NDC; per-pack figures are per-unit × pack quantity, shown only when the pack is denominated in the same measure NADAC prices.
Therapeutic equivalents
| Product | Labeler | Pack | NADAC/unit | TE | Status | Price vs. this |
|---|---|---|---|---|---|---|
| risedronate sodium 150 mg 47335-0928-60 | Sun | 1 tablet | $12.907 | AB | Availability likely | — |
| Risedronate Sodium 129 mg/1; 21 mg 59762-0406-01 | Mylan | 1 tablet | $12.907 | AB | Availability likely | — |
| Risedronate Sodium 150 mg 60505-3097-02 | Apotex | 1 tablet | $12.907 | AB | Availability likely | — |
| Risedronate Sodium 150 mgthis 65862-0870-11 | Aurobindo | 1 tablet | $12.907 | AB | Availability likely | — |
| Actonel 129 mg/1; 21 mg 00430-0478-01 | Allergan, | 1 tablet | $353.498 | AB | Availability likely | +2639% |
Where does this data come from?
- FDA openFDA NDC Directory · synced Oct 1, 2026
- FDA Orange Book · refreshed Oct 3, 2026
- CMS NADAC weekly file · file of Sep 30, 2026
Availability & generic status
This product is an FDA-approved generic. Other versions of the same drug are listed under Therapeutic equivalents, least expensive first.
Where does this data come from?
- FDA Orange Book · refreshed Oct 3, 2026
What it looks like
Where does this data come from?
- FDA label on DailyMed · label index refreshed Oct 1, 2026
Inactive Ingredients / Excipients
Inactive ingredients, also called excipients, are components of the drug product other than the active ingredient. They may include fillers, dyes, coatings, preservatives, flavors, or other formulation ingredients.
💡 Tap an ingredient (hover on desktop) to see what it is and why it’s used.
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UNII 68401960MK
Crospovidone is a synthetic polymer made from polyvinylpyrrolidone. It acts as a disintegrant, helping tablets break apart quickly in the stomach so the medicine dissolves and absorbs into the body.
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UNII L06K8R7DQK
A synthetic blue dye approved by the FDA for use in medications and foods. It serves as a colorant to make pills and liquids visually distinct and easier to identify.
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UNII RFW2ET671P
Hydroxypropyl cellulose is a plant-derived thickening agent made from cellulose. It acts as a binder to hold tablet ingredients together and as a film-former to coat tablets or control how fast the medicine releases.
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UNII 0WZ8WG20P6
Hypromellose 2910 is a plant-based cellulose derivative that acts as a thickener, binder, and film-coating agent. It helps control how quickly the medicine dissolves and protects the tablet or capsule from moisture and light.
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UNII 70097M6I30
Magnesium stearate is a salt made from magnesium and stearic acid, a fatty substance. It's used in tablets and capsules as a lubricant and glidant to help ingredients flow smoothly during manufacturing and prevent sticking.
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UNII OP1R32D61U
Microcrystalline cellulose is a purified form of cellulose, a natural fiber from plant sources. It acts as a binder and filler in tablets and capsules, helping hold ingredients together and give the medicine its shape and size.
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UNII B697894SGQ
Polyethylene glycol 400 is a clear, thick liquid made from petroleum-derived polymers. It acts as a solvent and humectant in medicines, helping dissolve active ingredients and retain moisture in the formulation.
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UNII Q662QK8M3B
Polyethylene glycol 8000 is a synthetic polymer made from ethylene oxide. It acts as a binder and filler in tablets and capsules, helping hold ingredients together and add bulk to the medicine.
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UNII ETJ7Z6XBU4
Silicon dioxide is a naturally occurring mineral used as a glidant and anti-caking agent. It helps powder ingredients flow smoothly and prevents clumping during manufacturing and storage.
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UNII 15FIX9V2JP
Titanium dioxide is a bright white mineral powder commonly used as a colorant and opacifying agent. It makes pills and tablets white or lighter in color and helps make coatings non-transparent.
10 inactive ingredients listed in the exact product block matched to this NDC.
Where does this data come from?
ingredient classCode="IACT" elements from the exact product block matched by this NDC. Label-section narrative from DailyMed / the openFDA label index is shown separately when available.- FDA label on DailyMed · label index refreshed Oct 1, 2026
- FDA openFDA NDC Directory · synced Oct 1, 2026
Inactive ingredient FAQ
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Manufacturer & labeler
Where does this data come from?
- FDA openFDA NDC Directory · synced Oct 1, 2026
- Drugs@FDA
Full prescribing information FDA SPL
🎯 Indications and Usage ▾
1 INDICATIONS AND USAGE Risedronate sodium tablets are a bisphosphonate indicated for: Treatment and prevention of postmenopausal osteoporosis ( 1.1 ) Treatment to increase bone mass in men with osteoporosis ( 1.2 ) Treatment and prevention of glucocorticoid-induced osteoporosis ( 1.3 ) Treatment of Paget’s disease ( 1.4 ) Limitations of Use Optimal duration of use has not been determined. For patients at low-risk for fracture, consider drug discontinuation after 3 to 5 years of use. ( 1.5 )
1.1Postmenopausal Osteoporosis Risedronate sodium tablets are indicated for the treatment and prevention of osteoporosis in postmenopausal women. In postmenopausal women with osteoporosis, risedronate sodium tablets reduce the incidence of vertebral fractures and a composite endpoint of nonvertebral osteoporosis-related fractures [see Clinical Studies (14.1 , 14.2 )] .
1.2Osteoporosis in Men Risedronate sodium tablets are is indicated for treatment to increase bone mass in men with osteoporosis.
1.3Glucocorticoid-Induced Osteoporosis Risedronate sodium tablets are indicated for the treatment and prevention of glucocorticoid-induced osteoporosis in men and women who are either initiating or continuing systemic glucocorticoid treatment (daily dosage of greater than or equal to 7.5 mg of prednisone or equivalent) for chronic diseases. Patients treated with glucocorticoids should receive adequate amounts of calcium and vitamin D.
1.4Paget’s Disease Risedronate sodium tablets are indicated for treatment of Paget’s disease of bone in men and women.
1.5Important Limitations of Use The optimal duration of use has not been determined. The safety and effectiveness of risedronate sodium tablets for the treatment of osteoporosis are based on clinical data of three years duration. All patients on bisphosphonate therapy should have the need for continued therapy re-evaluated on a periodic basis.
Patients at low-risk for fracture should be considered for drug discontinuation after 3 to 5 years of use. Patients who discontinue therapy should have their risk for fracture re-evaluated periodically.
⏱️ Dosage and Administration ▾
2 DOSAGE AND ADMINISTRATION Treatment of Postmenopausal Osteoporosis: 5 mg daily, 35 mg once-a-week, 75 mg two consecutive days each month, 150 mg once-a-month ( 2.1 ) Prevention of Postmenopausal Osteoporosis: 5 mg daily, 35 mg once-a-week ( 2.2 ) Men with Osteoporosis: 35 mg once-a-week ( 2.3 ) Glucocorticoid-Induced Osteoporosis: 5 mg daily ( 2.4 ) Paget’s Disease: 30 mg daily for 2 months ( 2.5 ) Instruct patients to: Swallow tablet whole with 6 to 8 ounces of plain water, at least 30 minutes before the first food, beverage, or medication of the day Avoid lying down for 30 minutes ( 2 ) Take supplemental calcium and vitamin D if dietary intake is inadequate ( 2.7 )
2.1Treatment of Postmenopausal Osteoporosis [see Indications and Usage (1.1) ] The recommended regimen is: one 5 mg tablet orally, taken daily or one 35 mg tablet orally, taken once-a-week or one 75 mg tablet orally, taken on two consecutive days for a total of two tablets each month or one 150 mg tablet orally, taken once-a-month
2.2Prevention of Postmenopausal Osteoporosis [see Indications and Usage (1.1) ] The recommended regimen is: one 5 mg tablet orally, taken daily or one 35 mg tablet orally, taken once-a-week or alternatively, one 75 mg tablet orally, taken on two consecutive days for a total of two tablets each month may be considered or alternatively, one 150 mg tablet orally, taken once-a-month may be considered
2.3Treatment to Increase Bone Mass in Men with Osteoporosis [see Indications and Usage (1.2) ] The recommended regimen is: one 35 mg tablet orally, taken once-a-week
2.4Treatment and Prevention of Glucocorticoid-Induced Osteoporosis [see Indications and Usage (1.3) ] The recommended regimen is: one 5 mg tablet orally, taken daily
2.5Treatment of Paget’s Disease [see Indications and Usage (1.4) ] The recommended treatment regimen is 30 mg orally once daily for 2 months. Retreatment may be considered (following post-treatment observation of at least 2 months) if relapse occurs, or if treatment fails to normalize serum alkaline phosphatase. For retreatment, the dose and duration of therapy are the same as for initial treatment.
No data are available on more than 1 course of retreatment.
2.6Important Administration Instructions Instruct patients to do the following: Take risedronate sodium tablets at least 30 minutes before the first food or drink of the day other than water, and before taking any oral medication or supplementation, including calcium, antacids, or vitamins to maximize absorption and clinical benefit, [see Drug Interactions (7.1) ] . Avoid the use of water with supplements, including mineral water, because they may have a higher concentration of calcium. Swallow risedronate sodium tablets whole with a full glass of plain water (6 to 8 ounces).
Avoid lying down for 30 minutes after taking the medication [see Warnings and Precautions (5.1) ] . Do not chew or suck the tablet because of a potential for oropharyngeal ulceration. Do not eat or drink anything except plain water, or take other medications for at least 30 minutes after taking risedronate sodium tablets.
2.7Recommendations for Calcium and Vitamin D Supplementation Instruct patients to take supplemental calcium and vitamin D if their dietary intake is inadequate; and to take calcium supplements, antacids, magnesium-based supplements or laxatives, and iron preparations at a different time of the day as they interfere with the absorption of risedronate sodium tablets.
2.8Administration Instructions for Missed Doses Instruct patients about missing risedronate sodium tablets dose as follows: If a dose of risedronate sodium tablets 35 mg once-a-week is missed: Take 1 tablet on the morning after they remember and return to taking 1 tablet once-a-week, as originally scheduled on their chosen day. Do not take 2 tablets on the same day. If one or both tablets of risedronate sodium tablets 75 mg on two consecutive days per month are missed, and the next month’s scheduled doses… [Excerpted — this section continues on DailyMed.]
💊 Dosage Forms and Strengths ▾
3 DOSAGE FORMS AND STRENGTHS 150 mg blue colored, circular shaped, film-coated biconvex tablets debossed with ‘Z’ on one side and ‘43’ on the other side. Tablets: 150 mg (3)
⛔ Contraindications ▾
4 CONTRAINDICATIONS Risedronate sodium tablets are 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 risedronate sodium tablets or any of its excipients. Angioedema, generalized rash, bullous skin reactions, Stevens-Johnson syndrome and toxic epidermal necrolysis have been reported [see Adverse Reactions (6.2) ] Abnormalities of the esophagus which delay esophageal emptying such as stricture or achalasia (4 , 5.2) Inability to stand or sit upright for at least 30 minutes (4 , 5.2) Hypocalcemia (4 , 5.3) Known hypersensitivity to any component of this product (4 , 6.2)
⚠️ Warnings and Cautions ▾
5 WARNINGS AND PRECAUTIONS Products Containing Same Active Ingredient : Patients receiving Atelvia should not be treated with risedronate sodium tablets ( 5.1 ) Upper Gastrointestinal Adverse Reactions can occur. Instruct patients to follow dosing instructions. Discontinue use if new or worsening symptoms occur ( 5.2 ) Hypocalcemia may worsen and must be corrected prior to use ( 5.3 ) Osteonecrosis of the Jaw has been reported ( 5.4 ) Severe Bone, Joint, Muscle Pain may occur.
Discontinue use if severe symptoms develop ( 5.5 , 6.2 ) Atypical Fractures Including Femoral Fractures have been reported. Patients with new thigh or groin pain should be evaluated to rule out a femoral fracture. Risk/benefit of continuing bisphosphonate therapy should be re-evaluated in these patients and interruption of bisphosphonate therapy should be considered ( 5.6 )
5.1Drug Products with the Same Active Ingredient Risedronate sodium tablets contain the same active ingredient found in Atelvia ® . A patient being treated with Atelvia should not receive risedronate sodium tablets.
5.2Upper Gastrointestinal Adverse Reactions Risedronate, like other bisphosphonates administered orally, may cause local irritation of the upper gastrointestinal mucosa. Because of these possible irritant effects and a potential for worsening of the underlying disease, caution should be used when risedronate is given to patients with active upper gastrointestinal problems (such as known Barrett’s esophagus, dysphagia, other esophageal diseases, gastritis, duodenitis or ulcers) [see Contraindications (4) , Adverse Reactions (6.1) , Information for Patients (17) ] .
Esophageal adverse experiences, such as esophagitis, esophageal ulcers and esophageal erosions, occasionally with bleeding and rarely followed by esophageal stricture or perforation, have been reported in patients receiving treatment with oral bisphosphonates. In some cases, these have been severe and required hospitalization. Physicians should therefore be alert to any signs or symptoms signaling a possible esophageal reaction and patients should be instructed to discontinue risedronate and seek medical attention if they develop dysphagia, odynophagia, retrosternal pain or new or worsening heartburn.
The risk of severe esophageal adverse experiences appears to be greater in patients who lie down after taking oral bisphosphonates and/or who fail to swallow it with the recommended full glass (6 to 8 ounces) of water, and/or who continue to take oral bisphosphonates after developing symptoms suggestive of esophageal irritation. Therefore, it is very important that the full dosing instructions are provided to, and understood by, the patient [see Dosage and Administration (2) ] . In patients who cannot comply with dosing instructions due to mental disability, therapy with risedronate should be used under appropriate supervision.
There have been post-marketing reports of gastric and duodenal ulcers with oral bisphosphonate use, some severe and with complications, although no increased risk was observed in controlled clinical trials.
5.3Mineral Metabolism Hypocalcemia has been reported in patients taking risedronate. Treat hypocalcemia and other disturbances of bone and mineral metabolism before starting risedronate therapy. Instruct patients to take supplemental calcium and vitamin D if their dietary intake is inadequate.
Adequate intake of calcium and vitamin D is important in all patients, especially in patients with Paget’s disease in whom bone turnover is significantly elevated [see Contraindications (4) , Adverse Reactions (6.1) , Information for Patients (17) ].
5.4Jaw Osteonecrosis Osteonecrosis of the jaw (ONJ), which can occur spontaneously, is generally associated with tooth extraction and/or local infection with delayed healing, and has been reported in patients taking bisphosphonates, including risedronate. Known risk factors for osteonecrosis of the jaw include invasive dental procedures (for example,… [Excerpted — this section continues on DailyMed.]
🤒 Adverse Reactions ▾
6 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) ] Glucocorticoid-Induced Osteoporosis [see Warnings and Precautions (5.8) ] Laboratory Test Interactions [see Warnings and Precautions (5.9) ] Most common adverse reactions reported in greater than 10% of patients treated with risedronate and with a higher frequency than placebo are: back pain, arthralgia, abdominal pain, and dyspepsia (6.1) Hypersensitivity reactions (angioedema, generalized rash, bullous skin reactions, Stevens-Johnson syndrome, and toxic epidermal necrolysis), and eye inflammation (iritis, uveitis) have been reported rarely (6.2) To report SUSPECTED ADVERSE REACTIONS, contact Aurobindo Pharma USA, Inc. at 1-866-850-2876 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch .
6.1Clinical Studies Experience Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice. Treatment of Postmenopausal Osteoporosis Daily Dosing The safety of risedronate sodium tablets 5 mg once daily in the treatment of postmenopausal osteoporosis was assessed in four randomized, double-blind, placebo-controlled multinational trials of 3232 women aged 38 to 85 years with postmenopausal osteoporosis.
The duration of the trials was up to three years, with 1619 patients exposed to placebo and 1613 patients exposed to risedronate sodium tablets 5 mg. Patients with pre-existing gastrointestinal disease and concomitant use of non-steroidal anti-inflammatory drugs, proton pump inhibitors, and H 2 antagonists were included in these clinical trials. All women received 1000 mg of elemental calcium plus vitamin D supplementation up to 500 international units per day if their 25-hydroxyvitamin D 3 level was below normal at baseline.
The incidence of all-cause mortality was 2% in the placebo group and 1.7% in the risedronate sodium tablets 5 mg daily group. The incidence of serious adverse events was 24.6% in the placebo group and 27.2% in the risedronate sodium tablets 5 mg group. The percentage of patients who withdrew from the study due to adverse events was 15.6% in the placebo group and 14.8% in the risedronate sodium tablets 5 mg group.
The most common adverse reactions reported in greater than 10 percent of subjects were: back pain, arthralgia, abdominal pain and dyspepsia. Table 1 lists adverse events from the Phase 3 postmenopausal osteoporosis trials reported in greater than or equal to 5% of patients. Adverse events are shown without attribution of causality.
Table 1 Adverse Events Occurring at a Frequency greater than or equal to 5% in Either Treatment Group Combined Phase 3 Postmenopausal Osteoporosis Treatment Trials Body System Placebo N = 1619 5 mg Risedronate Sodium Tablets N = 1613 % % Body as a Whole Infection 29.9
31.1Back Pain 26.1 28 Accidental Injury 16.8
16.9 Pain 14
14.1Abdominal Pain 9.9
12.2Flu Syndrome 11.6
10.5Headache 10.8
9.9Asthenia 4.5
5.4Neck Pain 4.7
5.4Chest Pain 5.1 5 Allergic Reaction Cardiovascular System 5.9
3.8Hypertension Digestive System 9.8
10.5Constipation 12.6
12.9 Diarrhea 10
10.8Dyspepsia 10.6
10.8Nausea Metabolic & Nutritional Disorders 11.2
10.5Peripheral Edema Musculoskeletal System 8.8
7.7Arthralgia 22.1
23.7Arthritis 10.1
9.6Traumatic Bone Fracture 12.3
9.3Joint Disorder 5.3 7 Myalgia 6.2
6.7Bone Pai… [Excerpted — this section continues on DailyMed.]
🔄 Drug Interactions ▾
7 DRUG INTERACTIONS No specific drug-drug interaction studies were performed. Risedronate is not metabolized and does not induce or inhibit hepatic microsomal drug-metabolizing enzymes (for example, Cytochrome P450). Calcium, antacids, or oral medications containing divalent cations interfere with the absorption of risedronate (7.1)
7.1Calcium Supplements/Antacids Co-administration of risedronate and calcium, antacids, or oral medications containing divalent cations will interfere with the absorption of risedronate.
7.2Hormone Replacement Therapy One study of about 500 early postmenopausal women has been conducted to date in which treatment with risedronate sodium tablets 5 mg daily plus estrogen replacement therapy was compared to estrogen replacement therapy alone. Exposure to study drugs was approximately 12 to 18 months and the primary endpoint was change in BMD. If considered appropriate, risedronate may be used concomitantly with hormone replacement therapy.
7.3Aspirin/Nonsteroidal Anti-Inflammatory Drugs Of over 5700 patients enrolled in the risedronate Phase 3 osteoporosis studies, aspirin use was reported by 31% of patients, 24% of whom were regular users (3 or more days per week). Forty-eight percent of patients reported NSAID use, 21% of whom were regular users. Among regular aspirin or NSAID users, the incidence of upper gastrointestinal adverse experiences in placebo-treated patients (24.8%) was similar to that in risedronate-treated patients (24.5%).
7.4H 2 Blockers and Proton Pump Inhibitors (PPIs) Of over 5700 patients enrolled in the risedronate Phase 3 osteoporosis studies, 21% used H 2 blockers and/or PPIs. Among these patients, the incidence of upper gastrointestinal adverse experiences in the placebo-treated patients was similar to that in risedronate-treated patients.
👥 Use in Specific Populations ▾
8 USE IN SPECIFIC POPULATIONS Pregnancy: Discontinue when pregnancy is recognized ( 8.1 ) Risedronate is not recommended for use in patients with severe renal impairment (creatinine clearance less than 30 mL/min) ( 5.6 , 8.6 , 12.3) Risedronate is not indicated for use in pediatric patients ( 8.4 )
8.1Pregnancy Risk Summary Available data on the use of risedronate in pregnant women are insufficient to inform a drug-associated risk of adverse maternal or fetal outcomes. Discontinue risedronate when pregnancy is recognized. In animal reproduction studies, daily oral administration of risedronate to pregnant rats during organogenesis decreased neonatal survival and body weight at doses approximately 5 and 26 times, respectively, the highest recommended human daily dose of 30 mg (based on body surface area, mg/m 2 ).
A low incidence of cleft palate was observed in fetuses of dams treated at doses approximately equal to the 30 mg human daily dose. Delayed skeletal ossification was observed in fetuses of dams treated at approximately 2.5 to 5 times the 30 mg human daily dose. Periparturient mortality due to maternal hypocalcemia occurred in dams and neonates upon daily oral administration of risedronate to pregnant rats during mating and/or gestation starting at doses equivalent to the 30 mg daily human dose.
Bisphosphonates are incorporated into the bone matrix, from which they are gradually released over a period of years. The amount of bisphosphonate incorporated into adult bone and available for release into the systemic circulation is directly related to the dose and duration of bisphosphonate use. Consequently, based on the mechanism of action of bisphosphonates, there is a potential risk of fetal harm, predominantly skeletal, if a woman becomes pregnant after completing a course of bisphosphonate therapy.
The impact of variables such as time between cessation of bisphosphonate therapy to conception, the particular bisphosphonate used, and the route of administration (intravenous versus oral) on this risk has not been studied. The estimated background risk of major birth defects and miscarriage for the indicated populations is unknown. All pregnancies have a background risk of birth defects, loss, or other adverse outcomes.
In the U.S. general population, the estimated background risks of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively. Data Animal Data In animal studies, pregnant rats received risedronate sodium during organogenesis at doses equivalent to 1 to 26 times the 30 mg human daily dose (based on body surface area, mg/m 2 ). Survival of neonates was decreased in dams treated during gestation with oral doses approximately 5 times the human dose, and body weight was decreased in neonates of dams treated with approximately 26 times the human dose.
A low incidence of cleft palate was observed in fetuses of dams treated with oral doses approximately equal to the human dose. The number of fetuses exhibiting incomplete ossification of sternebrae or skull of dams treated with approximately 2.5 times the human dose was significantly increased compared to controls. Both incomplete ossification and unossified sternebrae were increased in fetuses of dams treated with oral doses approximately 5 times the human dose.
No significant ossification effects were seen in fetuses of rabbits treated with oral doses approximately 7 times the human dose (the highest dose tested). However, 1 of 14 litters were aborted and 1 of 14 litters were delivered prematurely. Periparturient mortality due to maternal hypocalcemia occurred in dams and neonates when pregnant rats were treated daily during mating and/or gestation with oral doses equivalent to the human dose or higher.
8.2Lactation Risk Summary There are no data on the presence of risedronate in human milk, the effects on the breastfed infant, or the effects on milk production. A small degree of lacteal transfer occurred in n… [Excerpted — this section continues on DailyMed.]
🤰 Pregnancy ▾
8.1Pregnancy Risk Summary Available data on the use of risedronate in pregnant women are insufficient to inform a drug-associated risk of adverse maternal or fetal outcomes. Discontinue risedronate when pregnancy is recognized. In animal reproduction studies, daily oral administration of risedronate to pregnant rats during organogenesis decreased neonatal survival and body weight at doses approximately 5 and 26 times, respectively, the highest recommended human daily dose of 30 mg (based on body surface area, mg/m 2 ).
A low incidence of cleft palate was observed in fetuses of dams treated at doses approximately equal to the 30 mg human daily dose. Delayed skeletal ossification was observed in fetuses of dams treated at approximately 2.5 to 5 times the 30 mg human daily dose. Periparturient mortality due to maternal hypocalcemia occurred in dams and neonates upon daily oral administration of risedronate to pregnant rats during mating and/or gestation starting at doses equivalent to the 30 mg daily human dose.
Bisphosphonates are incorporated into the bone matrix, from which they are gradually released over a period of years. The amount of bisphosphonate incorporated into adult bone and available for release into the systemic circulation is directly related to the dose and duration of bisphosphonate use. Consequently, based on the mechanism of action of bisphosphonates, there is a potential risk of fetal harm, predominantly skeletal, if a woman becomes pregnant after completing a course of bisphosphonate therapy.
The impact of variables such as time between cessation of bisphosphonate therapy to conception, the particular bisphosphonate used, and the route of administration (intravenous versus oral) on this risk has not been studied. The estimated background risk of major birth defects and miscarriage for the indicated populations is unknown. All pregnancies have a background risk of birth defects, loss, or other adverse outcomes.
In the U.S. general population, the estimated background risks of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively. Data Animal Data In animal studies, pregnant rats received risedronate sodium during organogenesis at doses equivalent to 1 to 26 times the 30 mg human daily dose (based on body surface area, mg/m 2 ). Survival of neonates was decreased in dams treated during gestation with oral doses approximately 5 times the human dose, and body weight was decreased in neonates of dams treated with approximately 26 times the human dose.
A low incidence of cleft palate was observed in fetuses of dams treated with oral doses approximately equal to the human dose. The number of fetuses exhibiting incomplete ossification of sternebrae or skull of dams treated with approximately 2.5 times the human dose was significantly increased compared to controls. Both incomplete ossification and unossified sternebrae were increased in fetuses of dams treated with oral doses approximately 5 times the human dose.
No significant ossification effects were seen in fetuses of rabbits treated with oral doses approximately 7 times the human dose (the highest dose tested). However, 1 of 14 litters were aborted and 1 of 14 litters were delivered prematurely. Periparturient mortality due to maternal hypocalcemia occurred in dams and neonates when pregnant rats were treated daily during mating and/or gestation with oral doses equivalent to the human dose or higher.
🧒 Pediatric Use ▾
8.4Pediatric Use Risedronate is not indicated for use in pediatric patients. The safety and effectiveness of risedronate was assessed in a one-year, randomized, double-blind, placebo-controlled study of 143 pediatric patients (94 received risedronate) with osteogenesis imperfecta (OI). The enrolled population was predominantly patients with mild osteogenesis imperfecta (85% Type-I), aged 4 to less than 16 years, 50% male and 82% Caucasian, with a mean lumbar spine BMD Z-score of -2.08 (2.08 standard deviations below the mean for age-matched controls).
Patients received either a 2.5 mg (less than or equal to 30 kg body weight) or 5 mg (greater than 30 kg body weight) daily oral dose. After one year, an increase in lumbar spine BMD in the risedronate group compared to the placebo group was observed. However, treatment with risedronate did not result in a reduction in the risk of fracture in pediatric patients with osteogenesis imperfecta.
In risedronate-treated subjects, no mineralization defects were noted in paired bone biopsy specimens obtained at baseline and month 12. The overall safety profile of risedronate in OI patients treated for up to 12 months was generally similar to that of adults with osteoporosis. However, there was an increased incidence of vomiting compared to placebo.
In this study, vomiting was observed in 15% of children treated with risedronate and 6% of patients treated with placebo. Other adverse events reported in greater than or equal to 10% of patients treated with risedronate and with a higher frequency than placebo were: pain in the extremity (21% with risedronate versus 16% with placebo), headache (20% versus 8%), back pain (17% versus 10%), pain (15% versus 10%), upper abdominal pain (11% versus 8%), and bone pain (10% versus 4%).
🧓 Geriatric Use ▾
8.5Geriatric Use Of the patients receiving risedronate in postmenopausal osteoporosis studies [see Clinical Studies (14) ] , 47% were between 65 and 75 years of age, and 17% were over 75. The corresponding proportions were 26% and 11% in glucocorticoid-induced osteoporosis trials, and 40% and 26% in Paget’s disease trials. No overall differences in efficacy between geriatric and younger patients were observed in these studies.
In the male osteoporosis trial, 28% of patients receiving risedronate were between 65 and 75 years of age and 9% were over 75. The lumbar spine BMD response for risedronate compared to placebo was 5.6% for subjects less than 65 years and 2.9% for subjects greater than or equal to 65 years. No overall differences in safety between geriatric and younger patients were observed in the risedronate trials, but greater sensitivity of some older individuals cannot be ruled out.
🆘 Overdosage ▾
10 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. Milk or antacids containing calcium should be given to bind risedronate and reduce absorption of the drug.
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 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 30 mg human dose based on surface area (mg/m 2 ).
🧬 Clinical Pharmacology ▾
12 CLINICAL PHARMACOLOGY
12.1Mechanism 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.
12.2Pharmacodynamics Risedronate treatment decreases the elevated rate of bone turnover that is typically seen in postmenopausal osteoporosis. In clinical trials, administration of risedronate to postmenopausal women resulted in decreases in biochemical markers of bone turnover, including urinary deoxypyridinoline/creatinine and urinary collagen cross-linked N-telopeptide (markers of bone resorption) and serum bone-specific alkaline phosphatase (a marker of bone formation). At the 5 mg dose, decreases in deoxypyridinoline/creatinine were evident within 14 days of treatment.
Changes in bone formation markers were observed later than changes in resorption markers, as expected, due to the coupled nature of bone resorption and bone formation; decreases in bone-specific alkaline phosphatase of about 20% were evident within 3 months of treatment. Bone turnover markers reached a nadir of about 40% below baseline values by the sixth month of treatment and remained stable with continued treatment for up to 3 years. Bone turnover is decreased as early as 14 days and maximally within about 6 months of treatment, with achievement of a new steady-state that more nearly approximates the rate of bone turnover seen in premenopausal women.
In a 1-year study comparing daily versus weekly oral dosing regimens of risedronate for the treatment of osteoporosis in postmenopausal women, risedronate sodium tablets 5 mg daily and risedronate sodium tablets 35 mg once-a-week decreased urinary collagen cross-linked N-telopeptide by 60% and 61%, respectively. In addition, serum bone-specific alkaline phosphatase was also reduced by 42% and 41% in the risedronate sodium tablets 5 mg daily and risedronate sodium tablets 35 mg once-a-week groups, respectively. When postmenopausal women with osteoporosis were treated for 1 year with risedronate sodium tablets 5 mg daily or risedronate sodium tablets 75 mg two consecutive days per month, urinary collagen cross-linked N-telopeptide was decreased by 54% and 52%, respectively, and serum bone-specific alkaline phosphatase was reduced by 36% and 35%, respectively.
In a 1–year study comparing risedronate sodium tablets 5 mg daily versus risedronate sodium tablets 150 mg once-a-month in women with postmenopausal osteoporosis, urinary collagen cross-linked N-telopeptide was decreased by 52% and 49%, respectively, and serum bone-specific alkaline phosphatase was reduced by 31% and 32%, respectively. Osteoporosis in Men In a 2-year study of men with osteoporosis, treatment with risedronate sodium tablets 35 mg once-a-week resulted in a mean decrease from baseline compared to placebo of 16% (placebo 20%; risedronate sodium tablets 35 mg 37%) for the bone resorption marker urinary collagen cross-linked N-telopeptide, 45% (placebo -6%; risedronate sodium tablets 35 mg 39%) for the bone resorption marker serum C-telopeptide, and 27% (placebo -2%; risedronate sodium tablets 35 mg 25%) for the bone formation marker serum bone-specific alkaline phosphatase.
Glucocorticoid-Induced Osteoporosis Osteoporosis with glucocorticoid use occurs as a result of inhibited bone formation and increased bone resorption resulting in net bone loss. Risedronate sodium tablets decreases bone resorption without directly inhibiting bone formation. In two 1-year clinical trials in the treatment and prevention of glucocorticoid-induced osteoporosis, risedronate sodium tablets 5 mg d… [Excerpted — this section continues on DailyMed.]
🧬 Mechanism of Action ▾
12.1Mechanism 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.
📦 How Supplied / Storage and Handling ▾
16 HOW SUPPLIED/STORAGE AND HANDLING Risedronate Sodium Tablets USP, 150 mg are blue colored, circular shaped, film-coated biconvex tablets debossed with ‘Z’ on one side and ‘43’ on the other side. Unit-of-use blister package of 1 NDC 65862-870-11 Unit-of-use blister package of 3 NDC 65862-870-03 Store at 20° to 25°C (68° to 77°F). [See USP Controlled Room Temperature.]
📋 Description ▾
11 DESCRIPTION Risedronate sodium tablets, USP are a pyridinyl bisphosphonate that inhibits osteoclast-mediated bone resorption and modulates bone metabolism. Each risedronate sodium tablet, USP for oral administration contains the equivalent of 150 mg of anhydrous risedronate sodium in the form of the hemi-pentahydrate with small amounts of monohydrate. The molecular formula for risedronate sodium hemi-pentahydrate is C 7 H 10 NO 7 P 2 Na•2.5H 2 O.
The chemical name of risedronate sodium is [1-hydroxy-2-(3-pyridinyl)ethylidene]bis[phosphonic acid] monosodium salt. The chemical structure of risedronate sodium hemi-pentahydrate is the following: Molecular Weight: Anhydrous: 305.10 Hemi-pentahydrate: 350.13 Risedronate sodium is a white to off-white, crystalline powder. It is soluble in water and in aqueous solutions, and essentially insoluble in common organic solvents.
Inactive Ingredients Colloidal silicon dioxide, crospovidone, FD&C Blue#2/Indigo carmine aluminium Lake, hydroxypropyl cellulose, hypromellose, magnesium stearate, microcrystalline cellulose, polyethylene glycol and titanium dioxide. Chemical Structure
💬 Information for Patients ▾
17 PATIENT COUNSELING INFORMATION See FDA-approved patient labeling ( Medication Guide ) Instruct patients to read the Medication Guide before starting therapy with risedronate and to re-read it each time the prescription is renewed. Instruct patients that Atelvia and risedronate sodium tablets contain the same active ingredient and if they are taking Atelvia, they should not take risedronate sodium tablets [see Warnings and Precautions (5.1) ]. Instruct patients to pay particular attention to the dosing instructions as clinical benefits may be compromised by failure to take the drug according to instructions.
Specifically, risedronate should be taken at least 30 minutes before the first food or drink of the day other than water. Instruct patients to take risedronate while in an upright position (sitting or standing) with a full glass of plain water (6 to 8 ounces) to facilitate delivery to the stomach, and thus reduce the potential for esophageal irritation. Instruct patients not to lie down for 30 minutes after taking the medication [see Warnings and Precautions (5.1) ].
Instruct patients not to chew or suck on the tablet because of a potential for oropharyngeal irritation. Instruct patients that if they develop symptoms of esophageal disease (such as difficulty or pain upon swallowing, retrosternal pain or severe persistent or worsening heartburn) they should consult their physician before continuing risedronate. Instruct patients about missing risedronate doses as follows: If a dose of risedronate sodium 35 mg once-a-week is missed, they should take 1 tablet on the morning after they remember and return to taking 1 tablet once-a-week, as originally scheduled on their chosen day.
Patients should not take 2 tablets on the same day. If one or both tablets of risedronate sodium 75 mg on two consecutive days per month are missed, and the next month’s scheduled doses are more than 7 days away, the patient should be instructed as follows: If both tablets are missed, take one risedronate sodium 75 mg tablet in the morning after the day it is remembered and then the other tablet on the next consecutive morning. If only one risedronate sodium 75 mg tablet is missed, take the missed tablet in the morning after the day it is remembered.
Patients should then return to taking their risedronate sodium tablets 75 mg on two consecutive days per month as originally scheduled. Patients should not take more than two 75 mg tablets within 7 days. If one or both tablets of risedronate sodium 75 mg on two consecutive days per month are missed, and the next month's scheduled doses are within 7 days, patients should wait until their next month’s scheduled doses and then continue taking risedronate sodium 75 mg on two consecutive days per month as originally scheduled.
If the dose of risedronate sodium tablets 150 mg once-a-month is missed, and the next month’s scheduled dose is more than 7 days away, the patient should be instructed to take the missed tablet in the morning after the day it is remembered. Patients should then return to taking their risedronate sodium tablets 150 mg once-a-month as originally scheduled. Patients should not take more than one 150 mg tablet within 7 days.
If the dose of risedronate sodium tablets 150 mg once-a-month is missed, and the next month’s scheduled dose is within 7 days, patients should wait until their next month’s scheduled dose and then continue taking risedronate sodium tablets 150 mg once-a-month as originally scheduled. Instruct patients to take supplemental calcium and vitamin D if dietary intake is inadequate [see Warnings and Precautions (5.3) ] . Weight-bearing exercise should be considered along with the modification of certain behavioral factors, such as excessive cigarette smoking, and/or alcohol consumption, if these factors exist.
Instruct patients to take calcium supplements or calcium-, aluminum-, and magnesium-containing medications at a different time of the day than risedronate as these med… [Excerpted — this section continues on DailyMed.]
💬 Medication Guide ▾
Medication Guide Risedronate Sodium (ris ed′ roe nate soe′ dee um) Tablets, USP Read the Medication Guide that comes with risedronate sodium tablets before you start taking them and each time you get a refill. There may be new information. This Medication Guide does not take the place of talking with your doctor about your medical condition or your treatment.
Talk to your doctor if you have any questions about risedronate sodium tablets, there may be new information about them. What is the most important information I should know about risedronate sodium tablets? Risedronate sodium tablets can cause serious side effects including: 1.
Esophagus problems 2. Low calcium levels in your blood (hypocalcemia) 3. Severe jaw bone problems (osteonecrosis) 4.
Bone, joint, or muscle pain 5. Unusual breaks in thigh and other bones 1. Esophagus problems.
Some people who take risedronate sodium tablets may develop problems in the esophagus (the tube that connects the mouth and the stomach). These problems include irritation, inflammation, or ulcers of the esophagus which may sometimes bleed. It is important that you take risedronate sodium tablets exactly as prescribed to help lower your chance of getting esophagus problems.
(See the section “How should I take risedronate sodium tablets?”) Stop taking risedronate sodium tablets and call your doctor right away if you get chest pain, new or worsening heartburn, or have trouble or pain when you swallow. 2. Low calcium levels in your blood (hypocalcemia).
Risedronate sodium tablets may lower the calcium levels in your blood. If you have low blood calcium before you start taking risedronate sodium tablets, it may get worse during treatment. Your low blood calcium must be treated before you take risedronate sodium tablets.
Most people with low blood calcium levels do not have symptoms, but some people may have symptoms. Call your doctor right away if you have symptoms of low blood calcium such as: Spasms, twitches, or cramps in your muscles Numbness or tingling in your fingers, toes, or around your mouth Your doctor may prescribe calcium and vitamin D to help prevent low calcium levels in your blood, while you take risedronate sodium tablets. Take calcium and vitamin D as your doctor tells you to.
3. Severe jaw bone problems (osteonecrosis). Severe jaw bone problems may happen when you take risedronate sodium tablets.
Your doctor should examine your mouth before you start risedronate sodium tablets. Your doctor may tell you to see your dentist before you start risedronate sodium tablets. It is important for you to practice good mouth care during treatment with risedronate sodium tablets.
4. Bone, joint, or muscle pain. Some people who take risedronate sodium tablets develop severe bone, joint, or muscle pain.
5. Unusual breaks in thigh and other bones. Some people have had unusual bone breaks, including the thigh bone, when taking risedronate sodium tablets.
A break in the thigh bone can feel like a new pain in your hip, groin, or thigh. People taking risedronate sodium tablets can also have breaks in other bones. Call your doctor right away if you have any of these side effects.
What are risedronate sodium tablets ? Risedronate sodium tablets are a prescription medicine used to: Treat or prevent osteoporosis in women after menopause. Risedronate sodium tablets help increase bone mass and helps reduce the chance of having a spinal or non-spinal fracture (break).
Increase bone mass in men with osteoporosis. Treat or prevent osteoporosis in either men or women who are taking corticosteroid medicines. Treat certain men and women who have Paget’s disease of the bone.
It is not known how long risedronate sodium tablets work for the treatment and prevention of osteoporosis. You should see your doctor regularly to determine if risedronate sodium tablets are still right for you. Risedronate sodium tablets are not for use in children.
Who should not take risedronate sodium tablets ? Do not take risedronate… [Excerpted — this section continues on DailyMed.]
🧬 Pharmacokinetics ▾
12.3Pharmacokinetics Absorption Based on simultaneous modeling of serum and urine data, peak absorption after an oral dose is achieved at approximately 1 hour (T max ) and occurs throughout the upper gastrointestinal tract. The fraction of the dose absorbed is independent of dose over the range studied (single dose, from 2.5 mg to 30 mg; multiple dose, from 2.5 mg to 5 mg). Steady-state conditions in the serum are observed within 57 days of daily dosing.
Mean absolute oral bioavailability of the 30 mg tablet is 0.63% (90% CI: 0.54% to 0.75%) and is comparable to a solution. Food Effect The extent of absorption of a 30 mg dose (three 10 mg tablets) when administered 0.5 hours before breakfast is reduced by 55% compared to dosing in the fasting state (no food or drink for 10 hours prior to or 4 hours after dosing). Dosing 1 hour prior to breakfast reduces the extent of absorption by 30% compared to dosing in the fasting state.
Dosing either 0.5 hours prior to breakfast or 2 hours after dinner (evening meal) results in a similar extent of absorption. Risedronate is effective when administered at least 30 minutes before breakfast. Distribution The mean steady-state volume of distribution for risedronate is
13.8L/kg in humans. Human plasma protein binding of drug is about 24%. Preclinical studies in rats and dogs dosed intravenously with single doses of [ 14 C] risedronate indicate that approximately 60% of the dose is distributed to bone.
The remainder of the dose is excreted in the urine. After multiple oral dosing in rats, the uptake of risedronate in soft tissues was in the range of 0.001% to 0.01%. Metabolism There is no evidence of systemic metabolism of risedronate.
Excretion In young healthy subjects, approximately half of the absorbed dose of risedronate was excreted in urine within 24 hours, and 85% of an intravenous dose was recovered in the urine over 28 days. Based on simultaneous modeling of serum and urine data, mean renal clearance was 105 mL/min (CV = 34%) and mean total clearance was 122 mL/min (CV = 19%), with the difference primarily reflecting nonrenal clearance or clearance due to adsorption to bone. The renal clearance is not concentration dependent, and there is a linear relationship between renal clearance and creatinine clearance.
Unabsorbed drug is eliminated unchanged in feces. In osteopenic postmenopausal women, the terminal exponential half-life was 561 hours, mean renal clearance was 52 mL/min (CV = 25%), and mean total clearance was 73 mL/min (CV = 15%). Specific Populations Pediatric: Risedronate is not indicated for use in pediatric patients [see Pediatric Use (8.4) ] .
Gender: Bioavailability and pharmacokinetics following oral administration are similar in men and women. Geriatric: Bioavailability and disposition are similar in elderly (greater than 60 years of age) and younger subjects. No dosage adjustment is necessary.
Race: Pharmacokinetic differences due to race have not been studied. Renal Impairment: Risedronate is excreted unchanged primarily via the kidney. As compared to persons with normal renal function, the renal clearance of risedronate was decreased by about 70% in patients with creatinine clearance of approximately 30 mL/min.
Risedronate is not recommended for use in patients with severe renal impairment (creatinine clearance less than 30 mL/min) because of lack of clinical experience. No dosage adjustment is necessary in patients with a creatinine clearance greater than or equal to 30 mL/min. Hepatic Impairment: No studies have been performed to assess risedronate’s safety or efficacy in patients with hepatic impairment.
Risedronate is not metabolized in rat, dog, and human liver preparations. Insignificant amounts (less than 0.1% of intravenous dose) of drug are excreted in the bile in rats. Therefore, dosage adjustment is unlikely to be needed in patients with hepatic impairment.
Drug Interactions: No specific drug-drug interaction studies were performed. Risedronate is not m… [Excerpted — this section continues on DailyMed.]
🧬 Pharmacodynamics ▾
12.2Pharmacodynamics Risedronate treatment decreases the elevated rate of bone turnover that is typically seen in postmenopausal osteoporosis. In clinical trials, administration of risedronate to postmenopausal women resulted in decreases in biochemical markers of bone turnover, including urinary deoxypyridinoline/creatinine and urinary collagen cross-linked N-telopeptide (markers of bone resorption) and serum bone-specific alkaline phosphatase (a marker of bone formation). At the 5 mg dose, decreases in deoxypyridinoline/creatinine were evident within 14 days of treatment.
Changes in bone formation markers were observed later than changes in resorption markers, as expected, due to the coupled nature of bone resorption and bone formation; decreases in bone-specific alkaline phosphatase of about 20% were evident within 3 months of treatment. Bone turnover markers reached a nadir of about 40% below baseline values by the sixth month of treatment and remained stable with continued treatment for up to 3 years. Bone turnover is decreased as early as 14 days and maximally within about 6 months of treatment, with achievement of a new steady-state that more nearly approximates the rate of bone turnover seen in premenopausal women.
In a 1-year study comparing daily versus weekly oral dosing regimens of risedronate for the treatment of osteoporosis in postmenopausal women, risedronate sodium tablets 5 mg daily and risedronate sodium tablets 35 mg once-a-week decreased urinary collagen cross-linked N-telopeptide by 60% and 61%, respectively. In addition, serum bone-specific alkaline phosphatase was also reduced by 42% and 41% in the risedronate sodium tablets 5 mg daily and risedronate sodium tablets 35 mg once-a-week groups, respectively. When postmenopausal women with osteoporosis were treated for 1 year with risedronate sodium tablets 5 mg daily or risedronate sodium tablets 75 mg two consecutive days per month, urinary collagen cross-linked N-telopeptide was decreased by 54% and 52%, respectively, and serum bone-specific alkaline phosphatase was reduced by 36% and 35%, respectively.
In a 1–year study comparing risedronate sodium tablets 5 mg daily versus risedronate sodium tablets 150 mg once-a-month in women with postmenopausal osteoporosis, urinary collagen cross-linked N-telopeptide was decreased by 52% and 49%, respectively, and serum bone-specific alkaline phosphatase was reduced by 31% and 32%, respectively. Osteoporosis in Men In a 2-year study of men with osteoporosis, treatment with risedronate sodium tablets 35 mg once-a-week resulted in a mean decrease from baseline compared to placebo of 16% (placebo 20%; risedronate sodium tablets 35 mg 37%) for the bone resorption marker urinary collagen cross-linked N-telopeptide, 45% (placebo -6%; risedronate sodium tablets 35 mg 39%) for the bone resorption marker serum C-telopeptide, and 27% (placebo -2%; risedronate sodium tablets 35 mg 25%) for the bone formation marker serum bone-specific alkaline phosphatase.
Glucocorticoid-Induced Osteoporosis Osteoporosis with glucocorticoid use occurs as a result of inhibited bone formation and increased bone resorption resulting in net bone loss. Risedronate sodium tablets decreases bone resorption without directly inhibiting bone formation. In two 1-year clinical trials in the treatment and prevention of glucocorticoid-induced osteoporosis, risedronate sodium tablets 5 mg decreased urinary collagen cross-linked N-telopeptide (a marker of bone resorption), and serum bone-specific alkaline phosphatase (a marker of bone formation) by 50% to 55% and 25% to 30%, respectively, within 3 to 6 months after initiation of therapy.
Paget’s Disease Paget’s disease of bone is a chronic, focal skeletal disorder characterized by greatly increased and disordered bone remodeling. Excessive osteoclastic bone resorption is followed by osteoblastic new bone formation, leading to the replacement of the normal bone architecture by disorganized, enlarged, and we… [Excerpted — this section continues on DailyMed.]
🔬 Clinical Studies ▾
14 CLINICAL STUDIES
14.1Treatment of Osteoporosis in Postmenopausal Women The fracture efficacy of risedronate sodium tablets 5 mg daily in the treatment of postmenopausal osteoporosis was demonstrated in 2 large, randomized, placebo-controlled, double-blind studies that enrolled a total of almost 4000 postmenopausal women under similar protocols. The Multinational study (VERT MN) (risedronate sodium tablets 5 mg, N = 408) was conducted primarily in Europe and Australia; a second study was conducted in North America (VERT NA) (risedronate sodium tablets 5 mg, N = 821).
Patients were selected on the basis of radiographic evidence of previous vertebral fracture, and therefore, had established disease. The average number of prevalent vertebral fractures per patient at study entry was 4 in VERT MN, and 2.5 in VERT NA, with a broad range of baseline BMD levels. All patients in these studies received supplemental calcium 1000 mg/day.
Patients with low 25-hydroxyvitamin D 3 levels (approximately 40 nmol/L or less) also received supplemental vitamin D 500 international units/day. Effect on Vertebral Fractures Fractures of previously undeformed vertebrae (new fractures) and worsening of pre-existing vertebral fractures were diagnosed radiographically; some of these fractures were also associated with symptoms (that is, clinical fractures). Spinal radiographs were scheduled annually and prospectively planned analyses were based on the time to a patient’s first diagnosed fracture.
The primary endpoint for these studies was the incidence of new and worsening vertebral fractures across the period of 0 to 3 years. Risedronate sodium tablets 5 mg daily significantly reduced the incidence of new and worsening vertebral fractures and of new vertebral fractures in both VERT NA and VERT MN at all time points (Table 3). The reduction in risk seen in the subgroup of patients who had 2 or more vertebral fractures at study entry was similar to that seen in the overall study population.
Table 3 The Effect of Risedronate on the Risk of Vertebral Fractures VERT NA Proportion of Patients with Fracture (%) a Placebo N = 678 Risedronate Sodium Tablets 5 mg N = 696 Absolute Risk Reduction (%) Relative Risk Reduction (%) New and Worsening 0 to 1 Year 0 to 2 Years 0 to 3 Years 7.2 12.8 18.5 3.9 8 13.9 3.3 4.8 4.6 49 42 33 New 0 to 1 Year 0 to 2 Years 0 to 3 Years 6.4 11.7 16.3 2.4 5.8 11.3 4 5.9 5 65 55 41 VERT MN Placebo N = 346 Risedronate Sodium Tablets 5 mg N = 344 Absolute Risk Reduction (%) Relative Risk Reduction (%) New and Worsening 0 to 1 Year 0 to 2 Years 0 to 3 Years 15.3 28.3 34 8.2 13.9 21.8 7.1 14.4 12.2 50 56 46 New 0 to 1 Year 0 to 2 Years 0 to 3 Years 13.3 24.7 29 5.6 11.6 18.1 7.7 13.1 10.9 61 59 49 a Calculated by Kaplan-Meier methodology.
Effect on Osteoporosis-Related Nonvertebral Fractures In VERT MN and VERT NA, a prospectively planned efficacy endpoint was defined consisting of all radiographically confirmed fractures of skeletal sites accepted as associated with osteoporosis. Fractures at these sites were collectively referred to as osteoporosis-related nonvertebral fractures. Risedronate sodium tablets 5 mg daily significantly reduced the incidence of nonvertebral osteoporosis-related fractures over 3 years in VERT NA (8% versus 5%; relative risk reduction 39%) and reduced the fracture incidence in VERT MN from 16% to 11%.
There was a significant reduction from 11% to 7% when the studies were combined, with a corresponding 36% reduction in relative risk. Figure 1 shows the overall results as well as the results at the individual skeletal sites for the combined studies. Effect on Bone Mineral Density The results of 4 randomized, placebo-controlled trials in women with postmenopausal osteoporosis (VERT MN, VERT NA, BMD MN, BMD NA) demonstrate that risedronate sodium tablets 5 mg daily increases BMD at the spine, hip, and wrist compared to the effects seen with placebo.
Table 4 displays the significant increases in BMD seen at the l… [Excerpted — this section continues on DailyMed.]
🧪 Nonclinical Toxicology ▾
13 NONCLINICAL TOXICOLOGY
13.1Carcinogenesis, Mutagenesis, Impairment of Fertility Carcinogenesis In a 104-week carcinogenicity study, rats were administered daily oral doses up to approximately 8 times the maximum recommended human daily dose. There were no significant drug-induced tumor findings in male or female rats. The high dose male group was terminated early in the study (Week 93) due to excessive toxicity, and data from this group were not included in the statistical evaluation of the study results.
In an 80-week carcinogenicity study, mice were administered daily oral doses approximately 6.5 times the human dose. There were no significant drug-induced tumor findings in male or female mice. Mutagenesis Risedronate did not exhibit genetic toxicity in the following assays: In vitro bacterial mutagenesis in Salmonella and E. coli (Ames assay), mammalian cell mutagenesis in CHO/HGPRT assay, unscheduled DNA synthesis in rat hepatocytes and an assessment of chromosomal aberrations in vivo in rat bone marrow.
Risedronate was positive in a chromosomal aberration assay in CHO cells at highly cytotoxic concentrations (greater than 675 mcg/mL, survival of 6% to 7%). When the assay was repeated at doses exhibiting appropriate cell survival (29%), there was no evidence of chromosomal damage. Impairment of Fertility In female rats, ovulation was inhibited at an oral dose approximately 5 times the human dose.
Decreased implantation was noted in female rats treated with doses approximately 2.5 times the human dose. In male rats, testicular and epididymal atrophy and inflammation were noted at approximately 13 times the human dose. Testicular atrophy was also noted in male rats after 13 weeks of treatment at oral doses approximately 5 times the human dose.
There was moderate-to-severe spermatid maturation block after 13 weeks in male dogs at an oral dose approximately 8 times the human dose. These findings tended to increase in severity with increased dose and exposure time. Dosing multiples provided above are based on the recommended human dose of 30 mg/day and normalized using body surface area (mg/m 2 ).
Actual doses were 24 mg/kg/day in rats, 32 mg/kg/day in mice, and 8, 16 and 40 mg/kg/day in dogs.
13.2Animal Toxicology and/or Pharmacology Risedronate demonstrated potent anti-osteoclast, antiresorptive activity in ovariectomized rats and minipigs. Bone mass and biomechanical strength were increased dose-dependently at daily oral doses up to 4 and 25 times the human recommended oral dose of 5 mg for rats and minipigs, respectively. Risedronate treatment maintained the positive correlation between BMD and bone strength and did not have a negative effect on bone structure or mineralization.
In intact dogs, risedronate induced positive bone balance at the level of the bone remodeling unit at oral doses ranging from 0.5 to 1.5 times the 5 mg/day human daily dose. In dogs treated with an oral dose approximately 5 times the human daily dose, risedronate caused a delay in fracture healing of the radius. The observed delay in fracture healing is similar to other bisphosphonates.
This effect did not occur at a dose approximately 0.5 times the human daily dose. The Schenk rat assay, based on histologic examination of the epiphyses of growing rats after drug treatment, demonstrated that risedronate did not interfere with bone mineralization even at the highest dose tested, which was approximately 3500 times the lowest antiresorptive dose in this model (1.5 mcg/kg/day) and approximately 800 times the human daily dose of 5 mg. This indicates that risedronate administered at the therapeutic dose is unlikely to induce osteomalacia.
Dosing multiples provided above are based on the recommended human dose of 5 mg/day and normalized using body surface area (mg/m 2 ).
📄 Carcinogenesis, Mutagenesis, Impairment of Fertility ▾
13.1Carcinogenesis, Mutagenesis, Impairment of Fertility Carcinogenesis In a 104-week carcinogenicity study, rats were administered daily oral doses up to approximately 8 times the maximum recommended human daily dose. There were no significant drug-induced tumor findings in male or female rats. The high dose male group was terminated early in the study (Week 93) due to excessive toxicity, and data from this group were not included in the statistical evaluation of the study results.
In an 80-week carcinogenicity study, mice were administered daily oral doses approximately 6.5 times the human dose. There were no significant drug-induced tumor findings in male or female mice. Mutagenesis Risedronate did not exhibit genetic toxicity in the following assays: In vitro bacterial mutagenesis in Salmonella and E. coli (Ames assay), mammalian cell mutagenesis in CHO/HGPRT assay, unscheduled DNA synthesis in rat hepatocytes and an assessment of chromosomal aberrations in vivo in rat bone marrow.
Risedronate was positive in a chromosomal aberration assay in CHO cells at highly cytotoxic concentrations (greater than 675 mcg/mL, survival of 6% to 7%). When the assay was repeated at doses exhibiting appropriate cell survival (29%), there was no evidence of chromosomal damage. Impairment of Fertility In female rats, ovulation was inhibited at an oral dose approximately 5 times the human dose.
Decreased implantation was noted in female rats treated with doses approximately 2.5 times the human dose. In male rats, testicular and epididymal atrophy and inflammation were noted at approximately 13 times the human dose. Testicular atrophy was also noted in male rats after 13 weeks of treatment at oral doses approximately 5 times the human dose.
There was moderate-to-severe spermatid maturation block after 13 weeks in male dogs at an oral dose approximately 8 times the human dose. These findings tended to increase in severity with increased dose and exposure time. Dosing multiples provided above are based on the recommended human dose of 30 mg/day and normalized using body surface area (mg/m 2 ).
Actual doses were 24 mg/kg/day in rats, 32 mg/kg/day in mice, and 8, 16 and 40 mg/kg/day in dogs.
📄 Recent Major Changes ▾
Warnings and Precautions, Atypical Fractures Including Femoral Fractures ( 5.6 )............02/2026
📄 Package Label / Principal Display Panel ▾
PACKAGE LABEL-PRINCIPAL DISPLAY PANEL - 150 mg Blister Card (1 Unit-of-use) NDC 65862-870-11 Rx only Once-a-Month Risedronate Sodium Tablet, USP 150 mg AUROBINDO One-Month Supply (1 Tablet) PACKAGE LABEL-PRINCIPAL DISPLAY PANEL - 150 mg Blister Card (1 Unit-of-use)
PACKAGE LABEL-PRINCIPAL DISPLAY PANEL - 150 mg Blister Carton (1 Unit-of-use) NDC 65862-870-11 Rx only Once-a-Month Risedronate Sodium Tablet, USP 150 mg PHARMACIST: Dispense the accompanying Medication Guide to each patient. AUROBINDO One-Month Supply (1 Tablet) PACKAGE LABEL-PRINCIPAL DISPLAY PANEL - 150 mg Blister Carton (1 Unit-of-use)