Note: Avoid use of oral ibandronate in patients with swallowing difficulties, esophageal motility disorders, or the inability to stand or sit upright for ≥60 minutes. In patients treated for osteoporosis, correct hypocalcemia and vitamin D deficiency (eg, to a 25-hydroxyvitamin D level ≥20 ng/mL [≥50 nmol/L]) prior to initiating therapy and ensure adequate calcium and vitamin D intake during therapy (ES [Eastell 2019]; NAMS 2021; Rosen 2021; manufacturer’s labeling).
Breast cancer, metastatic bone disease (treatment; off-label use): IV: 6 mg over 1 to 2 hours every 3 to 4 weeks for up to 4 years (Body 2003; Diel 2004; Pecherstorfer 2006).
Hypercalcemia of malignancy (off-label use): IV: 2 to 6 mg as a single dose over 1 to 2 hours (Pecherstorfer 2003; Ralston 1997).
Osteoporosis, postmenopausal, fracture risk reduction:
Note: May be used in patients at risk for vertebral fractures; use has not been associated with reduction in hip or nonvertebral fractures (Adler 2016; ES [Eastell 2019]). Prior to use, evaluate and treat any potential causes of secondary osteoporosis (eg, severe vitamin D deficiency) (NOF [Cosman 2014]).
Patients with high fracture risk, including those with a history of vertebral fragility fracture, or those with a T-score of −2.5 or lower or a T-score between −1 and −2.5 at high fracture risk according to a risk assessment (NOF [Cosman 2014]):
Treatment:
Oral: 150 mg once monthly.
IV: 3 mg every 3 months.
Patients without high fracture risk, including those with a T-score between −1 and −2.5 and who are not at high fracture risk according to a risk assessment, but who desire pharmacologic therapy to prevent bone loss or fracture (Lewiecki 2021; NOF [Cosman 2014]):
Prevention: Oral: 150 mg once monthly.
Duration of therapy: The optimal duration of therapy has not been established. If discontinued, the decision to resume therapy is based on multiple factors, including decline in bone mineral density and risk factors for fracture (Adler 2016; ES [Eastell 2019]; Watts 2010).
Prostate cancer, metastatic, bone pain (alternative agent if radiation therapy is not an option; off-label use) IV: 6 mg as a single dose over 15 minutes (Hoskin 2015).
Missed doses:
Oral (once-monthly): If an oral dose is missed, administer the next morning after remembered if the next month's scheduled dose is >7 days away. If the next month's scheduled dose is within 7 days, wait until the next month's scheduled dose. Then return to the original scheduled day of the month on the once-monthly schedule; however, do not administer >150 mg within 7 days.
IV (once every 3 months): If an IV dose is missed, administer as soon as it can be rescheduled. Thereafter, administer every 3 months from the date of the last injection.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Osteoporosis: Oral, IV:
CrCl ≥30 mL/minute: No dosage adjustment necessary.
CrCl <30 mL/minute: Use is not recommended.
There are no dosage adjustments provided in the manufacturer's labeling (has not been studied); however, ibandronate does not undergo hepatic metabolism.
Refer to adult dosing.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Solution, Intravenous:
Boniva: 3 mg/3 mL (3 mL [DSC])
Solution, Intravenous [preservative free]:
Generic: 3 mg/3 mL (3 mL)
Tablet, Oral:
Boniva: 150 mg
Generic: 150 mg
Yes
An FDA-approved patient medication guide, which is available with the product information and as follows, must be dispensed with this medication:
Boniva injection: http://www.accessdata.fda.gov/drugsatfda_docs/label/2016/021858s022lbl.pdf#page=18
Boniva tablets: http://www.accessdata.fda.gov/drugsatfda_docs/label/2016/021455s021lbl.pdf#page=19
Oral: Administer 60 minutes before the first food or drink of the day (other than water) and prior to taking any oral medications or supplements (eg, calcium, antacids, vitamins). Ibandronate should be taken in an upright position with a full glass (6 to 8 oz) of plain water and the patient should avoid lying down for 60 minutes to minimize the possibility of GI side effects. Mineral water with a high calcium content should be avoided. The tablet should be swallowed whole; do not chew or suck. Do not eat or drink anything (except water) for 60 minutes following administration of ibandronate.
IV: Administer as a 15 to 30 second bolus IV; avoid paravenous or intraarterial administration (may cause tissue damage). Do not mix with calcium-containing solutions or other drugs. For osteoporosis, do not administer more frequently than every 3 months.
Off-label rates: Infuse over 1 to 2 hours for metastatic bone disease due to breast cancer and for hypercalcemia of malignancy (Body 2003; Pecherstorfer 2003; Ralston 1997). Infuse over 15 minutes for metastatic bone pain due to prostate cancer (Hoskin 2015).
Osteoporosis, postmenopausal, fracture risk reduction: Treatment and prevention of postmenopausal osteoporosis.
Breast cancer, metastatic bone disease (treatment); Hypercalcemia of malignancy; Prostate cancer, metastatic, bone pain (alternative agent)
Atypical femur fractures (AFF) have been reported with bisphosphonate use, including ibandronate. The fractures include subtrochanteric femur (bone just below the hip joint) and diaphyseal femur (long segment of the thigh bone). The benefits of therapy (when used for osteoporosis) generally outweigh the absolute risk of AFF within the first 5 years of treatment, especially in patients with high fracture risk (Ref). The risk decreases after bisphosphonate discontinuation (Ref). AFF is estimated to occur in ~0.2% of bisphosphonate users after ≥5 years of therapy (Ref).
Mechanism: Time-related. Long-term suppression of bone turnover may be primarily responsible; however, micro-damage accumulation and alterations of collagen cross-linking have also been postulated (Ref).
Onset: Delayed; most fractures have occurred in patients receiving bisphosphonates for at least 3 to 5 years (Ref). Patients may experience prodromal pain weeks or months before the fracture occurs (Ref).
Risk factors:
• Long-term treatment (>3 to 5 years) (Ref)
• Asian race (in North America) (Ref)
• Femoral bowing (Ref)
• Glucocorticoid use (>1 year) (Ref)
Esophagitis, dysphagia, esophageal ulcer, erosive esophagitis, esophageal stenosis (rare), and esophageal perforation (rare) have been reported with other bisphosphonates (Ref). Oropharyngeal ulcer has also been noted (Ref). Ibandronate appears to be well tolerated from a GI reaction standpoint (Ref). However, reactions may represent a class effect, including oral ibandronate. Experiencing a GI event increases the likelihood of decreased adherence at 1 year (Ref) or discontinuation (Ref).
Mechanism: GI mucosal irritation is secondary to the local effect on the gastric mucosa (as opposed to a systemic effect) (Ref).
Onset: Varied; dependent upon the type of mucosal injury but case reports have noted onset within 2 days to 12 months after initiation (Ref).
Risk factors:
• Oral administration (versus IV administration) (Ref)
• Incorrect administration technique (oral only) (ie, <180 mL water, lying down after administration) (Ref)
• Older adults (Ref)
• Concurrent nonsteroidal anti-inflammatory drug or antithrombotic use (Ref)
• Prior GI issues (Ref)
While transient hypocalcemia is expected with the use of ibandronate (and all bisphosphonates) secondary to their mechanism of action, cases of symptomatic hypocalcemia are rare with oral ibandronate (Ref). Intravenous ibandronate can cause both asymptomatic (Ref) and symptomatic hypocalcemia. Hypocalcemia is typically quickly reversible with either discontinuation of ibandronate or use of supportive care measures (Ref). In a systematic review of clinically significant hypocalcemia in patients receiving IV bisphosphonates for bone metastases (including ibandronate), incidence ranged from 1% to 2% (Ref). When compared to pamidronate, IV ibandronate appears to have a higher incidence of hypocalcemia (Ref).
Mechanism: By decreasing osteoclast activity, calcium is not released into the bloodstream, causing a transient decrease in blood calcium. In patients with normally functioning parathyroid glands, calcium homeostasis is regained shortly after starting the bisphosphonate (Ref).
Onset: IV: Rapid; hypocalcemia can occur within the first few days after IV infusion of ibandronate. Oral: Intermediate; hypocalcemia typically occurs within weeks of the start of oral ibandronate (Ref).
Risk factors:
• Baseline hypocalcemia (Ref)
• Impaired kidney function (Ref)
• Impaired parathyroid function (Ref)
• IV bisphosphonate (Ref)
• Vitamin D deficiency (Ref)
• Hypomagnesemia (Ref)
• Concurrent medications (eg, interferon-alfa, aminoglycosides, loop diuretics) (Ref)
• Close dosing intervals (Ref)
Acute phase reaction-like symptoms/flu-like symptoms are not life-threatening, reversible, and typically either not observed beyond the first dose of the bisphosphonate or symptoms are less significant with subsequent exposure (Ref). While more common when bisphosphonates are used IV (Ref), it has also been documented with oral use of ibandronate (Ref). The reaction can manifest as influenza-like symptoms, such as fatigue, arthralgia, and bone pain as well as fever and rigors (Ref). Resolution is usually observed within 2 to 3 days after symptom onset but may last up to 7 to 14 days (Ref).
Mechanism: Appears to be mediated by interleukin-6, tumor necrosis factor (TNF)-alpha, and other pro-inflammatory cytokines (Ref).
Onset: Rapid; typically manifests within the first 3 days (Ref).
Risk factors:
• IV dosing (Ref)
• Nitrogen-containing bisphosphonates (eg, ibandronate) (Ref)
• Less frequent oral dosing (Ref)
Osteonecrosis of the jaw (ONJ) was first described in the dental literature (Ref) with the use of IV bisphosphonates, and several case reports of ONJ with IV ibandronate exist. However, there is conflicting evidence of whether this risk is seen with oral bisphosphonates or is simply an increased risk in those who are treated with agents for osteoporosis (Ref). ONJ is most commonly reversible and not life-threatening; however, the possibility of ONJ significantly increases the risk of nonadherence (Ref).
Mechanism: Dose- and time-related; exact mechanism unknown, but several hypothesized mechanisms exist, such as over-suppression of bone turnover (Ref), mucosal toxicity (Ref), cytokine-mediated inflammation (Ref), and infection (Ref).
Onset: Varied; can be spontaneous or after insult, such as tooth extraction and/or dental implant procedures (Ref).
Risk factors:
• Alcohol use disorder (Ref)
• Anemia (Ref)()
• Cancer and anticancer therapy (Ref)
• Corticosteroid therapy (Ref)
• Dental extraction and/or dental implant procedures (Ref)
• Diabetes (Ref)
• Extended duration (>3 years) of bisphosphonate (Ref)
• High-dose, IV bisphosphonate (Ref)
• Immunological disorders (Ref)
• Oral surgery or trauma (Ref)
• Poor oral hygiene (Ref)
• Poorly fitting dental appliance (Ref)
• Radiotherapy to head and neck (Ref)
• Tobacco smoking (Ref)
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
1% to 10%:
Cardiovascular: Hypertension (oral: 6%)
Dermatologic: Skin rash (2%)
Gastrointestinal: Abdominal pain (5% to 8%), constipation (3% to 4%), diarrhea (3% to 5%), dyspepsia (4% to 6%), gastritis (IV: 2%), gastroenteritis (IV: 2%), nausea (2% to 5%)
Genitourinary: Cystitis (IV: 2%), urinary tract infection (2% to 3%)
Hypersensitivity: Acute phase reaction-like symptoms (9% to 10%)
Infection: Influenza (4% to 5%)
Local: Injection site reaction (IV: 2%)
Nervous system: Depression (IV: 1%), dizziness (2%), fatigue (IV: 3%), headache (3% to 4%), insomnia (1% to 2%)
Neuromuscular & skeletal: Arthralgia (6% to 10%), back pain (5% to 7%), limb pain (3% to 4%), localized osteoarthritis (2% to 3%), muscle cramps (oral: 2%), myalgia (2% to 3%)
Respiratory: Bronchitis (2% to 3%), flu-like symptoms (2% to 5%), nasopharyngitis (3% to 4%), upper respiratory tract infection (1% to 2%)
<1%: Ophthalmic: Scleritis, uveitis
Postmarketing:
Cardiovascular: Prolonged QT interval on ECG (Bonilla 2014)
Dermatologic: Bullous dermatitis, erythema multiforme (Song 2019), Stevens-Johnson syndrome
Endocrine & metabolic: Hypocalcemia (Papapetrou 2009)
Hypersensitivity: Anaphylactic shock, anaphylaxis, angioedema
Neuromuscular & skeletal: Femur fracture (diaphyseal or subtrochanteric) (Park-Wyllie 2011), musculoskeletal pain (bone, joint, or muscle; incapacitating), osteonecrosis (oro-facial sites including the external auditory canal), osteonecrosis of the jaw (Lewiecki 2011)
Ophthalmic: Iritis
Renal: Acute kidney injury
Respiratory: Bronchospasm, exacerbation of asthma
Known hypersensitivity to ibandronate or any component of the formulation; hypocalcemia; oral tablets are also contraindicated in patients unable to stand or sit upright for at least 60 minutes and in patients with abnormalities of the esophagus which delay esophageal emptying, such as stricture or achalasia.
Documentation of allergenic cross-reactivity for bisphosphonates is limited. However, because of similarities in chemical structure and/or pharmacologic actions, the possibility of cross-sensitivity cannot be ruled out with certainty.
Concerns related to adverse effects:
• Bone fractures: Atypical femur fractures (AFF) have been reported in patients receiving bisphosphonates. The fractures include subtrochanteric femur (bone just below the hip joint) and diaphyseal femur (long segment of the thigh bone). Some patients experience prodromal pain weeks or months before the fracture occurs. It is unclear if bisphosphonate therapy is the cause for these fractures; AFFs have also been reported in patients not taking bisphosphonates and in patients receiving glucocorticoids. Patients receiving long-term (>3 to 5 years) bisphosphonate therapy may be at an increased risk (Adler 2016; NOF [Cosman 2014]); however, benefits of therapy (when used for osteoporosis) generally outweigh absolute risk of AFF within the first 5 years of treatment, especially in patients with high fracture risk (Adler 2016; ES [Eastell 2019]). Patients presenting with thigh or groin pain with a history of receiving bisphosphonates should be evaluated for femur fracture. Consider interrupting bisphosphonate therapy in patients who develop a femoral shaft fracture; assess for fracture in the contralateral limb.
• Bone/joint/muscle pain: Infrequently, severe (and occasionally debilitating) bone, joint, and/or muscle pain have been reported during bisphosphonate treatment. The onset of pain ranged from a single day to several months. Discontinue intravenous ibandronate therapy in patients who experience severe symptoms; symptoms usually resolve upon discontinuation. Some patients experienced recurrence when rechallenged with the same drug or another bisphosphonate; avoid use in patients with a history of these symptoms in association with bisphosphonate therapy.
• GI mucosa irritation: May cause irritation to upper GI mucosa. Esophagitis, dysphagia, esophageal ulcers, esophageal erosions, and esophageal stricture (rare) have been reported with oral bisphosphonates; risk increases in patients unable to comply with dosing instructions. Use with caution in patients with dysphagia, esophageal disease, gastritis, duodenitis, or ulcers (may worsen underlying condition). Discontinue if new or worsening symptoms develop.
• Hypersensitivity: Allergic reactions, including anaphylactic reaction/shock (some fatal), angioedema, bronchospasm, exacerbation of asthma, rash, Stevens-Johnson syndrome, erythema multiforme, and dermatitis bullous have been reported; discontinue if hypersensitivity reaction occurs.
• Hypocalcemia: Hypocalcemia has been reported with the use of bisphosphonates. Prior to therapy initiation, hypocalcemia must be corrected; ensure adequate calcium and vitamin D intake.
• Influenza-like illness/acute phase reaction: A transient acute phase reaction (eg, fever, chills, pain/myalgia, or other influenza-like symptoms) may occur, typically within 3 days following the initial infusion; resolution is usually observed within 48 hours after symptom onset but may rarely last >7 days (Popp 2017; Sieber 2013).
• Ocular effects: Uveitis and scleritis have been reported with ibandronate; patients presenting with signs of ocular inflammation may require further ophthalmologic evaluation.
• Osteonecrosis of the jaw: Osteonecrosis of the jaw (ONJ), also referred to as medication-related osteonecrosis of the jaw (MRONJ), has been reported in patients receiving bisphosphonates. Known risk factors for MRONJ include invasive dental procedures (eg, tooth extraction, dental implants, boney surgery), cancer diagnosis, concomitant therapy (eg, chemotherapy, corticosteroids, angiogenesis inhibitors), poor oral hygiene, ill-fitting dentures, and comorbid disorders (anemia, coagulopathy, infection, preexisting dental or periodontal disease). Risk may increase with increased duration of bisphosphonate use. According to a position paper by the American Association of Maxillofacial Surgeons (AAOMS), MRONJ has been associated with bisphosphonates and other antiresorptive agents (denosumab), and antiangiogenic agents (eg, bevacizumab, sunitinib) used for the treatment of osteoporosis or malignancy; risk is significantly higher in cancer patients receiving antiresorptive therapy compared to patients receiving osteoporosis treatment (regardless of medication used or dosing schedule). MRONJ risk is also increased with monthly IV antiresorptive therapy compared to the minimal risk associated with oral bisphosphonate use, although risk appears to increase with oral bisphosphonates when duration of therapy exceeds 4 years (AAOMS [Ruggiero 2014]). The manufacturer's labeling states that discontinuing bisphosphonates in patients requiring invasive dental procedures may reduce the risk of ONJ and clinical judgment by physician and/or oral surgeon should be used. However, the AAOMS suggests there is currently no evidence that interrupting oral bisphosphonate therapy alters the risk of ONJ following tooth extraction, and that no alternations or delay in any procedure common to oral/maxillofacial surgeons, periodontists, and other dental providers is necessary in patients receiving oral bisphosphonates for <4 years who have no clinical risk factors (special considerations apply to patients receiving dental implants). Conversely, in patients receiving oral bisphosphonates for >4 years or in patients receiving oral bisphosphonates for <4 years who have also taken corticosteroids or antiangiogenic medications concomitantly, the AAOMS recommends considering a 2-month drug free period prior to invasive dental procedures based on a theoretical benefit. Patients developing ONJ during therapy should receive care by an oral surgeon (AAOMS [Ruggiero 2014]). According to the manufacturer, discontinuation of oral bisphosphonate therapy should be considered (based on risk/benefit evaluation) in patients who develop ONJ.
Disease-related concerns:
• Bariatric surgery: Altered absorption and ulceration risk: Avoid oral bisphosphates after bariatric surgery; inadequate oral absorption and potential anastomotic ulceration may occur. If therapy is indicated, IV administered bisphosphonates are recommended.
• Osteoporosis in survivors of adult cancers (nonmetastatic disease): Survivors of adult cancers with nonmetastatic disease who have osteoporosis (T score of -2.5 or lower in femoral neck, total hip, or lumbar spine) or who are at increased risk of osteoporotic fractures, should be offered bone modifying agents (utilizing the osteoporosis-indicated dose) to reduce the risk of fracture. For patients without hormonal responsive cancers, when clinically appropriate, estrogens may be administered along with other bone modifying agents (ASCO [Shapiro 2019]). The choice of bone modifying agent (eg, oral or IV bisphosphonates or subQ denosumab) should be based on several factors (eg, patient preference, potential adverse effects, quality of life considerations, availability, adherence, cost). Adequate calcium and vitamin D intake, exercise (using a combination of exercise types), as well as lifestyle modifications (if indicated), should also be encouraged.
• Renal impairment: Use not recommended with severe renal impairment (CrCl <30 mL/minute). Intravenous bisphosphonate use has been associated with renal deterioration, including acute renal failure.
None known.
Aminoglycosides: May enhance the hypocalcemic effect of Bisphosphonate Derivatives. Risk C: Monitor therapy
Angiogenesis Inhibitors (Systemic): May enhance the adverse/toxic effect of Bisphosphonate Derivatives. Specifically, the risk for osteonecrosis of the jaw may be increased. Risk C: Monitor therapy
Deferasirox: Bisphosphonate Derivatives may enhance the adverse/toxic effect of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased. Risk C: Monitor therapy
Inhibitors of the Proton Pump (PPIs and PCABs): May diminish the therapeutic effect of Bisphosphonate Derivatives. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents: May enhance the adverse/toxic effect of Bisphosphonate Derivatives. Both an increased risk of gastrointestinal ulceration and an increased risk of nephrotoxicity are of concern. Risk C: Monitor therapy
Polyvalent Cation Containing Products: May decrease the serum concentration of Bisphosphonate Derivatives. Management: Avoid administration of oral medications containing polyvalent cations within: 2 hours before or after tiludronate/clodronate/etidronate; 60 minutes after oral ibandronate; or 30 minutes after alendronate/risedronate. Risk D: Consider therapy modification
Food may reduce absorption; mean oral bioavailability is decreased up to 90% when given with food. Management: Take with a full glass (6-8 oz) of plain water, at least 60 minutes prior to any food, beverages, or medications. Mineral water with a high calcium content should be avoided. Wait at least 60 minutes after taking ibandronate before taking anything else.
Underlying causes of osteoporosis should be evaluated and treated prior to considering bisphosphonate therapy in premenopausal women; effective contraception is recommended when bisphosphonate therapy is required (Pepe 2020). Bisphosphonates are incorporated into the bone matrix and gradually released over time. Because exposure prior to pregnancy may theoretically increase the risk of fetal harm, most sources recommend discontinuing bisphosphonate therapy in females of reproductive potential as early as possible prior to a planned pregnancy. Use in premenopausal females should be reserved for special circumstances when rapid bone loss is occurring; a bisphosphonate with the shortest half-life should then be used (Bhalla 2010; Pereira 2012; Stathopoulos 2011).
It is not known if bisphosphonates cross the placenta, but based on their lower molecular weight, fetal exposure is expected (Djokanovic 2008; Stathopoulos 2011).
Information related to the use of ibandronate in pregnancy is limited (El-Safadi 2012).
Bisphosphonates are incorporated into the bone matrix and gradually released over time. The amount available in the systemic circulation varies by drug, dose, and duration of therapy. Theoretically, there may be a risk of fetal harm when pregnancy follows the completion of therapy (hypocalcemia, low birth weight, and decreased gestation have been observed in some case reports); however, available data have not shown that exposure to bisphosphonates during pregnancy significantly increases the risk of adverse fetal events (Djokanovic 2008; Green 2014; Levy 2009; Machairiotis 2019; Sokal 2019; Stathopoulos 2011). Exposed infants should be monitored for hypocalcemia after birth (Djokanovic 2008; Stathopoulos 2011).
It is not known if ibandronate is present in breast milk.
Ensure adequate calcium and vitamin D intake; if dietary intake is inadequate, dietary supplementation is recommended. Patients should consume:
Calcium: 1,000 mg/day (males: 50 to 70 years of age) or 1,200 mg/day (females ≥51 years of age and males ≥71 years of age) (IOM 2011; NOF [Cosman 2014]).
Vitamin D: 800 to 1,000 units daily (age ≥50 years) (NOF [Cosman 2014]). Recommended dietary allowance (RDA): 600 units daily (age ≤70 years) or 800 units daily (age ≥71 years) (IOM 2011).
Osteoporosis: Serial bone mineral density (BMD) should be evaluated at baseline and every 1 to 3 years on treatment (usually at ~2 years following initiation of therapy, then more or less frequently depending on patient-specific factors and stability of BMD) (AACE/ACE [Camacho 2020]; ES [Eastell 2019]; NOF [Cosman 2014]); evaluate BMD every 2 to 4 years during a drug holiday (ES [Eastell 2019]); serum creatinine prior to each IV dose; annual measurements of height and weight, assessment of chronic back pain; serum calcium and 25(OH)D; may consider measuring biochemical markers of bone turnover (eg, fasting serum CTX or urinary NTX) at baseline, 3 months, and 6 months, to assess treatment response, adherence to therapy, and/or possible malabsorption (ES [Eastell 2019]).
A bisphosphonate which inhibits bone resorption via actions on osteoclasts or on osteoclast precursors; decreases the rate of bone resorption, leading to an indirect increase in bone mineral density.
Distribution: Terminal Vd: 90 L; 40% to 50% of circulating ibandronate binds to bone
Protein binding: 85.7% to 99.5%
Metabolism: Not metabolized
Bioavailability: Oral: Minimal; reduced ~90% following standard breakfast
Half-life elimination:
Oral: 150 mg dose: Terminal: 37 to 157 hours
IV: Terminal: ~5 to 25 hours
Time to peak, plasma: Oral: 0.5 to 2 hours
Excretion: Urine (50% to 60% of absorbed dose, excreted as unchanged drug); feces (unabsorbed drug)
Renal function impairment: Patients with CrCl 40 to 70 mL/minute had 55% higher AUC and patients with CrCl 30 mL/minute had more than a 2-fold increase in exposure.
Geriatric: Progressive age-related changes in renal function may alter the elimination of ibandronate in elderly patients.
Solution (Ibandronate Sodium Intravenous)
3 mg/3 mL (per mL): $100.00 - $168.40
Tablets (Boniva Oral)
150 mg (per each): $229.14
Tablets (Ibandronate Sodium Oral)
150 mg (per each): $138.73 - $165.12
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