Fosamax Information
Fosamax (Alendronate) Description
Fosamax (Alendronate) (alendronate sodium) is a bisphosphonate that acts as a specific inhibitor of osteoclast-mediated bone resorption. Bisphosphonates are synthetic analogs of pyrophosphate that bind to the hydroxyapatite found in bone.
Alendronate sodium is chemically described as (4-amino-1-hydroxybutylidene) bisphosphonic acid monosodium salt trihydrate.
The empirical formula of alendronate sodium is CHNNaOP•3HO and its formula weight is 325.12. The structural formula is:
Alendronate sodium is a white, crystalline, nonhygroscopic powder. It is soluble in water, very slightly soluble in alcohol, and practically insoluble in chloroform.
Tablets Fosamax (Alendronate) for oral administration contain 6.53, 13.05, 45.68, 52.21 or 91.37 mg of alendronate monosodium salt trihydrate, which is the molar equivalent of 5, 10, 35, 40 and 70 mg, respectively, of free acid, and the following inactive ingredients: microcrystalline cellulose, anhydrous lactose, croscarmellose sodium, and magnesium stearate. Tablets Fosamax (Alendronate) 10 mg also contain carnauba wax.
Each bottle of the oral solution contains 91.35 mg of alendronate monosodium salt trihydrate, which is the molar equivalent to 70 mg of free acid. Each bottle also contains the following inactive ingredients: sodium citrate dihydrate and citric acid anhydrous as buffering agents, sodium saccharin, artificial raspberry flavor, and purified water. Added as preservatives are sodium propylparaben 0.0225% and sodium butylparaben 0.0075%.
Fosamax (Alendronate) Clinical Pharmacology
(also see )
Intravenous ranitidine was shown to double the bioavailability of oral alendronate. The clinical significance of this increased bioavailability and whether similar increases will occur in patients given oral H-antagonists is unknown.
In healthy subjects, oral prednisone (20 mg three times daily for five days) did not produce a clinically meaningful change in the oral bioavailability of alendronate (a mean increase ranging from 20 to 44%).
Products containing calcium and other multivalent cations are likely to interfere with absorption of alendronate.
Osteoporosis is characterized by low bone mass that leads to an increased risk of fracture. The diagnosis can be confirmed by the finding of low bone mass, evidence of fracture on x-ray, a history of osteoporotic fracture, or height loss or kyphosis, indicative of vertebral (spinal) fracture. Osteoporosis occurs in both males and females but is most common among women following the menopause, when bone turnover increases and the rate of bone resorption exceeds that of bone formation. These changes result in progressive bone loss and lead to osteoporosis in a significant proportion of women over age 50. Fractures, usually of the spine, hip, and wrist, are the common consequences. From age 50 to age 90, the risk of hip fracture in white women increases 50-fold and the risk of vertebral fracture 15- to 30-fold. It is estimated that approximately 40% of 50-year-old women will sustain one or more osteoporosis-related fractures of the spine, hip, or wrist during their remaining lifetimes. Hip fractures, in particular, are associated with substantial morbidity, disability, and mortality.
Daily oral doses of alendronate (5, 20, and 40 mg for six weeks) in postmenopausal women produced biochemical changes indicative of dose-dependent inhibition of bone resorption, including decreases in urinary calcium and urinary markers of bone collagen degradation (such as deoxypyridinoline and cross-linked N-telopeptides of type I collagen). These biochemical changes tended to return toward baseline values as early as 3 weeks following the discontinuation of therapy with alendronate and did not differ from placebo after 7 months.
Long-term treatment of osteoporosis with Fosamax (Alendronate) 10 mg/day (for up to five years) reduced urinary excretion of markers of bone resorption, deoxypyridinoline and cross-linked N-telopeptides of type l collagen, by approximately 50% and 70%, respectively, to reach levels similar to those seen in healthy premenopausal women. Similar decreases were seen in patients in osteoporosis prevention studies who received Fosamax (Alendronate) 5 mg/day. The decrease in the rate of bone resorption indicated by these markers was evident as early as one month and at three to six months reached a plateau that was maintained for the entire duration of treatment with Fosamax (Alendronate) . In osteoporosis treatment studies Fosamax (Alendronate) 10 mg/day decreased the markers of bone formation, osteocalcin and bone specific alkaline phosphatase by approximately 50%, and total serum alkaline phosphatase by approximately 25 to 30% to reach a plateau after 6 to 12 months. In osteoporosis prevention studies Fosamax (Alendronate) 5 mg/day decreased osteocalcin and total serum alkaline phosphatase by approximately 40% and 15%, respectively. Similar reductions in the rate of bone turnover were observed in postmenopausal women during one-year studies with once weekly Fosamax (Alendronate) 70 mg for the treatment of osteoporosis and once weekly Fosamax (Alendronate) 35 mg for the prevention of osteoporosis. These data indicate that the rate of bone turnover reached a new steady-state, despite the progressive increase in the total amount of alendronate deposited within bone.
As a result of inhibition of bone resorption, asymptomatic reductions in serum calcium and phosphate concentrations were also observed following treatment with Fosamax (Alendronate) . In the long-term studies, reductions from baseline in serum calcium (approximately 2%) and phosphate (approximately 4 to 6%) were evident the first month after the initiation of Fosamax (Alendronate) 10 mg. No further decreases in serum calcium were observed for the five-year duration of treatment; however, serum phosphate returned toward prestudy levels during years three through five. Similar reductions were observed with Fosamax (Alendronate) 5 mg/day. In one-year studies with once weekly Fosamax (Alendronate) 35 and 70 mg, similar reductions were observed at 6 and 12 months. The reduction in serum phosphate may reflect not only the positive bone mineral balance due to Fosamax (Alendronate) but also a decrease in renal phosphate reabsorption.
Sustained use of glucocorticoids is commonly associated with development of osteoporosis and resulting fractures (especially vertebral, hip, and rib). It occurs both in males and females of all ages. Osteoporosis occurs as a result of inhibited bone formation and increased bone resorption resulting in net bone loss. Alendronate decreases bone resorption without directly inhibiting bone formation.
In clinical studies of up to two years' duration, Fosamax (Alendronate) 5 and 10 mg/day reduced cross-linked N-telopeptides of type I collagen (a marker of bone resorption) by approximately 60% and reduced bone-specific alkaline phosphatase and total serum alkaline phosphatase (markers of bone formation) by approximately 15 to 30% and 8 to 18%, respectively. As a result of inhibition of bone resorption, Fosamax (Alendronate) 5 and 10 mg/day induced asymptomatic decreases in serum calcium (approximately 1 to 2%) and serum phosphate (approximately 1 to 8%).
Paget's disease of bone is a chronic, focal skeletal disorder characterized by greatly increased and disorderly 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 weakened bone structure.
Clinical manifestations of Paget's disease range from no symptoms to severe morbidity due to bone pain, bone deformity, pathological fractures, and neurological and other complications. Serum alkaline phosphatase, the most frequently used biochemical index of disease activity, provides an objective measure of disease severity and response to therapy.
Fosamax (Alendronate) decreases the rate of bone resorption directly, which leads to an indirect decrease in bone formation. In clinical trials, Fosamax (Alendronate) 40 mg once daily for six months produced significant decreases in serum alkaline phosphatase as well as in urinary markers of bone collagen degradation. As a result of the inhibition of bone resorption, Fosamax (Alendronate) induced generally mild, transient, and asymptomatic decreases in serum calcium and phosphate.
Fosamax (Alendronate) Animal Pharmacology
The relative inhibitory activities on bone resorption and mineralization of alendronate and etidronate were compared in the Schenk assay, which is based on histological examination of the epiphyses of growing rats. In this assay, the lowest dose of alendronate that interfered with bone mineralization (leading to osteomalacia) was 6000-fold the antiresorptive dose. The corresponding ratio for etidronate was one to one. These data suggest that alendronate administered in therapeutic doses is highly unlikely to induce osteomalacia.
Fosamax (Alendronate) Indications And Usage
Fosamax (Alendronate) is indicated for:
The safety and effectiveness of Fosamax (Alendronate) for the treatment of osteoporosis are based on clinical data of four years duration. The optimal duration of use has not been determined. All patients on bisphosphonate therapy should have the need for continued therapy re-evaluated on a periodic basis.
Fosamax (Alendronate) Warnings
Fosamax (Alendronate) , 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 Fosamax (Alendronate) is given to patients with active upper gastrointestinal problems (such as known Barrett's esophagus, dysphagia, other esophageal diseases, gastritis, duodenitis, or ulcers).
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 including Fosamax (Alendronate) . 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 Fosamax (Alendronate) 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 including Fosamax (Alendronate) and/or who fail to swallow oral bisphosphonates including Fosamax (Alendronate) with the recommended full glass (6-8 oz) of water, and/or who continue to take oral bisphosphonates including Fosamax (Alendronate) 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 ). In patients who cannot comply with dosing instructions due to mental disability, therapy with Fosamax (Alendronate) 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.
Fosamax (Alendronate) Precautions
Causes of osteoporosis other than estrogen deficiency, aging, and glucocorticoid use should be considered.
Hypocalcemia must be corrected before initiating therapy with Fosamax (Alendronate) (see ). Other disorders affecting mineral metabolism (such as vitamin D deficiency) should also be effectively treated. In patients with these conditions, serum calcium and symptoms of hypocalcemia should be monitored during therapy with Fosamax (Alendronate) .
Presumably due to the effects of Fosamax (Alendronate) on increasing bone mineral, small, asymptomatic decreases in serum calcium and phosphate may occur, especially in patients with Paget's disease, in whom the pretreatment rate of bone turnover may be greatly elevated and in patients receiving glucocorticoids, in whom calcium absorption may be decreased.
Ensuring adequate calcium and vitamin D intake is especially important in patients with Paget's disease of bone and in patients receiving glucocorticoids.
In post marketing experience, severe and occasionally incapacitating bone, joint, and/or muscle pain has been reported in patients taking bisphosphonates that are approved for the prevention and treatment of osteoporosis (see ). This category of drugs includes Fosamax (Alendronate) (alendronate). Most of the patients were postmenopausal women. The time to onset of symptoms varied from one day to several months after starting the drug. Discontinue use if severe symptoms develop. Most patients had relief of symptoms after stopping. A subset had recurrence of symptoms when rechallenged with the same drug or another bisphosphonate.
In placebo-controlled clinical studies of Fosamax (Alendronate) , the percentages of patients with these symptoms were similar in the Fosamax (Alendronate) and placebo groups.
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 Fosamax (Alendronate) . Known risk factors for osteonecrosis of the jaw include invasive dental procedures (e.g., tooth extraction, dental implants, boney surgery), diagnosis of cancer, concomitant therapies (e.g., chemotherapy, corticosteroids), poor oral hygiene, and co-morbid disorders (e.g., periodontal and/or other pre-existing dental disease, anemia, coagulopathy, infection, ill-fitting dentures).
For patients requiring invasive dental procedures, discontinuation of bisphosphonate treatment may reduce the risk for ONJ. Clinical judgment of the treating physician and/or oral surgeon should guide the management plan of each patient based on individual benefit/risk assessment.
Patients who develop osteonecrosis of the jaw while on bisphosphonate therapy should receive care by an oral surgeon. In these patients, extensive dental surgery to treat ONJ may exacerbate the condition. Discontinuation of bisphosphonate therapy should be considered based on individual benefit/risk assessment.
Atypical, low-energy, or low trauma fractures of the femoral shaft have been reported in bisphosphonate-treated patients. These fractures can occur anywhere in the femoral shaft from just below the lesser trochanter to above the supracondylar flare and are transverse or short oblique in orientation without evidence of comminution. Causality has not been established as these fractures also occur in osteoporotic patients who have not been treated with bisphosphonates.
Atypical femur fractures most commonly occur with minimal or no trauma to the affected area. They may be bilateral and many patients report prodromal pain in the affected area, usually presenting as dull, aching thigh pain, weeks to months before a complete fracture occurs. A number of reports note that patients were also receiving treatment with glucocorticoids (e.g. prednisone) at the time of fracture.
Any patient with a history of bisphosphonate exposure who presents with thigh or groin pain should be suspected of having an atypical fracture and should be evaluated to rule out an incomplete femur fracture. Patients presenting with an atypical fracture should also be assessed for symptoms and signs of fracture in the contralateral limb. Interruption of bisphosphonate therapy should be considered, pending a risk/benefit assessment, on an individual basis.
The risk versus benefit of Fosamax (Alendronate) for treatment at daily dosages of glucocorticoids less than 7.5 mg of prednisone or equivalent has not been established (see ). Before initiating treatment, the hormonal status of both men and women should be ascertained and appropriate replacement considered.
A bone mineral density measurement should be made at the initiation of therapy and repeated after 6 to 12 months of combined Fosamax (Alendronate) and glucocorticoid treatment.
The efficacy of Fosamax (Alendronate) for the treatment of glucocorticoid-induced osteoporosis has been shown in patients with a median bone mineral density which was 1.2 standard deviations below the mean for healthy young adults.
The efficacy of Fosamax (Alendronate) has been established in studies of two years' duration. The greatest increase in bone mineral density occurred in the first year with maintenance or smaller gains during the second year. Efficacy of Fosamax (Alendronate) beyond two years has not been studied.
The efficacy of Fosamax (Alendronate) in respect to fracture prevention has been demonstrated for vertebral fractures. However, this finding was based on very few fractures that occurred primarily in postmenopausal women. The efficacy for prevention of non-vertebral fractures has not been demonstrated.
Harderian gland (a retro-orbital gland not present in humans) adenomas were increased in high-dose female mice (p=0.003) in a 92-week oral carcinogenicity study at doses of alendronate of 1, 3, and 10 mg/kg/day (males) or 1, 2, and 5 mg/kg/day (females). These doses are equivalent to 0.12 to 1.2 times a maximum recommended daily dose of 40 mg (Paget's disease) based on surface area, mg/m. The relevance of this finding to humans is unknown.
Parafollicular cell (thyroid) adenomas were increased in high-dose male rats (p=0.003) in a 2-year oral carcinogenicity study at doses of 1 and 3.75 mg/kg body weight. These doses are equivalent to 0.26 and 1 times a 40 mg human daily dose based on surface area, mg/m. The relevance of this finding to humans is unknown.
Alendronate was not genotoxic in the microbial mutagenesis assay with and without metabolic activation, in an mammalian cell mutagenesis assay, in an alkaline elution assay in rat hepatocytes, and in an chromosomal aberration assay in mice. In an chromosomal aberration assay in Chinese hamster ovary cells, however, alendronate gave equivocal results.
Alendronate had no effect on fertility (male or female) in rats at oral doses up to 5 mg/kg/day (1.3 times a 40 mg human daily dose based on surface area, mg/m).
The efficacy and safety of Fosamax (Alendronate) were examined in a randomized, double-blind, placebo-controlled two-year study of 139 pediatric patients, aged 4-18 years, with severe osteogenesis imperfecta. One-hundred-and-nine patients were randomized to 5 mg Fosamax (Alendronate) daily (weight
Fosamax (Alendronate) is not indicated for use in children.
(For clinical adverse experiences in children, see .)
Fosamax (Alendronate) Adverse Reactions
In clinical studies of up to five years in duration adverse experiences associated with Fosamax (Alendronate) usually were mild, and generally did not require discontinuation of therapy.
Fosamax (Alendronate) has been evaluated for safety in approximately 8000 postmenopausal women in clinical studies.
The following adverse reactions have been reported in post-marketing use:
Body as a Whole:
Gastrointestinal:
Localized osteonecrosis of the jaw, generally associated with tooth extraction and/or local infection with delayed healing, has been reported rarely (see ).
Musculoskeletal:
Nervous system:
Skin:
Special Senses:
Fosamax (Alendronate) Overdosage
Significant lethality after single oral doses was seen in female rats and mice at 552 mg/kg (3256 mg/m) and 966 mg/kg (2898 mg/m), respectively. In males, these values were slightly higher, 626 and 1280 mg/kg, respectively. There was no lethality in dogs at oral doses up to 200 mg/kg (4000 mg/m).
No specific information is available on the treatment of overdosage with Fosamax (Alendronate) . Hypocalcemia, hypophosphatemia, and upper gastrointestinal adverse events, such as upset stomach, heartburn, esophagitis, gastritis, or ulcer, may result from oral overdosage. Milk or antacids should be given to bind alendronate. Due to the risk of esophageal irritation, vomiting should not be induced and the patient should remain fully upright.
Dialysis would not be beneficial.
Fosamax (Alendronate) Dosage And Administration
Fosamax (Alendronate) must be taken one-half hour before the first food, beverage, or medication of the day with plain water only (see ). Other beverages (including mineral water), food, and some medications are likely to reduce the absorption of Fosamax (Alendronate) (see ). Waiting less than 30 minutes, or taking Fosamax (Alendronate) with food, beverages (other than plain water) or other medications will lessen the effect of Fosamax (Alendronate) by decreasing its absorption into the body.
Fosamax (Alendronate) should only be taken upon arising for the day. To facilitate delivery to the stomach and thus reduce the potential for esophageal irritation, a Fosamax (Alendronate) tablet should be swallowed with a full glass of water (6-8 oz). To facilitate gastric emptying Fosamax (Alendronate) oral solution should be followed by at least 2 oz (a quarter of a cup) of water. Patients should not lie down for at least 30 minutes until after their first food of the day. Fosamax (Alendronate) should not be taken at bedtime or before arising for the day. Failure to follow these instructions may increase the risk of esophageal adverse experiences (see , ).
Patients should receive supplemental calcium and vitamin D, if dietary intake is inadequate (see ).
No dosage adjustment is necessary for the elderly or for patients with mild-to-moderate renal insufficiency (creatinine clearance 35 to 60 mL/min). Fosamax (Alendronate) is not recommended for patients with more severe renal insufficiency (creatinine clearance
Fosamax (Alendronate) How Supplied
No. 3759 — Tablets Fosamax (Alendronate) , 5 mg, are white, round, uncoated tablets with an outline of a bone image on one side and code MRK 925 on the other. They are supplied as follows:
No. 3797 — Tablets Fosamax (Alendronate) , 10 mg, are white, oval, wax-polished tablets with code MRK on one side and 936 on the other. They are supplied as follows:
No. 3813 — Tablets Fosamax (Alendronate) , 35 mg, are white, oval, uncoated tablets with code 77 on one side and a bone image on the other. They are supplied as follows:
No. 8457 — Tablets Fosamax (Alendronate) , 40 mg, are white, triangular-shaped, uncoated tablets with code MSD 212 on one side and Fosamax (Alendronate) on the other. They are supplied as follows:
No. 3814 — Tablets Fosamax (Alendronate) , 70 mg, are white, oval, uncoated tablets with code 31 on one side and an outline of a bone image on the other. They are supplied as follows:
No. 3833 — Oral Solution Fosamax (Alendronate) , 70 mg, is a clear, colorless solution with a raspberry flavor and is supplied as follows:
Fosamax (Alendronate) Medication Guide
Read the Medication Guide that comes with Fosamax (Alendronate) before you start taking it 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 treatment. Talk to your doctor if you have any questions about Fosamax (Alendronate) .
Fosamax (Alendronate) is a prescription medicine used to:
It is not known how long Fosamax (Alendronate) works for the treatment and prevention of osteoporosis. You should see your doctor regularly to determine if Fosamax (Alendronate) is still right for you.
Fosamax (Alendronate) is not for use in children.
Especially tell your doctor if you take:
Know the medicines you take. Keep a list of them and show it to your doctor and pharmacist each time you get a new medicine.
After swallowing Fosamax (Alendronate) tablet or oral solution, wait at least 30 minutes:
If you miss a dose of Fosamax (Alendronate) , do not take it later in the day. Take your missed dose on the next morning after you remember and then return to your normal schedule. Do not take 2 doses on the same day.
If you take too much Fosamax (Alendronate) , call your doctor. Do not try to vomit. Do not lie down.
Fosamax (Alendronate) may cause serious side effects.
You may get allergic reactions, such as hives or, in rare cases, swelling of your face, lips, tongue, or throat.
Tell your doctor if you have any side effect that bothers you or that does not go away.
These are not all the possible side effects of Fosamax (Alendronate) . For more information, ask your doctor or pharmacist.
Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.
Medicines are sometimes prescribed for purposes other than those listed in a Medication Guide. Do not use Fosamax (Alendronate) for a condition for which it was not prescribed. Do not give Fosamax (Alendronate) to other people, even if they have the same symptoms you have. It may harm them.
This Medication Guide summarizes the most important information about Fosamax (Alendronate) . If you would like more information, talk with your doctor. You can ask your doctor or pharmacist for information about Fosamax (Alendronate) that is written for health professionals. For more information, go to: www.Fosamax (Alendronate) .com or call 1-800-622-4477 (toll-free).
Active ingredient: alendronate sodium
Inactive ingredients: cellulose, lactose, croscarmellose sodium, magnesium stearate.
In addition the 10 mg tablet also contains carnauba wax.
Active ingredient: alendronate monosodium salt trihydrate
Inactive ingredients: sodium citrate dihydrate, citric acid anhydrous, sodium saccharin, artificial raspberry flavor, water, sodium propylparaben 0.0225%, sodium butylparaben 0.0075%.
Merck Sharp & Dohme Corp., a subsidiary of Whitehouse Station, NJ 08889, USA
Copyright © 2010 Merck Sharp & Dohme Corp., a subsidiary of All rights reserved
Revised July 2011
6013412
This Medication Guide has been approved by the U.S. Food and Drug Administration.
Fosamax (Alendronate) Principal Display Panel - Bottle Label Mg
Fosamax (Alendronate) 10 mg(Alendronate Sodium Tablets)
Merck Sharp & Dohme Corp., a subsidiary ofMERCK & CO., INC.Whitehouse Station, NJ 08889, USA
Alendronate Sodium (active ingred.)Made in Ireland. Formulated in USA.
Dispense the accompanying Medication Guide to each patient.
30 Tablets
NDC 0006-0936-31
Each tablet contains 13.05 mg Alendronate Sodium (10 mg free acid equivalent).
Store in a well-closed container at room temperature, 15 - 30°C (59 - 86°F).
USUAL ADULT DOSAGE: 10 mg once a day. See accompanying circular for complete dosage information.
Rx only
962220430 | No. 3797
Fosamax (Alendronate) Principal Display Panel - Bi Fold Card, Outer Mg
ONCE WEEKLYFosamax (Alendronate) 35 mg(Alendronate Sodium Tablets)
Dispense the enclosed Medication Guide to each patient.
Each tablet contains 45.68 mg alendronate sodium (35 mg free acid equivalent)
4 TabletsNo. 3813
Rx only
USUAL ADULT DOSAGE:ONE 35 mg TABLET ONCE WEEKLY
See accompanying circular for complete dosage information.
Merck Sharp & Dohme Corp., a subsidiary ofMERCK & CO., INC.Whitehouse Station, NJ 08889, USA
Alendronate Sodium (active ingred.) Made in Ireland.Formulated in USA.
Fosamax (Alendronate) Principal Display Panel - Bi Fold Card, Outer Mg
ONCE WEEKLYFosamax (Alendronate) 70 mg(Alendronate Sodium Tablets)
Dispense the enclosed Medication Guide to each patient.
Each tablet contains 91.37 mg alendronate sodium (70 mg free acid equivalent)
4 TabletsNo. 3814
Rx only
USUAL ADULT DOSAGE:ONE 70 mg TABLET ONCE WEEKLY
See accompanying circular for complete dosage information.
Merck Sharp & Dohme Corp., a subsidiary ofMERCK & CO., INC.Whitehouse Station, NJ 08889, USA
Alendronate Sodium (active ingred.) Made in Ireland.Formulated in USA.
Fosamax (Alendronate) Principal Display Panel - Bottle Label Mg Per Ml
75 mL
NDC 0006-3833-01
ONCE WEEKLYFosamax (Alendronate) 70 mg(Alendronate Sodium) Oral Solution
70 mg per 75 mL
Dispense the accompanying Medication Guide to each patient.
Each bottle contains 91.35 mg alendronate sodium (70 mg free acid equivalent) in 75 mL of oral solution.
Mark the day of the week you prefer to take Fosamax (Alendronate) 70 mg, and remember to take one bottle each week, on that day.
Store at 25°C (77°F), excursions permitted to 15-30°C (59-86°F). [See USP Controlled Room Temperature.]
Do not freeze.
Rx only
USUAL ADULT DOSAGE: One bottle (75 mL) of 70 mg oral solution taken once weekly at least one-half hour before the first food, beverage or medication of the day followed by at least 2 ounces (a quarter of a cup) of plain water. Do not lie down until after the first food of the day.
See accompanying circular for complete dosage information.
Merck Sharp & Dohme Corp., a subsidiary ofMERCK & CO., INC., Whitehouse Station, NJ 08889, USA
Alendronate Sodium (active ingred.) Made in Ireland.Formulated in USA.
Inactive Ingredients: Sodium citrate dihydrate and citric acid anhydrous as buffering agents, sodium saccharin, artificial raspberry flavor, and purified water. Added as preservatives are sodium propylparaben 0.0225% and sodium butylparaben 0.0075%.
9934102
