RISEDRONATE SODIUM tablet, delayed release

Country: United States

Language: English

Source: NLM (National Library of Medicine)

Active ingredient:

RISEDRONATE SODIUM HEMI-PENTAHYDRATE (UNII: HU2YAQ274O) (RISEDRONIC ACID - UNII:KM2Z91756Z), RISEDRONATE SODIUM MONOHYDRATE (UNII: F67L43UT5C) (RISEDRONIC ACID - UNII:KM2Z91756Z)

Available from:

Greenstone LLC

INN (International Name):

RISEDRONATE SODIUM HEMI-PENTAHYDRATE

Composition:

RISEDRONATE SODIUM ANHYDROUS 30.1 mg

Administration route:

ORAL

Prescription type:

PRESCRIPTION DRUG

Therapeutic indications:

Risedronate sodium delayed-release is indicated for the treatment of osteoporosis in postmenopausal women. In postmenopausal women, risedronate sodium has been shown to reduce the incidence of vertebral fractures and a composite endpoint of nonvertebral osteoporosis-related fractures [see Clinical Studies (14.1) ].  The optimal duration of use has not been determined. The safety and effectiveness of Risedronate sodium delayed-release for the treatment of osteoporosis are based on clinical data of one year 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. Risedronate sodium delayed-release is contraindicated in patients with the following conditions: - Abnormalities of the esophagus which delay esophageal emptying such as stricture or achalasia [see Warnings and Precautions (5.2) ] - Inability to stand or sit upright for at least 30 minutes [see Dosage and Administration (2) , Warnings and Precautions (5.2) ] - Hypocalcemia [see  Warnings and Precautions (5.3) ] - Known hypersensitivity to any component of this product. Angioedema, generalized rash, bullous skin reactions, Stevens-Johnson syndrome and toxic epidermal necrolysis have been reported [see  Adverse Reactions (6.2) ] Risk Summary Available data on use of Risedronate sodium delayed-release in pregnant women are insufficient to inform drug-associated risk of adverse maternal or fetal outcomes. Discontinue Risedronate sodium delayed-release 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/m2 ), the dose indicated for treatment of Paget’s disease. 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 weeks to years. The amount of bisphosphonate incorporated into adult bone available for release into the systemic circulation is directly related to the dose and duration of bisphosphonate use. Consequently, based on 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 2-4% and 15-20%, respectively. Data Animal D ata In animal studies, pregnant rats received risedronate sodium during organogenesis at doses 1 to 26 times the human Paget’s disease dose of 30 mg/day (based on body surface area, mg/m2 ). Survival of neonates was decreased in rats treated during gestation with oral doses approximately 5 times the human dose and body weight was decreased in neonates from dams treated with approximately 26 times the human dose. A low incidence of cleft palate was observed in fetuses from female rats 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. Risk Summary There are no data to assess 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 nursing rats. The concentration of the drug in animal milk does not necessarily predict the concentration of drug in human milk. However, when a drug is present in animal milk, it is likely that the drug will be present in human milk. The developmental and health benefits of breast-feeding should be considered along with the mother’s clinical need for Risedronate sodium delayed-release and any potential adverse effects on the breast-fed child from Risedronate sodium delayed-release or from the underlying maternal condition. Data Animal Data Risedronate was detected in neonates of lactating rats given a single oral dose of risedronate at 24-hours post-dosing, indicating a small degree of lacteal transfer. Infertility There are no data available in humans. Female and male fertility may be impaired based on animal studies demonstrating adverse effects of Risedronate sodium delayed-release on fertility parameters [see Nonclinical Toxicology (13.1) ] . Risedronate sodium delayed-release is not indicated for use in pediatric patients. The safety and effectiveness of risedronate sodium immediate-release 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 OI (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 sodium immediate-release group compared to the placebo group was observed. However, treatment with risedronate sodium immediate-release did not result in a reduction in the risk of fracture in pediatric patients with OI. In risedronate sodium immediate-release 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 sodium immediate-release and 6% of patients treated with placebo. Other adverse reactions reported in greater than or equal to 10% of patients treated with risedronate sodium immediate-release and with a higher frequency than placebo were: pain in the extremity (21% with risedronate sodium immediate-release 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%). Of the patients receiving Risedronate sodium delayed-release in postmenopausal osteoporosis studies, 59% were 65 and over, while 13% were 75 and over. No overall differences in safety or effectiveness were observed between these patients and younger patients, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out. Risedronate sodium delayed-release 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. No studies have been performed to assess risedronate sodium’s safety or efficacy in patients with hepatic impairment. Risedronate is not metabolized in human liver preparations. Dosage adjustment is unlikely to be needed in patients with hepatic impairment.

Product summary:

Risedronate sodium delayed-release tablets are: 35 mg, yellow, oval-shaped, and engraved with EC 35 on one side. NDC 59762-0407-4       Dose pack of 4 tablets Store at controlled room temperature 20° to 25° C (68° to 77° F) [see USP].

Authorization status:

New Drug Application Authorized Generic

Patient Information leaflet

Greenstone LLC
----------
Medication Guide
Risedronate sodium delayed-release
tablets
Read this Medication Guide that comes with Risedronate sodium
delayed-release 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 your treatment. Talk to your
doctor if you have any questions about Risedronate sodium
delayed-release, there may be new
information about it.
What is the most important information I should know about Risedronate
sodium delayed-release?
Risedronate sodium delayed-release 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 thigh bone fractures
1. Esophagus problems.
Some people who take Risedronate sodium delayed-release 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 delayed-release
exactly as prescribed to help
lower your chance of getting esophagus problems. (See the section
“How should I take
Risedronate sodium delayed-release?”)
•
Stop taking Risedronate sodium delayed-release 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 delayed-release may lower the calcium levels in
your blood. If you have low blood
calcium before you start taking Risedronate sodium delayed-release, it
may get worse during treatment.
Your low blood calcium must be treated before you take Risedronate
sodium delayed-release. 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

Summary of Product characteristics

RISEDRONATE SODIUM- RISEDRONATE SODIUM TABLET, DELAYED RELEASE
GREENSTONE LLC
----------
HIGHLIGHTS OF PRESCRIBING INFORMATION
THESE HIGHLIGHTS DO NOT INCLUDE ALL THE INFORMATION NEEDED TO USE
RISEDRONATE
SODIUM DELAYED-RELEASE SAFELY AND EFFECTIVELY. SEE FULL PRESCRIBING
INFORMATION
FOR RISEDRONATE SODIUM DELAYED-RELEASE.
RISEDRONATE SODIUM DELAYED-RELEASE TABLETS
INITIAL U.S. APPROVAL: 1998
INDICATIONS AND USAGE
Risedronate sodium is a bisphosphonate in a delayed-release
formulation and is indicated for treatment of
postmenopausal osteoporosis (1.1)
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 (1.2)
DOSAGE AND ADMINISTRATION
One 35 mg delayed-release tablet once-a-week (2.1)
Instruct patients to:
Take Risedronate sodium delayed-release in the morning immediately
_following breakfast_ with at least
4 ounces of plain water (2.2)
Avoid lying down for 30 minutes after taking Risedronate sodium
delayed-release (2.2)
Take supplemental calcium and vitamin D if dietary intake is
inadequate (2.3)
DOSAGE FORMS AND STRENGTHS
Delayed-release tablets: 35 mg (3)
CONTRAINDICATIONS
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 PRECAUTIONS
_Products Containing Same Active Ingredient_: Patients receiving
Risedronate sodium immediate-
release should not be treated with Risedronate sodium delayed-release
(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 Femur