Aclasta, 5 mg/100 ml 100 ml
€401.02 €347.55
Out of stock
(E-mail when Stock is available)
Pharmacodynamics
Zoledronic acid, a member of the class of aminobisphosphonates, acts primarily on bone tissue, inhibits osteoclast activity and bone resorption. Selective action of bisphosphonates on bone tissue is based on high affinity for mineralized bone tissue.
After IV administration zoledronic acid rapidly redistributes into bone tissue and, like other bisphosphonates, localizes mainly in the sites of remodeling. The main molecular target of zoledronic acid in the osteoclast is the enzyme farnesyl pyrophosphate synthetase (FPS); however, other mechanisms of action of the drug are not excluded.
The prolonged period of action of the drug is determined by the high affinity to the active center of FPS and the expressed affinity to the mineralized bone tissue. On experimental models of accelerated osteoresorption it was shown that zoledronic acid significantly inhibits bone resorption without undesirable effect on formation, mineralization and mechanical properties of the bone tissue, reduces osteoclast activity and activation rate of new remodeling foci both in trabecular and cortical (Haversian) bone parts without causing formation of fibrous bone tissue and aberrant osteoid accumulation. Except for the high antiresorptive action, the effect of zoledronic acid on bone tissue is similar to that of other bisphosphonates.
The use of Aclasta in patients with postmenopausal osteoporosis (femoral neck bone mineral density T-criterion values of less than 2.5) showed a statistically significant 70% reduction in the risk of vertebral fractures by the end of the 3rd year of treatment, and a 60-70% reduction in the risk of one or more new/repeated fractures and moderate/severe vertebral fractures. In patients with osteoporosis aged 75 years and older, treatment with Aclasta achieved a 61% reduction in the risk of vertebral fractures.
Treatment with Aclasta reduced the relative risk of nonvertebral fractures of any localization, (including fractures of the phalanges and facial bones of the skull) by 33%. Administration of the drug for 3 years in patients with postmenopausal osteoporosis showed the increase of bone mineral density (BMD) of lumbar vertebrae, femur in general, femoral neck, and distal radius by 6.9; 6; 5, and 3.2% on the average respectively.
Aclast therapy for 1 year in patients with postmenopausal osteoporosis showed a decrease in the activity of bone ALP isoenzyme, N-terminal collagen propeptide type I (PINP) and β-C-terminal telopeptides of blood to the premenopausal value. No further decrease in the blood content of bone remodeling markers was noted with repeated injections of the drug for 3 years.
Application of Aclasta for 3 years significantly reduced the rate of growth loss in patients, and helped to shorten the period of immobilization in postmenopausal women with osteoporosis and vertebral fractures, including by reducing the intensity of pain syndrome.
Injection of the drug in patients (men and women) with fractures of the proximal femur (which occurred due to minimal trauma and required surgical intervention) resulted in a 35% reduction of the frequency of subsequent osteoporotic fractures of any localization compared to placebo (of which clinically significant vertebral fractures – by 46%, nonvertebral fractures – by 27%).
The relative risk of fatal outcomes (regardless of their cause) was reduced by 28% with the use of Aclasta in this category of patients. In patients with femoral fractures the use of Aclasta over 2 years showed 5.4% and 4.3% increase of MPC of femur in general and femoral neck region, respectively.
A once-daily use in men with primary (senile) or secondary (hypogonadism) osteoporosis showed a marked increase in MPC of lumbar vertebrae for 2 years.
In patients with GCS-induced osteoporosis, Aclasta also significantly increased BMD without adversely affecting bone structure and mineralization. When Aclasta was used once every 2 years to prevent postmenopausal osteoporosis in women with osteopenia and postmenopause duration of less and more than 5 years, a 6.3% and 5.4% increase in the lumbar spine BMD was observed, respectively. When the drug was administered once every 2 years, the MPC of the femur was increased by 4.7 and 3.2% in women with postmenopause duration of less than and more than 5 years, respectively.
In women with varying duration of postmenopause, administration of Aclasta once every 2 years resulted in a 44-46% reduction in blood β-C-terminal telopeptide concentrations (to premenopausal levels) and a 55-40% reduction in type I collagen N-terminal propeptide (PINP).
The treatment with Aclasta in patients with Paget’s bone disease showed statistically significant, rapid and prolonged therapeutic response, normalization of bone metabolism and plasma ALP activity.
The drug is also highly effective in patients previously treated with oral bisphosphonates.
It was found that in the majority of patients with zoledronic acid the therapeutic response is maintained throughout the entire period of treatment (about 2 years). Expressed decrease of pain syndrome at 6 months after a single injection of Aclasta in dose of 5 mg is comparable to analgesic effect of risedronic acid in dose of 30 mg/day.
In patients with postmenopausal osteoporosis and Paget’s disease zoledronic acid has no effect on the qualitative state of normal bone tissue, does not disturb bone remodeling and mineralization processes and helps to maintain normal trabecular bone architectonics.
Pharmacokinetics
Pharmacokinetic data were obtained after single and repeated 5- and 15-minute infusions of 2, 4, 8 and 16 mg zoledronic acid in 64 patients. The pharmacokinetic parameters were independent of the drug dose. After initiation of the drug, the plasma concentration of zoledronic acid increases rapidly, reaching a maximum at the end of the infusion.
After the end of infusion a rapid decrease of zoledronic acid concentration in plasma occurs (to the level of <10% of Cmax – after 4 hours and to <1% of Cmax – after 24 hours), then during long period low concentration of the preparation in plasma is maintained (not exceeding 0.1% of Cmax).
Zoledronic acid is excreted by kidneys in 3 phases: rapid biphasic excretion from the systemic blood stream with T1/2 of 0.24 h (α-phase) and 1.87 h (β-phase) and long phase with a final T1/2 of 146 h (γ-phase).
The rapid decrease of the drug concentration (α- and β-phase) in plasma is probably due to the rapid distribution of zoledronic acid in bone tissue and its excretion by the kidneys. No cumulation of the drug was observed with repeated injections every 28 days. Zoledronic acid is not metabolized and is excreted unchanged by the kidneys.
In the first 24 hours, (39±16)% of the administered dose is detected in the urine. The remaining amount of the drug is bound exclusively to the bone tissue, after which slow release of zoledronic acid back from the bone tissue into the systemic bloodstream and its excretion by the kidneys is observed. Total plasma clearance of the drug is (5.04±2.5) l/h and does not depend on the dose, sex, age, race and body weight of the patient.
The variability of zoledronic acid plasma clearance in the same patient and in different patients was found to be 36% and 34%, respectively. Increasing infusion time from 5 to 15 min leads to a 30% decrease in zoledronic acid concentration at the end of infusion, but does not affect the bioavailability of the drug. Binding of zoledronic acid to plasma proteins is low (43-55%) and does not depend on its concentration.
Pharmacokinetics in special clinical cases
Renal clearance of zoledronic acid correlates with creatinine Cl and is (75±33)% of creatinine Cl, with mean values of (84±29) ml/min (range, 22-143 ml/min) in 64 patients included in the pharmacokinetic study.
The slight increase in AUC (30-40%) in mild and moderate renal function impairment, compared with normal, and the absence of drug cumulation with repeated administration regardless of renal function, suggest that no dose adjustment of zoledronic acid is necessary in mild (creatinine Cl – 50-80 ml/min) and moderate (creatinine Cl – 30-50 ml/min) renal function impairment.
Indications
Active ingredient
Composition
1 vial (100 ml) contains:
Active ingredient:
5 mg zoledronic acid monohydrate;
Associates:
Mannitol;
Sodium citrate;
water for injection.
How to take, the dosage
Intravenously, using a valve infusion system providing a constant infusion rate, for at least 15 min. Adequate hydration of the body should be ensured before administering Aclasta. This is particularly important in patients over 65 years of age and in patients receiving diuretic therapy.
For the treatment of postmenopausal osteoporosis in women and osteoporosis in men, the recommended dose of Aclasta is 5 mg (one bottle of the drug is 100 ml solution) intravenously once a year. If dietary intake of calcium and vitamin D is insufficient, patients should be prescribed additional calcium and vitamin D preparations.
In order to prevent repeated fractures in patients with proximal femur fractures, the recommended dose of Aclasta is 5 mg (one bottle of the drug is 100 ml solution) intravenously once a year. In patients with a recent (up to 90 days) fracture of the proximal femur, it is recommended that a single dose of high-dose vitamin D (50000 to 125000 ME or orally or intramuscularly) be given two weeks before infusion of Aclasta. After a single high-dose vitamin D administration, patients are advised to take calcium (1000 mg/day) and vitamin D (800 ME/day) daily for 14 days before infusion of Aclasta. After infusion, patients should also take calcium and vitamin D preparations for one year.
According to data of clinical trials, the best results in increase of bone mineral density have been achieved with Aclasta administration in 6 to 12 weeks after surgical intervention for fracture of the femur. For the treatment of GCS-induced osteoporosis, the recommended dose of Aclasta is 5 mg (one bottle of the drug is 100 ml solution) intravenously once a year. If dietary intake of calcium and vitamin D is insufficient, calcium and vitamin D supplements should be prescribed for patients with osteoporosis.
In order to prevent postmenopausal osteoporosis, the recommended dose of Aclasta is 5 mg (one bottle of the drug is 100 ml solution) intravenously once every 2 years. An annual fracture risk assessment and assessment of clinical response to therapy should be performed to decide whether a repeat infusion is necessary.
The adequate intake of calcium and vitamin D is very important for the prevention of postmenopausal osteoporosis. If dietary intake is insufficient, supplementation with preparations of calcium and vitamin D is recommended.
A single dose of 5 mg of Aclasta intravenously is recommended for the treatment of Paget’s bone disease. Because Peggett’s bone disease is characterized by high bone metabolism, all patients with this disease are recommended to take daily calcium (at least 500 mg of elemental calcium twice daily) and vitamin D for the first 10 days after administration of Aclast.
Retreatment with Aclasta for Paget’s bone disease. Currently, there are no specific recommendations for re-treatment of Paget’s bone disease. Patients who responded to Aclasta therapy showed a prolonged period of remission after its single administration.
The possibility of reintroduction of Aclasta may be considered if relapse of the disease is found in patients based on the following criteria: absence of normalization of serum ALP activity, its increase with time, and presence of clinical signs of Paget’s bone disease detected at physical examination 12 months after the first dose of Aclasta.
Patients with impaired renal function. In patients with a creatinine Cl >35 ml/min, no dose adjustment is required.
Patients with impaired hepatic function. Patients with impaired liver function do not require dose adjustment of the drug.
Patients of advanced age (>65 years). No dose adjustment of the drug is required because the bioavailability, distribution and excretion of the drug are similar in patients of different ages.
Instructions for use of the drug. When preparing and carrying out infusion the rules of asepsis should be observed. Before administering the drug Aclasta should visually assess the quality and color of the solution. The drug must not be used if the color changes or appearance of insoluble visible particles.
Aklasta should not be mixed or injected with any other drug. Aclasta should not be allowed in contact with any solutions containing calcium or any other divalent cations. A separate infusion system should always be used for the administration of the drug. At the end of infusion of Aclasta the unused solution remaining in the bottle must not be used.
Aclasta solution should preferably be used immediately after opening the vial. Unused solution can be stored in the refrigerator at 2-8 °C for a maximum of 24 hours. If the solution is refrigerated, it should be kept indoors until it reaches room temperature before administration.
Interaction
Special studies on interaction of zoledronic acid with other medicinal products have not been conducted. Zoledronic acid does not undergo systemic metabolism and does not affect human cytochrome P450 isoenzymes in vitro.
Zoledronic acid has a low degree of binding to plasma proteins (approximately 43-55%); interaction due to displacement of drugs with high degree of binding to proteins from binding sites is unlikely.
Zoledronic acid is excreted by the kidneys. Caution should be exercised when concomitant use of Aclasta with drugs that may significantly affect renal function (e.g. aminoglycosides) and drugs that cause dehydration (e.g. diuretics). In patients with impaired renal function, the systemic bioavailability of these drugs may be increased when Aclasta is used with drugs that are mainly excreted by the kidneys.
Pharmaceutical Interactions and Compatibility
The Aclasta solution is not compatible with solutions containing calcium (e.g. in the same IV drip system).
Special Instructions
The physician should inform patients about the main manifestations of hypocalcemia and ensure regular monitoring of patients at risk.
The therapy with Aclasta in patients with Paget’s Bone Disease should only be given by qualified physicians with experience in treating this condition.
Paracetamol or ibuprofen may be given immediately after infusion of Aclasta to reduce the incidence of some NSAIDs noted within 3 days of administration.
Zoledronic acid is the active ingredient in both Aclasta and Zometa (a treatment for cancer patients), but these drugs are not interchangeable and should not be used concomitantly. In the presence of hypocalcemia, adequate doses of calcium and vitamin D should be treated before starting Aclasta. Other existing mineral metabolism disorders (e.g., following thyroid and parathyroid surgery, hypoparathyroidism or decreased intestinal calcium absorption) should also be treated and patients with hypocalcemia should be monitored regularly.
Kidney function disorders. The following guidelines should be followed to reduce the risk of renal impairment:
Aclasta is not recommended for use in patients with severe renal dysfunction (Cl creatinine less than 35 mL/min) because there are limited data on the safety of the drug in this patient population.
Caution should be exercised when concomitant use of Aclasta with drugs that may have significant effect on renal function.
Physical creatinine levels in plasma should be determined before initiating the drug. During drug therapy, transient increase of creatinine in plasma may be higher in patients with a history of renal impairment compared to patients with normal renal function. Plasma creatinine should be monitored regularly when Aclasta is used in patients with risk factors for renal impairment.
Adequate hydration of the body should be achieved before administration of Aclasta. This is particularly important in patients aged >65 years and in patients receiving diuretic therapy.
The dose of the drug in a single intravenous infusion should not exceed 5 mg, and Aclasta should be infused for at least 15 minutes.
Osteonecrosis of the jaw. Risk factors for osteonecrosis include oncological diseases, concomitant therapy (e.g., chemotherapy, radiation therapy, GCS treatment) and the presence of other comorbidities (e.g., anemia, coagulopathies, infections, a history of dental disease). Although a causal relationship between osteonecrosis of the jaw and bisphosphonate intake has not been established, dental surgery should be avoided because the recovery time after said surgery may be longer. Prior to treatment with bisphosphonates, patients with risk factors (cancer, chemotherapy, GCS treatment, poor oral hygiene) should have a dental examination and the necessary preventive procedures should be performed in advance. If osteonecrosis of the jaw develops against the background of bisphosphonate therapy, dental surgery may worsen the condition of patients. There is no evidence that interrupting treatment with bisphosphonates prior to dental interventions reduces the risk of osteonecrosis of the jaw. Treatment tactics for an individual patient should be based on an individual risk/benefit assessment.
Impact on the ability to drive vehicles and operate machinery. There is no data about the effect of the drug Aclasta on the ability to drive vehicles and operate mechanisms; however due to the possibility of side effects (including blurred vision, lethargy and others) care should be taken when driving vehicles and operating mechanisms.
Contraindications
Side effects
Treatment of various types of osteoporosis, Paget’s bone disease and prevention of new fractures in men and women with fractures of the proximal femur.
. When 5 mg of Aclasta was given intravenously once a year to treat postmenopausal osteoporosis in women, osteoporosis in men, prevention of new fractures in men and women with proximal femur fractures, prevention and treatment of GCS-induced osteoporosis, and treatment of Paget’s bone disease, most adverse events (AEs) were mild to moderate.
After IV administration of Aclasta in these patients the most frequently observed NIs were as follows: fever (18.1%), myalgia (9.4%), flu-like syndrome (7.8%), arthralgia (6.8%), headache (6.5%) – usually lasting not more than 3 days (“post-dose” symptoms). Most of the above-mentioned NIs observed within 3 days after drug administration were mild to moderate in severity.
The severity of these NIHs decreased significantly when the drug was repeatedly administered. The following are the possible NFRs (according to treating physicians) associated with treatment of various types of osteoporosis, Paget’s disease and prevention of new fractures in men and women with proximal femur fractures.
Nervous system disorders: often – headache, dizziness; sometimes – lethargy*, paresthesia, somnolence, tremor, fainting.
Sensory system disorders: sometimes – conjunctivitis, eye pain, vertigo; rarely – uveitis*, episcleritis, iritis.
Respiratory system: sometimes – shortness of breath*, cough.
The digestive system: often – nausea, vomiting, diarrhea; sometimes – anorexia*, decreased appetite, dyspepsia*, abdominal pain*, dry mouth, esophagitis*, gastroesophageal reflux, pain in the upper abdomen, constipation.
Skin and subcutaneous tissue: sometimes – rash, hyperhidrosis*, itching, erythema.
Skeletal-muscular system and connective tissue disorders: frequent – arthralgia*, myalgia*; bone pain, back and limb pain; sometimes – neck pain, joint swelling*, muscle cramps, shoulder girdle pain, chest pain* of musculoskeletal origin, weakness in muscles, stiffness in muscles* and joints*, arthritis, musculoskeletal pain.
Urinary system disorders: sometimes – increase in blood creatinine level, pollakiuria, proteinuria.
Hematopoietic system: sometimes – anemia.
The cardiovascular system: sometimes – increase in blood pressure, sudden redness of the face.
Infections and infestations: sometimes – influenza, nasopharyngitis.
The body in general: very often – fever; often – flu-like syndrome, chills, increased fatigue*, asthenia, pain*, general malaise; infrequently – peripheral edema, feeling of thirst*, increased excitability*, chest pain (not associated with heart disease).
*Note: In individual studies, the frequency of these NIHs increased as follows: very common – myalgia, arthralgia, increased fatigue, pain; common – lethargy, shortness of breath, dyspepsia, esophagitis, abdominal pain, hyperhidrosis, muscle stiffness, joint swelling, muscle-skeletal pain in the chest, joint stiffness, anorexia, feelings of thirst, increased excitability; infrequent – uveitis.
In separate studies, the following ONs have been reported with a lower frequency in the Aclasta group compared to patients who did not receive the drug: red eyes, elevated C-reactive protein, hypocalcemia, taste disorders, toothache, gastritis, palpitations, site-of-injection reactions.
In patients with postmenopausal osteoporosis, the overall incidence of atrial fibrillation with Aclasta therapy was 2.5% (96 of 3862 patients) compared to 1.9% (75 of 3852 patients) in those not treated with Aclasta (placebo group). In 1.3% of patients (51 patients out of 3862) treated with Aclasta and in 0.6% (22 patients out of 3852) in the placebo group, this adverse event was considered serious. The cause of the increased incidence of atrial fibrillation during therapy with Aclasta has not been established in this study. The increased incidence of atrial fibrillation seen in this study compared with placebo has not been seen in other clinical studies of zoledronic acid.
Prevention of postmenopausal osteoporosis
The overall safety profile of Aclasta for the prevention of postmenopausal osteoporosis (PMO) was comparable to that of PMO treatment, with the exception of NPOs occurring within 3 days of infusion: pain, fever, chills, myalgia, nausea, headache, increased fatigue, and arthralgia, the frequency of which was higher in women who received the drug to prevent PMO. Most of these NS were mild to moderate in severity and subsided within 3 days of onset. The severity of these NIHs was significantly reduced with repeated administration of the drug.
The following are the possible NTs that may be related to the use of DME prophylaxis (according to treating physicians):
(1) NFRs reported more than once with Aclast for PMO prophylaxis that have not been reported with the drug for treatment of various types of osteoporosis, Paget’s bone disease, and for prevention of new fractures in men and women with proximal femur fractures;
(2) NTs, the incidence of which was higher in women who received the drug for the prevention of PMT (compared to other patient categories).
Mental disorders: sometimes anxiety.
Nervous system disorders: very common – headache; common – tremor, lethargy; infrequent – hypersensitivity, taste disorders.
An organ of vision: often – conjunctivitis, pain in the eyes, iritis; infrequent – blurred vision.
The digestive system: very often – nausea; often – anorexia, abdominal pain, pain in the upper abdomen, constipation.
Skin and subcutaneous tissue: often – increased sweating at night.
Musculoskeletal and connective tissue disorders: very often – myalgia; often – musculoskeletal pain, muscle spasm, pain in the chest of musculoskeletal origin, pain in the jaw, pain in the neck; infrequently – pain in the side.
As to the body in general and reactions at the site of administration: very often – pain, chills; often – peripheral edema, reactions at the site of administration, noncardiac pain in the chest area.
Change in laboratory findings
Patients with postmenopausal osteoporosis showed a decrease of serum calcium concentration (less than 1.87 mmol/L) in 0.2% of cases with Aclasta without clinical signs of hypocalcemia.
When the drug was used in patients with femoral fractures, osteoporosis in men and osteoporosis caused by GCS administration, decrease of plasma calcium concentration less than 1.87 mmol/l was not observed.
When using the drug in patients for prevention of postmenopausal osteoporosis there was no decrease in plasma calcium concentration less than 1.87 mmol/l. In about 1% of patients with Paget’s disease transient hypocalcemia accompanied by clinical manifestations was found.
Kidney function abnormalities. During intravenous administration of bisphosphonates, including zoledronic acid, there have been cases of renal dysfunction manifested by increased blood creatinine concentration and in rare cases – acute renal failure. Impaired renal function during the use of zoledronic acid was observed in patients with either a history of renal pathology or additional risk factors (e.g., cancer requiring chemotherapy, nephrotoxic drugs, diuretics or severe dehydration). Most of these patients were treated with zoledronic acid at a dose of 4 mg every 3-4 weeks, but in some cases, impaired renal function has been observed after a single dose of zoledronic acid. The incidence of plasma creatinine elevation and renal failure did not differ from placebo in patients with postmenopausal osteoporosis when treated with Aclasta for 3 years. In patients treated with Aclasta there was a slightly more frequent transient increase in blood creatinine within 10 days after infusion compared to placebo (1.8 and 0.8%, respectively).
In men with osteoporosis, the rate of change in creatinine clearance and development of renal function abnormalities was similar to that in the alendronic acid group when Aclasta was used for 2 years.
In patients with GCS-induced osteoporosis with Aclasta therapy, the rates of change in creatinine clearance and renal function impairment were similar to those in the risedronic acid group.
Reactions at the site of administration. In 0.7% of patients with postmenopausal osteoporosis, there was redness, swelling and/or pain at the injection site when Aclasta was used.
In patients with femoral fractures, the incidence of injection site reactions was comparable to that in the placebo group. In men with osteoporosis the Aclasta reaction rate was 2.6% (compared to 1.4% in the alendronic acid group). In patients with osteoporosis caused by the use of GCS, no reactions at the site of drug administration were observed. When using the drug to prevent postmenopausal osteoporosis, the rate of reactions at the site of administration of Aclasta was 1.1% (compared to 2.0% in the placebo group).
Osteonecrosis of the jaw. Cases of osteonecrosis (most frequently of the jaw) occurred mainly in cancer patients treated with bisphosphonates after tooth extraction or other dental manipulations. Most patients had symptoms of local infection and inflammation, including osteomyelitis. In clinical studies in patients with osteoporosis, a case of osteonecrosis of the jaw occurred in 1 patient taking Aclasta and in 2 patients taking placebo. In all three cases there was resolution of the process. In Aclasta use in patients with hip fractures, in male osteoporosis and GCS-induced osteoporosis, as well as in treatment for prevention of postmenopausal osteoporosis no cases of osteonecrosis of the jaw were observed.
Manual reports of adverse events
The following adverse events have been reported in clinical practice during treatment with Aclasta without any indication of a causal relationship to the use of the drug (frequency of adverse events has not been established): Hypersensitivity reactions, including in rare cases bronchoobstruction, urticaria, angioedema and isolated reports of the development of anaphylactic reactions, includingincluding anaphylactic shock. In rare cases during the use of Aclasta in clinical practice, renal dysfunction, including renal failure requiring hemodialysis, especially in patients with either a history of renal impairment or additional risk factors (e.g. concomitant therapy with nephrotoxic agents, diuretics or severe dehydration) were observed in patients.
In very rare cases, the following adverse events have been reported: dehydration due to fever, vomiting, and diarrhea after drug administration; marked BP reduction in patients with risk factors, osteonecrosis of the jaw, scleritis, and ocular inflammation.
Overdose
There are currently limited clinical data on cases of drug overdose. Patients who have received a dose of the drug that exceeds the recommended dose should be monitored by a physician.
Symptoms: In acute zoledronic acid overdose (limited data) renal dysfunction including renal failure, hypocalcemia, hypophosphatemia, hypomagnesemia have been reported.
Treatment: In case of overdose of the drug accompanied by clinical symptomatology (numbness, tingling sensation, especially in the mouth region, muscle cramps, etc.) intravenous administration of solutions containing calcium ions, magnesium and phosphates is indicated.
Pregnancy use
The drug Aclasta is contraindicated in pregnancy and during lactation (breastfeeding).
There are no data on the use of zoledronic acid in pregnant women.
The presence of teratogenic action in one of the experimental rodent species has been shown in experimental studies.
Potential risk when used in humans is unknown.
Weight | 0.170 kg |
---|---|
Shelf life | 3 years |
Conditions of storage | At a temperature not exceeding 25 °C |
Manufacturer | Fresenius Kabi Austria GmbH, Austria |
Medication form | solution for infusion |
Brand | Fresenius Kabi Austria GmbH |
Related products
Buy Aclasta, 5 mg/100 ml 100 ml with delivery to USA, UK, Europe and over 120 other countries.