Ibandronic acid 6mg/6ml solution for infusion vials
Requires a prescription from a doctor or prescriber
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MHRA alerts for Ibandronic acid
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Ibandronic acid
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
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Suspected adverse reactions reported for Ibandronic acid
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4 branded products available
MHRA licensed products
View all licensed products for Ibandronic acid on the MHRA register
Bondronat 6mg/6ml concentrate for solution for infusion vials
Ibandronic acid 6mg/6ml concentrate for solution for infusion vials
WHO defined daily dose (DDD)
6 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(3)
Bisphosphonates for treating osteoporosis (TA464)
Denosumab for the prevention of skeletal-related events in adults with bone metastases from solid tumours (TA265)
Romosozumab for treating severe osteoporosis (TA791)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 9 · Randomised trials: 2 · 1975–2026
Showing the 50 most relevant studies, sorted by most relevant.
Wang WY, Chen LH, Ma WJ, et al.
2023
- Osteoporosis, Postmenopausal
- Spinal Fractures
- Teriparatide
Mann RS, Chopra I, Kilic A, et al.
2026
The majority of clinical research continues to focus on evaluating the efficacy of teriparatide and bisphosphonates in the treatment of osteoporosis. This systematic review gathered data from extensive research assessing the efficacy, safety, and clinical outcomes of various medications. The objective was to determine the effectiveness and clinical implications of teriparatide and bisphosphonates in the treatment of postmenopausal osteoporosis. We analyzed 15 comprehensive studies, encompassing randomized controlled trials (RCTs), systematic reviews, and meta-analyses. The primary studies included large trials and several medium-sized trials that examined changes in bone mineral density (BMD), fracture risk, and adverse outcomes. Teriparatide significantly lowered vertebral fracture risk compared with risedronate in patients with severe osteoporosis and increased lumbar spine BMD to a comparable extent as alendronate, though via a distinct anabolic mechanism. Combination therapy with zoledronic acid resulted in greater BMD gains than either agent alone. Most adverse events were mild and transient, including injection-site reactions, nausea, and dizziness, with no significant difference in serious adverse event rates compared with bisphosphonates. Network meta-analyses indicate that romosozumab may achieve greater early spine BMD gains than teriparatide. Teriparatide is effective in lowering vertebral fracture risk and enhancing BMD in postmenopausal osteoporosis. Anabolic agents, including teriparatide, are recommended as first-line therapy for patients at very high risk of fractures (e.g., very low BMD with prevalent fractures or fractures occurring during glucocorticoid therapy), followed by a transition to antiresorptive therapy. Treatment selection should be guided by guideline-based risk stratification rather than applying a uniform stepwise approach.
Abstract licence: CC BY
Mun S, Chalasani R, Van de Vel G, et al.
2025
Spinal cord injury (SCI) causes significant bone loss as a long-term complication, increasing fracture risk and healthcare costs. Bisphosphonates are widely studied for mitigating bone loss since they can prevent fractures and preserve rehabilitation potential in acute SCI patients. Zoledronic acid, in particular, stands out due to its high potency, dosing convenience, and better patient adherence. This review aims to evaluate the efficacy of bisphosphonates, particularly zoledronic acid, in mitigating bone loss in acute SCI. A systematic review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines using PubMed, ScienceDirect, PubMed Central (PMC), Google Scholar, and Cochrane Central Register of Controlled Trials (CENTRAL) databases. Studies from January 1, 2016, to December 31, 2024, on bisphosphonate use within six months of SCI were included. Randomized controlled trials using zoledronic acid as the intervention and meta-analyses or systematic reviews covering all bisphosphonates were selected based on predefined inclusion and exclusion criteria. Eight studies, comprising three meta-analyses and five randomized controlled trials with 729 participants, were selected after quality assessment using Assessment of Multiple Systematic Reviews 2 (AMSTAR 2) and a revised Cochrane risk of bias tool for randomized trials (RoB 2). Seven studies demonstrated significant bone mineral density (BMD) improvements at the total hip, four at the lumbar spine, two at the trochanter, and five at the femoral neck. Two meta-analyses performed subgroup analyses of zoledronic acid, demonstrating substantial bone loss reduction, although comparisons with other bisphosphonates were lacking. Reductions in bone resorption markers, such as C-terminal telopeptide (CTX), were observed in five studies. While zoledronic acid exhibits strong anti-resorptive effects and allows for practical intravenous administration, its limited impact on bone formation markers, such as P1NP, and inconsistent BMD improvements across skeletal sites require further investigation. Future studies should assess long-term outcomes, utilize advanced imaging techniques, and directly compare zoledronic acid with other bisphosphonates.
Abstract licence: CC BY
Zheng G, Meng L, Li D, et al.
2026
BackgroundMalignant bone tumors are one of the most painful types of cancer, and their pain is very difficult to manage. Pain-relieving methods such as radiotherapy, Bone-Modifying Agents (BMAs), and radiopharmaceuticals have been explored in different studies and found to be effective pain control measures and also prevention of skeletal-related events (SREs). This meta-analysis analyzes the global burden of pain in malignant bone tumors with an emphasis on severity, health outcomes, and the efficacy of pain management interventions.MethodsNineteen randomized controlled trials and comparative studies were selected, which included patients with Malignant Bone Tumors. Treatments involved External Beam Radiotherapy (EBRT) in single or multi-fractions, BMAs (zoledronic acid, ibandronate, pamidronate, denosumab), and radiopharmaceuticals (Radium-223, Strontium-89, Samarium-153) either alone or in combination. Random-effects models were used to compute standardized mean differences (SMDs), with the evaluation of heterogeneity, Jadad score, and GRADE quality.ResultsInterventions across all subgroups were effective at relieving pain and protecting bones. One-time EBRT was shown to be as effective as standard multi-fraction treatments (SMD 0.04, 95% CI -0.02-0.1) for pain management. BMA-based treatments yielded contradictory results: denosumab versus zoledronic acid did not show a significant difference (SMD 0.01, 95% CI -0.02-0.05), whereas bisphosphonates alone resulted in a significant uplift (SMD 0.12, 95% CI 0.05-0.2, pConclusionsRadiotherapy, BMAs, and radiopharmaceuticals, either singly or in tandem, are well-tolerated for managing pain and preventing SREs in patients with malignant bone tumors, thereby providing patients with various ways to enhance their quality of life.
Abstract licence: CC BY
P. Barrett-Lee, A. Casbard, J. Abraham, et al.
The Lancet. Oncology, 2014
- Bone Neoplasms
- Breast Neoplasms
- Diphosphonates
D.A. Bossio, K.M. Scow
Microbial Ecology, 1998
Eric Jauniaux, Adrian Watson, Graham Burton
American Journal of Obstetrics and Gynecology, 2001
Hong Xie, J.J. Pasternak, Bernard R. Glick
Current Microbiology, 1996
Randy M. Becker, Guoyao Wu, Joseph A. Galanko, et al.
The Journal of Pediatrics, 2000
N.V. Grygorievа
Bolʹ, Sustavy, Pozvonočnik, 2019
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
195 found
Half-life
37-157 hours
Mechanism
Bisphosphonates are taken into the bone where they bind to hydroxyapatite.
Food interactions
2 warnings
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
0.63%
[A203153]
In a study of healthy males, a 10mg oral dose had a Tmax of 1.1±0.6h…
Half-life
37-157 hours
[L13805][L13808]
Protein binding
85.7-99.5%
Volume of distribution
90-368L
[A203153][L13805][L13808]
…
Metabolism
[L13805][L13808]
Elimination
[A203153][L13805][L13808]
Clearance
84-160mL/min
[L13805][L13808]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Ibandronate was granted FDA approval on 16 May 2003.[L13805]
[L13805][L13808]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 784 interactions
[L13805][L13808]
Oral overdose can be managed by giving patients milk or antacids to bind excess unabsorbed ibandronate.
[L13805]
Overdoses can be managed by providing intravenous electrolytes and dialysis is not expected to remove excess drug from serum.
[L13805][L13808]
Osteoclasts mediate resorption of bone.[A6366] When osteoclasts bind to bone they form podosomes, ring structures of F-actin.[A6366] Disruption of the podosomes causes osteoclasts to detach from bones, preventing bone resorption.[A6366]
Nitrogen containing bisphosphonates such as ibandronate are known to induce apoptosis of hematopoietic tumor cells by inhibiting the components of the mevalonate pathway farnesyl diphosphate synthase, farnesyl diphosphate, and geranylgeranyl diphosphate.[A202769][A203147] These components are essential for post-translational prenylation of GTP-binding proteins like Rap1.[A202769] The lack of prenylation of these proteins interferes with their function, and in the case of Rap1, leads to apoptosis.[A202769] ibandronate also activated caspase-3 which contribute to apoptosis.[A203150]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A203153]
In a study of healthy males, a 10mg oral dose had a Tmax of 1.1±0.6h and a Cmax of 4.1±2.6ng/mL.
[A203162]
The Tmax is approximately 1 hour, while Cmax varies depending on dose.
[A203162]
A 2mg intravenous dose of ibandronate has an AUC of 316ng\*h/mL, a 4mg intravenous dose of ibandronate has an AUC of 581ng\*h/mL, and a 6mg intravenous dose of ibandronate has an AUC of 908ng\*h/mL.
[A203159]
[L13805][L13808]
[L13808]
[A203153][L13805][L13808]
[L13805][L13808]
[A203153][L13805][L13808]
[L13805][L13808]
Proteins and enzymes this drug interacts with in the body
ATC M05BA06
ATC M05BB09
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Additional database identifiers
Drugs Product Database (DPD)
11519
ChemSpider
54839
BindingDB
12577
PDB
BFQ
ZINC
ZINC000001533877
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4249
GeneCards
GGPS1
GenBank Gene Database
AB017971
GenBank Protein Database
4520350
Guide to Pharmacology
643
UniProt Accession
GGPPS_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3631
GenAtlas
FDPS
GeneCards
FDPS
GenBank Gene Database
J05262
GenBank Protein Database
182399
Guide to Pharmacology
644
UniProt Accession
FPPS_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72