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MHRA alerts for Tiludronic 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 Tiludronic 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 Tiludronic acid
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1 branded products available
WHO defined daily dose (DDD)
400 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
Check stock at pharmacies and supply information
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Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & safety information
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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: 3 · 1938–2026
Showing the 50 most relevant studies, sorted by most relevant.
Journal of the American College of Toxicology, 1987
Chris M. Riggs, Sarah L. Thompson, Jenny K.Y. Wong, et al.
2020
Landis W. Doner, Kevin B. Hicks
Analytical Biochemistry, 1981
Herrera-Calderon O, Herrera-Ramírez A, Cardona-G W, et al.
2023
Colorectal cancer (CRC) is the third most common cancer diagnosed worldwide and is the second leading cause of cancer-related death due to an insufficiency prognosis and is generally diagnosed in the last step of development. The Peruvian flora has a wide variety of medicinal plants with therapeutic potential in several diseases. Dodonaea viscosa Jacq. is a plant used to treat inflammatory process as well as gastrointestinal diseases. The aim of this study was to examine the cytotoxic, antiproliferative, and cell death-inducing effects of D. viscosa on colorectal cancer cells (SW480 and SW620). The hydroethanolic extract was obtained by maceration at 70% ethanol, the phytochemical constituents were identified by LC-ESI-MS. D. viscosa revealed 57 compounds some of them are: isorhamnetin, kaempferol, quercetin, methyl dodovisate B, hardwickiic acid, viscosol, and dodonic acid. Regarding the antitumoral activity, D. viscosa induced cytotoxic and antiproliferative activity in both SW480 and SW620 cancer cells, accompanied with, important changes in mitochondrial membrane potential, formation of the Sub G0/G1 population and increasing levels of apoptotic biomarkers (caspase 3 and the tumor suppressor protein p53) in the metastatic derivative cell line (SW620), suggesting an intrinsic apoptotic process after the treatment with the hydroethanolic extract of D. viscosa.
Abstract licence: CC BY
Alhaidhal BA, Alsulais FM, Mothana RA, et al.
2024
- Citrobacter koseri
- Anti-Bacterial Agents
- Molecular Dynamics Simulation
Citrobacter koseri causes infection in people who are immunocompromised. Without effective antibiotics, these infections can become severe and life-threatening, so effective drugs are essential to treat these infections. Utilizing subtractive genomics, 2699 ORFs were predicted and translated into amino acid sequences. Metabolic pathway analysis and subcellular localization helped define the roles of key bacterial proteins. Two druggable proteins, WP_012000829.1 and WP_275157394.1, were discovered as promising targets. Alpha Fold provided 3D structures, and a library of 1600 echinoderm metabolites was docked against these proteins, with Ampicillin, Levofloxacin, and Doxycycline as controls. Notably, CMNPD13085 and CMNPD15632 exhibited the highest binding affinities for WP_012000829.1 and WP_275157394.1, respectively. Molecular dynamics simulations and MM-GBSA binding free energy complemented docking results. However, acknowledging the reliance on computational validations, the study emphasizes the need for essential in-vitro research to transform these potential inhibitors into therapeutic drugs.
Abstract licence: CC BY-NC-ND
Nedashkovskaya O, Baldaev S, Ivaschenko A, et al.
2025
A novel, strictly aerobic, non-motile, and pink-pigmented bacterium, designated 7Alg 153T, was isolated from the Pacific green alga Cladophora stimpsonii. Strain 7Alg 153T was able to grow at 4-32 °C in the presence of 1.5-4% NaCl and hydrolyze L-tyrosine, gelatin, aesculin, Tweens 20, 40, and 80 and urea, as well as produce catalase, oxidase, and nitrate reductase. The novel strain 7Alg 153T showed the highest similarity of 96.75% with Pseudaestuariivita rosea H15T, followed by Thalassobius litorarius MME-075T (96.60%), Thalassobius mangrovi GS-10T (96.53%), Tritonibacter litoralis SM1979T (96.45%), and Marivita cryptomonadis CL-SK44T (96.38%), indicating that it belongs to the family Roseobacteraceae, the order Rhodobacteales, the class Alphaproteobacteria, and the phylum Pseudomonadota. The respiratory ubiquinone was Q-10. The main polar lipids were phosphatidylethanolamine, phosphatidylglycerol, diphosphatidylglycerol, phosphatidylcholine, two unidentified aminolipids, and one unidentified lipid. The predominant cellular fatty acids (>5%) were C18:1 ω7c, C16:0, C18:0, and 11-methyl C18:1 ω7c. The 7Alg 153T genome is composed of a single circular chromosome of 3,786,800 bp and two circular plasmids of 53,157 bp and 37,459 bp, respectively. Pan-genome analysis showed that the 7Alg 153T genome contains 33 genus-specific clusters spanning 92 genes. The COG20-annotated singletons were more often related to signal transduction mechanisms, cell membrane biogenesis, transcription, and transport, and the metabolism of amino acids. The complete photosynthetic gene cluster (PGC) for aerobic anoxygenic photosynthesis (AAP) was found on a 53 kb plasmid. Based on the phylogenetic evidence and phenotypic and chemotaxonomic characteristics, the novel isolate represents a novel genus and species within the family Roseobacteraceae, for which the name Algirhabdus cladophorae gen. nov., sp. nov. is proposed. The type strain is 7Alg 153T (=KCTC 72606T = KMM 6494T).
Abstract licence: CC BY
Brit Solvor Lyse Riska, Nina Gunnes, Trine Finnes, et al.
Archives of Osteoporosis, 2024
- Zoledronic Acid
- Hip Fractures
- Ambulatory Care
Acid, 2025
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
87 found
Half-life
150 hours
Mechanism
Bisphosphonates are taken into the bone where they bind to hydroxyapatite.
Food interactions
4 warnings
Human targets
6 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
400mg
Half-life
150 hours
[L4763]
…
Protein binding
90%
[L4763]
It is mostly bound to albumin.
[L4763]
Volume of distribution
30L
[A1923]
…
Metabolism
[L4763]
Elimination
60%
[L4763]
Clearance
0.68L/h
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Tiludronic acid was granted FDA approval on 7 March 1997.[L4763]
[L4763]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 841 interactions
[L4763]
Patients given doses of 6mg/kg/day for 2 days have experienced acute renal failure and death.
[L4763]
Treat overdose with symptomatic and supportive care.
[L4763]
Dialysis will not be useful for removal of the drug from serum.
[L4763]
Osteoclasts mediate resorption of bone.[A6366] When osteoclasts bind to bone they form podosomes, ring structures of F-actin.[A6366] Tiludronate inhibits protein-tyrosine-phosphatase, which increases tyrosine phosphorylation, and disrupts podosome formation.[A6366][L4763] Tiludronic acid also inhibits V-ATPases in the osteoclast, though the exact subunits are unknown, preventing F-actin from forming podosomes.[A202229][A202247] Disruption of the podosomes causes osteoclasts to detach from bones, preventing bone resorption.[A6366]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A1923]
Tiludronic acid has an oral bioavailability of 2-11% with an average of 6%.
[A1923]
[L4763]
The terminal phase half life is approximately 40h after a single IV dose of 10-30mg.
[A1923]
[L4763]
It is mostly bound to albumin.
[L4763]
[A1923]
Due to the unknown clearance rate from bone, this may underestimate the true volume of distribution.
[A1923]
[L4763]
[L4763]
[A1923][L4763]
Approximately 50% of tilurdronic acid binds to bone but the rate of clearance from the bone is unknown.
[A1923]
Proteins and enzymes this drug interacts with in the body
PMID:18559503
Dephosphorylates cellular tyrosine kinases, such as ERBB2 and PTK2B/PYK2, and thereby regulates signaling via ERBB2 and PTK2B/PYK2 .
PMID:17329398 PMID:27134172
Selectively dephosphorylates ERBB2 phosphorylated at 'Tyr-1112', 'Tyr-1196', and/or 'Tyr-1248' PMID:27134172
PMID:14739280 PMID:29925997
Dephosphorylates and negatively regulate several receptor tyrosine kinases (RTKs) such as EGFR, PDGFR and FGFR, thereby modulating their signaling activities .
PMID:21258366 PMID:9733788
When recruited to immunoreceptor tyrosine-based inhibitory motif (ITIM)-containing receptors such as immunoglobulin-like transcript 2/LILRB1, programmed cell death protein 1/PDCD1, CD3D, CD22, CLEC12A and other receptors involved in immune regulation, initiates their dephosphorylation and subsequently inhibits downstream signaling events .
PMID:11907092 PMID:14739280 PMID:37932456 PMID:38166031
Modulates the signaling of several cytokine receptors including IL-4 receptor .
PMID:9065461
Additionally, targets multiple cytoplasmic signaling molecules including STING1, LCK or STAT1 among others involved in diverse cellular processes including modulation of T-cell activation or cGAS-STING signaling .
PMID:34811497 PMID:38532423
Within the nucleus, negatively regulates the activity of some transcription factors such as NFAT5 via direct dephosphorylation. Also acts as a key transcriptional regulator of hepatic gluconeogenesis by controlling recruitment of RNA polymerase II to the PCK1 promoter together with STAT5A PMID:37595871
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
ATC M05BA05
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)
Tiludronic acid
Additional database identifiers
Drugs Product Database (DPD)
11362
ChemSpider
54905
BindingDB
50442524
ZINC
ZINC000001531010
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9645
GeneCards
PTPN12
UniProt Accession
PTN12_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9658
GeneCards
PTPN6
UniProt Accession
PTN6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9669
GeneCards
PTPRE
GenBank Gene Database
X54134
GenBank Protein Database
35792
UniProt Accession
PTPRE_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:865
GeneCards
ATP6V0A1
UniProt Accession
VPP1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18481
GeneCards
ATP6V0A2
UniProt Accession
VPP2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11647
GeneCards
TCIRG1
UniProt Accession
VPP3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:866
GeneCards
ATP6V0A4
UniProt Accession
VPP4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:855
GeneCards
ATP6V0C
UniProt Accession
VATL_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:861
GeneCards
ATP6V0B
UniProt Accession
VATO_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:851
GeneCards
ATP6V1A
GenBank Gene Database
L09235
GenBank Protein Database
291868
UniProt Accession
VATA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:854
GeneCards
ATP6V1B2
GenBank Gene Database
M60346
GenBank Protein Database
179563
Guide to Pharmacology
812
UniProt Accession
VATB2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:853
GeneCards
ATP6V1B1
UniProt Accession
VATB1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:856
GeneCards
ATP6V1C1
UniProt Accession
VATC1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18264
GeneCards
ATP6V1C2
UniProt Accession
VATC2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:13527
GeneCards
ATP6V1D
UniProt Accession
VATD_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:13724
GeneCards
ATP6V0D1
UniProt Accession
VA0D1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18266
GeneCards
ATP6V0D2
UniProt Accession
VA0D2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:863
GeneCards
ATP6V0E1
UniProt Accession
VA0E1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:857
GeneCards
ATP6V1E1
UniProt Accession
VATE1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18125
GeneCards
ATP6V1E2
UniProt Accession
VATE2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:21723
GeneCards
ATP6V0E2
UniProt Accession
VA0E2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:16832
GeneCards
ATP6V1F
UniProt Accession
VATF_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:864
GeneCards
ATP6V1G1
UniProt Accession
VATG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:862
GeneCards
ATP6V1G2
UniProt Accession
VATG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18265
GeneCards
ATP6V1G3
UniProt Accession
VATG3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18303
GeneCards
ATP6V1H
UniProt Accession
VATH_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:868
GeneCards
ATP6AP1
UniProt Accession
VAS1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_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