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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.
EudraVigilance
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Suspected adverse reactions reported for Tiludronic acid
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
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 BNF/ATC 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
Official UK regulator monitoring and safety alerts
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. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. 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 all 21 studies.
Reviews & meta-analyses: 9 · 1934–2025
Showing all 21 studies, sorted by most relevant.
Wei Jia, G. Xie, Weiping Jia
Nature reviews. Gastroenterology & hepatology, 2017
- Gastrointestinal Microbiome
- Bile Acids and Salts
- Biological Transport
F. Röhrig, A. Schulze
Nature Reviews Cancer, 2016
- Fatty Acids
- Neoplasms
- Disease Progression
Muhammad Naveed, V. Hejazi, Muhammad Abbas, et al.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2018
- Chlorogenic Acid
- Hypoglycemic Agents
- Obesity
Nikos Koundouros, G. Poulogiannis
British Journal of Cancer, 2019
- Phosphoinositide-3 Kinase Inhibitors
- Epigenome
- Fatty Acids
A common feature of cancer cells is their ability to rewire their metabolism to sustain the production of ATP and macromolecules needed for cell growth, division and survival. In particular, the importance of altered fatty acid metabolism in cancer has received renewed interest as, aside their principal role as structural components of the membrane matrix, they are important secondary messengers, and can also serve as fuel sources for energy production. In this review, we will examine the mechanisms through which cancer cells rewire their fatty acid metabolism with a focus on four main areas of research. (1) The role of de novo synthesis and exogenous uptake in the cellular pool of fatty acids. (2) The mechanisms through which molecular heterogeneity and oncogenic signal transduction pathways, such as PI3K-AKT-mTOR signalling, regulate fatty acid metabolism. (3) The role of fatty acids as essential mediators of cancer progression and metastasis, through remodelling of the tumour microenvironment. (4) Therapeutic strategies and considerations for successfully targeting fatty acid metabolism in cancer. Further research focusing on the complex interplay between oncogenic signalling and dysregulated fatty acid metabolism holds great promise to uncover novel metabolic vulnerabilities and improve the efficacy of targeted therapies.
Abstract licence: CC BY
J. Gootenberg, O. Abudayyeh, Jeong Wook Lee, et al.
Science (New York, N.Y.), 2017
- Zika Virus Infection
- Zika Virus
- Circulating Tumor DNA
Rapid, inexpensive, and sensitive nucleic acid detection may aid point-of-care pathogen detection, genotyping, and disease monitoring. The RNA-guided, RNA-targeting clustered regularly interspaced short palindromic repeats (CRISPR) effector Cas13a (previously known as C2c2) exhibits a "collateral effect" of promiscuous ribonuclease activity upon target recognition. We combine the collateral effect of Cas13a with isothermal amplification to establish a CRISPR-based diagnostic (CRISPR-Dx), providing rapid DNA or RNA detection with attomolar sensitivity and single-base mismatch specificity. We use this Cas13a-based molecular detection platform, termed Specific High-Sensitivity Enzymatic Reporter UnLOCKing (SHERLOCK), to detect specific strains of Zika and Dengue virus, distinguish pathogenic bacteria, genotype human DNA, and identify mutations in cell-free tumor DNA. Furthermore, SHERLOCK reaction reagents can be lyophilized for cold-chain independence and long-term storage and be readily reconstituted on paper for field applications.
Abstract licence: CC BY-NC-SA
P. Chomczyński, N. Sacchi
Analytical biochemistry, 1987
H. Ohkawa, N. Ohishi, K. Yagi
Analytical biochemistry, 1979
- Thiobarbiturates
- Carbon Tetrachloride
- Hydrogen-Ion Concentration
V. L. Singleton, J. Rossi
American Journal of Enology and Viticulture, 1965
Leon M Larcher, Ianthe L. Pitout, Niall P. Keegan, et al.
Nucleic Acid Therapeutics, 2023
- DNA, Catalytic
- RNA
Nucleic acids drugs have been proven in the clinic as a powerful modality to treat inherited and acquired diseases. However, key challenges including drug stability, renal clearance, cellular uptake, and movement across biological barriers (foremost the blood-brain barrier) limit the translation and clinical efficacy of nucleic acid-based therapies, both systemically and in the central nervous system. In this study we provide an overview of an emerging class of nucleic acid therapeutic, called DNAzymes. In particular, we review the use of chemical modifications and carrier molecules for the stabilization and/or delivery of DNAzymes in cell and animal models. Although this review focuses on DNAzymes, the strategies described are broadly applicable to most nucleic acid technologies. This review should serve as a general guide for selecting chemical modifications to improve the therapeutic performance of DNAzymes.
Abstract licence: CC BY
Jillian Belgrad, H. Fakih, Anastasia Khvorova
Nucleic Acid Therapeutics, 2024
- Nucleic Acids
- Drug Delivery Systems
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 medications. 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 the following publications:
Show earlier publications
Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q2823312), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.