Delamanid 50mg tablets
Requires a prescription from a doctor or prescriber
Delamanid is an anti-tuberculosis agent derived from the nitro-dihydro-imidazooxazole class of compounds that inhibits mycolic acid synthesis of bacterial cell wall [A31965].
Safety information for pregnancy and breastfeeding
Pregnancy
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
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 Delamanid
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Submit a Yellow Card report to the MHRA
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
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
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Suspected adverse reactions reported for Delamanid
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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)
200 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
Pharmacy stock checkers
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 the 50 most relevant studies.
Reviews & meta-analyses: 26 · Randomised trials: 12 · 2011–2026
Showing the 50 most relevant studies, sorted by most relevant.
Suha Kadura, Nicholas King, Maria Nakhoul, et al.
Journal of Antimicrobial Chemotherapy, 2020
- Pharmaceutical Preparations
- Mycobacterium tuberculosis
- Nitroimidazoles
Florian von Groote-Bidlingmaier, R. F. Patientia, Epifanio Sánchez, et al.
The Lancet Respiratory Medicine, 2019
- Isoniazid
- Nitroimidazoles
- Oxazoles
Emanuele Pontali, Giovanni Sotgiu, Simon Tiberi, et al.
European Respiratory Journal, 2018
- Antitubercular Agents
- Nitroimidazoles
- Oxazoles
Lia D’Ambrosio, Rosella Centis, Simon Tiberi, et al.
Journal of Thoracic Disease, 2017
Mohammad Javad Nasiri, Moein Zangiabadian, Erfan Arabpour, et al.
International Journal of Infectious Diseases, 2022
- Nitroimidazoles
- Tuberculosis, Multidrug-Resistant
- Antitubercular Agents
Kelly E. Dooley, Susan L. Rosenkranz, Francesca Conradie, et al.
The Lancet Infectious Diseases, 2021
- Antitubercular Agents
- Electrocardiography
- Nitroimidazoles
Luisa María Nieto Ramírez, Karina Quintero Vargas, Gustavo Díaz
Antibiotics, 2020
Tuberculosis (TB) remains the deadliest Infectious disease worldwide, partially due to the increasing dissemination of multidrug and extensively drug-resistant (MDR/XDR) strains. Drug regimens containing the new anti-TB drugs bedaquiline (BDQ) and delamanid (DLM) appear as a last resort for the treatment of MDR or XDR-TB. Unfortunately, resistant cases to these drugs emerged just one year after their introduction in clinical practice. Early detection of resistant strains to BDQ and DLM is crucial to preserving the effectiveness of these drugs. Here, we present a systematic review aiming to define all available genotypic variants linked to different levels of resistance to BDQ and DLM that have been described through whole genomic sequencing (WGS) and the available drug susceptibility testing methods. During the review, we performed a thorough analysis of 18 articles. BDQ resistance was associated with genetic variants in Rv0678 and atpE, while mutations in pepQ were linked to a low-level of resistance for BDQ. For DLM, mutations in the genes ddn, fgd1, fbiA, and fbiC were found in phenotypically resistant cases, while all the mutations in fbiB were reported only in DLM-susceptible strains. Additionally, WGS analysis allowed the detection of heteroresistance to both drugs. In conclusion, we present a comprehensive panel of gene mutations linked to different levels of drug resistance to BDQ and DLM.
Abstract licence: CC BY 4.0
Syeda Hoorulain Ahmed, Hoorain Haider, Abdul Moeed, et al.
Indian Journal of Tuberculosis, 2023
- Antitubercular Agents
- Nitroimidazoles
- Oxazoles
O. Putra, Yulistiani Yulistiani, S. Soedarsono, et al.
International Journal of Mycobacteriology, 2023
- Antitubercular Agents
- Tuberculosis, Multidrug-Resistant
- Nitroimidazoles
Giovanni Battista Migliori, Emanuele Pontali, Giovanni Sotgiu, et al.
International Journal of Molecular Sciences, 2017
- Antitubercular Agents
- Nitroimidazoles
- Oxazoles
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
None known
Half-life
30 to 38 hours
Mechanism
Delamanid is a prodrug that requires biotransformation via via the mycobacterial…
Food interactions
2 warnings
Human targets
None mapped
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
100 mg
[A31968]…
Half-life
30 to 38 hours
[L1407]
Protein binding
99.5%
[L1407]
Volume of distribution
100 L
Metabolism
13%
Elimination
5%
[A31967]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L1407]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 461 interactions
[L1407]
Studies of genotoxicity and carcinogenic potential reveal no significant effects on humans.
Delamanid and/or its metabolites have the potential to affect cardiac repolarisation via blockade of hERG potassium channels. During repeat-dose studies in dogs, foamy macrophages were observed in lymphoid tissue of various organs with delamanid treatment although clinical relevance of this finding was not established. Repeat-dose toxicity studies in rabbits revealed an inhibitory effect of delamanid and/or its metabolites on clotting factors II, VII, IX, and X via inhibition of vitamin K production .
[L1407][A31966]
Embryo-fetal toxicity was observed at maternally toxic dosages in reproductive studies involving rabbits .
[L1407]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A31968]
Steady-state concentration is reached after 10-14 days .
[A31978]
Delamanid plasma exposure increases less than proportionally with increasing dose. In animal models (dog, rat, mouse), the oral bioavailability of delamanid was reported to be 35%–60% .
[A31966]
The absolute oral bioavailability in humans is estimated to range from 25 to 47% .
[A31967]
Oral bioavailability in humans is enhanced when administered with a standard meal, by about 2.7 fold compared to fasting conditions [L1407] because delamanid exhibits poor water solubility .
[A31967]
[L1407]
[L1407]
[L1407]
[L1407]
The metabolism of delamanid may also be mediated by hepatic CYP1A1, CYP2D6, and CYP2E1 to a lesser extent [31966]. Four major metabolites (M1–M4) have been identified in plasma in patients receiving delamanid where M1 and M3 accounts for 13%–18% of the total plasma exposure in humans .
[A31968]
While they do not retain significant pharmacological activity, they may still contribute to QT prolongation .
[A31967]
This is especially true for the main metabolite of delamanid, M1 (DM-6705) .
[A31966][A31967]
Delamanid is predominantly metabolized by serum albumin to form M1 (DM-6705) via hydrolytic cleavage of the 6-nitro-2,3-dihydroimidazo[2,1-b] oxazole moiety. The formation of this major metabolite is suggested to be a crucial starting point in the metabolic pathway of delamanid .
[A31968]
M1 (DM-6705) can be further catalyzed by three pathways.
In the first metabolic pathway, DM-6705 undergoes hydroxylation of the oxazole moiety to form M2 ((4RS,5S)-DM-6720), followed by CYP3A4-mediated oxidation of hydroxyl group and tautomerization of oxazole to an imino-ketone metabolite, M3 ((S)-DM-6718) .
[A31968]
The second metabolic pathway involves the hydrolysis and deamination of the oxazole amine to form M4 (DM-6704) followed by hydroxylation to M6 ((4R,5S)-DM-6721) and M7 ((4S,5S)-DM-6722) and oxidation of oxazole to another ketone metabolite, M8 ((S)-DM-6717) .
[A31968]
The third pathway involves the hydrolytic cleavage of the oxazole ring to form M5 (DM-6706) .
[A31968]
[A31967]
Enzymes involved in drug metabolism — important for understanding drug interactions
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
Appears to function in modulating the activity of the immune system during the acute-phase reaction
ATC J04AK06
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Delamanid
Additional database identifiers
ChemSpider
4981055
ZINC
ZINC000043100810
UniProt Accession
DDN_MYCTU
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8498
GenAtlas
ORM1
GeneCards
ORM1
GenBank Gene Database
X02544
GenBank Protein Database
757907
UniProt Accession
A1AG1_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q15408413), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.