Zanubrutinib 80mg capsules
Requires a prescription from a doctor or prescriber
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Safety monitoring data
Yellow Card reports
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Suspected adverse reactions reported for Zanubrutinib
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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 Zanubrutinib
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Brukinsa 80mg capsules
WHO defined daily dose (DDD)
320 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(7)
Zanubrutinib for treating Waldenstrom's macroglobulinaemia (TA833)
Zanubrutinib for treating chronic lymphocytic leukaemia (TA931)
Zanubrutinib for treating relapsed or refractory mantle cell lymphoma (TA1081)
Zanubrutinib for treating marginal zone lymphoma after anti-CD20-based treatment (TA1001)
Zanubrutinib with obinutuzumab for treating relapsed or refractory B-cell follicular lymphoma after 2 or more treatments (terminated appraisal) (TA978)
Non-Hodgkin lymphoma: diagnosis and management (NG52)
Pirtobrutinib for treating relapsed or refractory chronic lymphocytic leukaemia after a BTK inhibitor (TA1173)
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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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: 27 · Randomised trials: 12 · 2019–2026
Showing the 50 most relevant studies, sorted by most relevant.
Constantine S. Tam, Stephen Opat, Shirley D’Sa, et al.
Blood, 2020
- Adenine
- Antineoplastic Combined Chemotherapy Protocols
- Waldenstrom Macroglobulinemia
Constantine S. Tam, Jennifer R. Brown, Brad S. Kahl, et al.
The Lancet Oncology, 2022
- COVID-19
- Leukemia, Lymphocytic, Chronic, B-Cell
- Sequoia
Lijie Xing, Qiang He, Linna Xie, et al.
Haematologica, 2021
Steven R. Hwang, Jacqueline Wang, Zizhong Tian, et al.
HemaSphere, 2023
Stożek-Tutro A, Małowicka M, Janiszewska K, et al.
2026
- Antineoplastic Agents
- Antineoplastic Combined Chemotherapy Protocols
- Leukemia, Lymphocytic, Chronic, B-Cell
ObjectiveTo assess the real-world effectiveness of first-line targeted therapies (1LTT) for chronic lymphocytic leukemia (CLL) and compare these outcomes with those reported in randomized controlled trials (RCT).MethodsA systematic review of MEDLINE and EMBASE was conducted to identify real-world data (RWD). Key endpoints included progression-free survival (PFS), overall survival (OS), time-to-next treatment (TTNT), and treatment discontinuation due to adverse events (TdAE). CRD42024549185.ResultsIbrutinib (IBR) demonstrated consistent effectiveness in multiple RWD studies, with 12- and 24-month OS rates of 87-100% and 78-100%, respectively, and PFS rates of 76-94% and 68-94%, respectively, aligning with the results of the RESONATE-2 trial. Zanubrutinib (ZAN) showed a 36-month OS rate of 92% and a PFS rate of 84%, consistent with the outcomes of the SEQUOIA trial. For acalabrutinib (ACA), 12- and 24-month OS was 86-94% and 76-88%, PFS 92% and 81%, respectively, in line with the ELEVATE-TN trial, similarly, for venetoclax+obinutuzumab (VEN+OBI), 12-and 24-month OS was 94% and 86-94%, PFS 94% and 88%-92%, consistent with the CLL14 trial results. In contrast, idelalisib+rituximab (IDE+RTX) was associated with lower 24-month OS (77%), PFS (68%), and the highest TdAE rate (63%).ConclusionsAmong 1LTT for CLL, IBR has the most extensive and consistent RWD, with results mirroring RCT outcomes. ZAN, ACA and VEN+OBI show promising results based on RWD, however, these data are less extensive but consistent with RCT outcomes. Findings highlight the value of RWD and the need for more robust data on newer agents.
Abstract licence: CC BY-NC-ND
Helal F. Hetta, Ayman Salama, Turki A. Aljuaid, et al.
Pharmaceuticals, 2026
Zetong Cai
Theoretical and Natural Science, 2025
A. Jamil, Z. Qureshi, Rimsha Siddique, et al.
Discover Medicine, 2025
T. Munir, P. Sportoletti, L. Mohseninejad, et al.
Blood, 2025
Peter Hillmen, Barbara Eichhorst, Jennifer R. Brown, et al.
Journal of Clinical Oncology, 2022
- Atrial Fibrillation
- Leukemia, Lymphocytic, Chronic, B-Cell
- Lymphoma, B-Cell
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
2 to 4 hours
Mechanism
Bruton's tyrosine kinase (BTK) is a non-receptor kinase and a signalling molecul…
Food interactions
4 warnings
Human targets
15 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
160 mg
Half-life
160 mg
[L10163]
Protein binding
94%
[L10163]
Volume of distribution
95%
[L10163]
Metabolism
[L10163]
Its metabolites have not been characterized.
Elimination
320 mg
Clearance
37%
[L10163]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Zanubrutinib was granted accelerated approval by the FDA in November 2019 based on clinical trial results that demonstrated an 84% overall response rate from zanubrutinib therapy in patients with MCL,[L10166] which measures the proportion of patients in a trial whose tumour is entirely or partially destroyed by a drug.[L10169] It is currently marketed under the trade name BRUKINSA™ and is available as oral capsules. In August 2021, the FDA granted accelerated approval to zanubrutinib for the treatment of adults with Waldenström’s macroglobulinemia.[L39030] This indication is valid in the US, Europe, and Canada.[L39367] In September 2021, zanubrutinib was granted another accelerated approval for the treatment of relapsed or refractory marginal zone lymphoma who have received at least one anti-CD20-based regimen.[L39025] In October 2022, the EMA's Committee for Medicinal Products for Human Use (CHMP) recommended zanubrutinib be granted marketing authorization for the treatment of chronic lymphocytic leukemia.[L43737]
- Mantle cell lymphoma (MCL) in adults who have received at least one prior therapy.
[L10163][L40788]
- Waldenström’s macroglobulinemia in adults.
[L10163][L40788][L49976]
- Relapsed or refractory marginal zone lymphoma (MZL) in adults who have received at least one anti-CD20-based regimen.
[L10163][L40788][L49976]
- Chronic lymphocytic leukemia (CLL) [L44727][L49976] or small lymphocytic lymphoma (SLL) in adults.
[L44727]
- Refractory or relapsed follicular lymphoma, in combination with [obinutuzumab], in adults who have received at least two prior systemic therapies.
[L49971][L49976][L50612]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 573 interactions
Zanubrutinib inhibits BTK by forming a covalent bond with cysteine 481 residue in the adenosine triphosphate (ATP)–binding pocket of BTK, which is the enzyme's active site. This binding specificity is commonly seen with other BTK inhibitors. Due to this binding profile, zanubrutinib may also bind with varying affinities to related and unrelated ATP-binding kinases that possess a cysteine residue at this position.[A187958] By blocking the BCR signalling pathway, zanubrutinib inhibits the proliferation, trafficking, chemotaxis, and adhesion of malignant B cells, ultimately leading to reduced tumour size.[L10163] Zanubrutinib was also shown to downregulate programmed death-ligand 1 (PD-1) expression and cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) on CD4+ T cells.[A187949]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L10163]
The Cmax and AUC of zanubrutinib increase in a dose-proportional manner and there is minimal systemic accumulation after repeated dosing. The median Tmax is 2 hours.
[L10163]
[L10163]
[L10163]
[L10163]
[L10163]
Its metabolites have not been characterized.
[L10163]
[L10163]
Proteins and enzymes this drug interacts with in the body
PMID:19290921
Binding of antigen to the B-cell antigen receptor (BCR) triggers signaling that ultimately leads to B-cell activation .
PMID:19290921
After BCR engagement and activation at the plasma membrane, phosphorylates PLCG2 at several sites, igniting the downstream signaling pathway through calcium mobilization, followed by activation of the protein kinase C (PKC) family members .
PMID:11606584
PLCG2 phosphorylation is performed in close cooperation with the adapter protein B-cell linker protein BLNK .
PMID:11606584
BTK acts as a platform to bring together a diverse array of signaling proteins and is implicated in cytokine receptor signaling pathways .
PMID:16517732 PMID:17932028
Plays an important role in the function of immune cells of innate as well as adaptive immunity, as a component of the Toll-like receptors (TLR) pathway .
PMID:16517732
The TLR pathway acts as a primary surveillance system for the detection of pathogens and are crucial to the activation of host defense .
PMID:16517732
Especially, is a critical molecule in regulating TLR9 activation in splenic B-cells .
PMID:16517732 PMID:17932028
Within the TLR pathway, induces tyrosine phosphorylation of TIRAP which leads to TIRAP degradation .
PMID:16415872
BTK also plays a critical role in transcription regulation .
PMID:19290921
Induces the activity of NF-kappa-B, which is involved in regulating the expression of hundreds of genes .
PMID:19290921
BTK is involved on the signaling pathway linking TLR8 and TLR9 to NF-kappa-B .
PMID:19290921
Acts as an activator of NLRP3 inflammasome assembly by mediating phosphorylation of NLRP3 .
PMID:34554188
Transiently phosphorylates transcription factor GTF2I on tyrosine residues in response to BCR .
PMID:9012831
GTF2I then translocates to the nucleus to bind regulatory enhancer elements to modulate gene expression .
PMID:9012831
ARID3A and NFAT are other transcriptional target of BTK .
PMID:16738337
BTK is required for the formation of functional ARID3A DNA-binding complexes .
PMID:16738337
There is however no evidence that BTK itself binds directly to DNA .
PMID:16738337
BTK has a dual role in the regulation of apoptosis .
PMID:9751072
Plays a role in STING1-mediated induction of type I interferon (IFN) response by phosphorylating DDX41 PMID:25704810
PMID:10805725 PMID:27153536 PMID:2790960 PMID:35538033
Known ligands include EGF, TGFA/TGF-alpha, AREG, epigen/EPGN, BTC/betacellulin, epiregulin/EREG and HBEGF/heparin-binding EGF .
PMID:12297049 PMID:15611079 PMID:17909029 PMID:20837704 PMID:27153536 PMID:2790960 PMID:7679104 PMID:8144591 PMID:9419975
Ligand binding triggers receptor homo- and/or heterodimerization and autophosphorylation on key cytoplasmic residues. The phosphorylated receptor recruits adapter proteins like GRB2 which in turn activates complex downstream signaling cascades. Activates at least 4 major downstream signaling cascades including the RAS-RAF-MEK-ERK, PI3 kinase-AKT, PLCgamma-PKC and STATs modules .
PMID:27153536
May also activate the NF-kappa-B signaling cascade .
PMID:11116146
Also directly phosphorylates other proteins like RGS16, activating its GTPase activity and probably coupling the EGF receptor signaling to the G protein-coupled receptor signaling .
PMID:11602604
Also phosphorylates MUC1 and increases its interaction with SRC and CTNNB1/beta-catenin .
PMID:11483589
Positively regulates cell migration via interaction with CCDC88A/GIV which retains EGFR at the cell membrane following ligand stimulation, promoting EGFR signaling which triggers cell migration .
PMID:20462955
Plays a role in enhancing learning and memory performance (By similarity).
Plays a role in mammalian pain signaling (long-lasting hypersensitivity) (By similarity)
Regulates outgrowth and stabilization of peripheral microtubules (MTs). Upon ERBB2 activation, the MEMO1-RHOA-DIAPH1 signaling pathway elicits the phosphorylation and thus the inhibition of GSK3B at cell membrane. This prevents the phosphorylation of APC and CLASP2, allowing its association with the cell membrane.
In turn, membrane-bound APC allows the localization of MACF1 to the cell membrane, which is required for microtubule capture and stabilization
Required for mammary gland differentiation, induction of milk proteins and lactation. Acts as cell-surface receptor for the neuregulins NRG1, NRG2, NRG3 and NRG4 and the EGF family members BTC, EREG and HBEGF. Ligand binding triggers receptor dimerization and autophosphorylation at specific tyrosine residues that then serve as binding sites for scaffold proteins and effectors.
Ligand specificity and signaling is modulated by alternative splicing, proteolytic processing, and by the formation of heterodimers with other ERBB family members, thereby creating multiple combinations of intracellular phosphotyrosines that trigger ligand- and context-specific cellular responses. Mediates phosphorylation of SHC1 and activation of the MAP kinases MAPK1/ERK2 and MAPK3/ERK1. Isoform JM-A CYT-1 and isoform JM-B CYT-1 phosphorylate PIK3R1, leading to the activation of phosphatidylinositol 3-kinase and AKT1 and protect cells against apoptosis.
Isoform JM-A CYT-1 and isoform JM-B CYT-1 mediate reorganization of the actin cytoskeleton and promote cell migration in response to NRG1. Isoform JM-A CYT-2 and isoform JM-B CYT-2 lack the phosphotyrosine that mediates interaction with PIK3R1, and hence do not phosphorylate PIK3R1, do not protect cells against apoptosis, and do not promote reorganization of the actin cytoskeleton and cell migration. Proteolytic processing of isoform JM-A CYT-1 and isoform JM-A CYT-2 gives rise to the corresponding soluble intracellular domains (4ICD) that translocate to the nucleus, promote nuclear import of STAT5A, activation of STAT5A, mammary epithelium differentiation, cell proliferation and activation of gene expression.
The ERBB4 soluble intracellular domains (4ICD) colocalize with STAT5A at the CSN2 promoter to regulate transcription of milk proteins during lactation. The ERBB4 soluble intracellular domains can also translocate to mitochondria and promote apoptosis
Phosphorylation leads to ITK autophosphorylation and full activation. Once activated, phosphorylates PLCG1, leading to the activation of this lipase and subsequent cleavage of its substrates. In turn, the endoplasmic reticulum releases calcium in the cytoplasm and the nuclear activator of activated T-cells (NFAT) translocates into the nucleus to perform its transcriptional duty.
Phosphorylates 2 essential adapter proteins: the linker for activation of T-cells/LAT protein and LCP2. Then, a large number of signaling molecules such as VAV1 are recruited and ultimately lead to lymphokine production, T-cell proliferation and differentiation .
PMID:12186560 PMID:12682224 PMID:21725281
Required for TCR-mediated calcium response in gamma-delta T-cells, may also be involved in the modulation of the transcriptomic signature in the Vgamma2-positive subset of immature gamma-delta T-cells (By similarity). Phosphorylates TBX21 at 'Tyr-530' and mediates its interaction with GATA3 (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
ATC L01EL03
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)
Zanubrutinib
Additional database identifiers
Drugs Product Database (DPD)
23569
ChemSpider
64835237
BindingDB
250082
ZINC
ZINC000584641430
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1133
GenAtlas
BTK
GeneCards
BTK
GenBank Gene Database
X58957
GenBank Protein Database
312467
Guide to Pharmacology
1948
UniProt Accession
BTK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3236
GenAtlas
EGFR
GeneCards
EGFR
GenBank Gene Database
X00588
GenBank Protein Database
757924
Guide to Pharmacology
1797
UniProt Accession
EGFR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3430
GenAtlas
ERBB2
GeneCards
ERBB2
GenBank Gene Database
M11767
GenBank Protein Database
553282
Guide to Pharmacology
2019
UniProt Accession
ERBB2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3432
GeneCards
ERBB4
Guide to Pharmacology
1799
UniProt Accession
ERBB4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6171
GenAtlas
ITK
GeneCards
ITK
GenBank Gene Database
D13720
GenBank Protein Database
399658
Guide to Pharmacology
2046
UniProt Accession
ITK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1079
GeneCards
BMX
Guide to Pharmacology
1942
UniProt Accession
BMX_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6192
GenAtlas
JAK2
GeneCards
JAK2
GenBank Gene Database
AF058925
Guide to Pharmacology
2048
UniProt Accession
JAK2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11719
GeneCards
TEC
Guide to Pharmacology
2238
UniProt Accession
TEC_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1057
GeneCards
BLK
Guide to Pharmacology
1940
UniProt Accession
BLK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6193
GenAtlas
JAK3
GeneCards
JAK3
GenBank Gene Database
U57096
Guide to Pharmacology
2049
UniProt Accession
JAK3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9617
GeneCards
PTK6
Guide to Pharmacology
2182
UniProt Accession
PTK6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3697
GeneCards
FGR
Guide to Pharmacology
2024
UniProt Accession
FGR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3955
GeneCards
FRK
Guide to Pharmacology
2025
UniProt Accession
FRK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6524
GenAtlas
LCK
GeneCards
LCK
GenBank Gene Database
X05027
GenBank Protein Database
36808
Guide to Pharmacology
2053
UniProt Accession
LCK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12434
GeneCards
TXK
Guide to Pharmacology
2268
UniProt Accession
TXK_HUMAN
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:2615
GeneCards
CYP2B6
GenBank Gene Database
M29874
GenBank Protein Database
181296
Guide to Pharmacology
1324
UniProt Accession
CP2B6_HUMAN
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:17450
GeneCards
CYP3A43
GenBank Gene Database
AF319634
GenBank Protein Database
12642642
UniProt Accession
CP343_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2640
GeneCards
CYP3A7
GenBank Gene Database
D00408
GenBank Protein Database
220149
UniProt Accession
CP3A7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_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