Lorlatinib 25mg tablets
Requires a prescription from a doctor or prescriber
Lorlatinib is a third-generation ALK tyrosine kinase inhibitor (TKI) for patients with ALK-positive metastatic non-small cell lung cancer[L39905] which was first approved by the US FDA in November of 2018.
Safety information for pregnancy and breastfeeding
Pregnancy
Breastfeeding
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
Yellow Card
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Drug safety updates
MHRA alerts for Lorlatinib
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 Lorlatinib
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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 Lorlatinib
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Learn about EU pharmacovigilance and safety monitoring
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
MHRA licensed products
View all licensed products for Lorlatinib on the MHRA register
Lorviqua 25mg tablets
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(4)
Lorlatinib for previously treated ALK-positive advanced non-small-cell lung cancer (TA628)
Lorlatinib for ALK-positive advanced non-small-cell lung cancer that has not been treated with an ALK inhibitor (TA1103)
Brigatinib for ALK-positive advanced non-small-cell lung cancer that has not been previously treated with an ALK inhibitor (TA670)
Dabrafenib plus trametinib for treating BRAF V600 mutation-positive advanced non-small-cell lung cancer (TA898)
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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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: 26 · Randomised trials: 2 · 2016–2026
Showing the 50 most relevant studies, sorted by most relevant.
Alice T Shaw, Enriqueta Felip, Todd M Bauer, et al.
The Lancet Oncology, 2017
S. Ou, H. Kilvert, J. Candlish, et al.
Lung cancer, 2024
Jonathan N. Priantti, M. Vilbert, F. D. de Moraes, et al.
Cancers, 2024
Huang Y, Chu Q, Wang J, et al.
2025
- Carcinoma, Non-Small-Cell Lung
- Lung Neoplasms
- Protein Kinase Inhibitors
PurposeTo assess the possible effect of anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors (TKIs) on the health-related quality of life (HRQoL) in patients with ALK-positive non-small cell lung cancer (NSCLC).MethodsA systematic search was performed in PubMed, Web of Science, Embase, and ClinicalTrials.gov to identify literature published between January 2010 and January 2025. Publications reported quantitative assessments of HRQoL in ALK-positive NSCLC patients treated with ALK-TKIs were included. Meta-analyses were performed using random effect models.ResultsA total of 805 records were identified, of which 21 were analyzed in the meta-analysis. Compared to crizotinib, next-generation ALK-TKIs showed statistically significant delayed time to deterioration (TTD) in global health status measured by the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Core 30 (EORTC QLQ-C30) (hazard ratio [HR]: 0.80; 95% confidence interval [CI]: 0.67 to 0.96). Brigatinib and alectinib demonstrated superior TTD in fatigue symptom score of EORTC QLQ-C30 compared to crizotinib (HR: 0.71; 95% CI: 0.54 to 0.92). Regarding between-arm comparisons from baseline, brigatinib and lorlatinib outperformed crizotinib in global health status, physical and emotional functioning, and symptoms scores of nausea and vomiting, fatigue, constipation, and appetite loss using EORTC QLQ-C30.ConclusionsThis study is by far the most comprehensive systematic review and meta-analysis on HRQoL among ALK-positive NSCLC patients treated with ALK-TKIs. These findings extended prior literature by conducting a granular comparison of all available ALK-TKIs across multiple endpoints and highlighted the improved performance of next-generation ALK-TKIs in enhancing HRQoL for ALK-positive NSCLC patients.
Abstract licence: CC BY
B. Solomon, Geoffrey Liu, E. Felip, et al.
Journal of Clinical Oncology, 2024
James A. Fletcher, M.B.B.S., William J. Mullally, MBBCh BAO, Rahul Ladwa, MPhil, et al.
JTO Clinical and Research Reports, 2024
J. Naik, Norma Beavers, F. Nilsson, et al.
Applied Health Economics and Health Policy, 2023
Valentini I, Rumi F, Di Brino E, et al.
2026
- Carcinoma, Non-Small-Cell Lung
- Lung Neoplasms
- Lactams, Macrocyclic
BackgroundLorlatinib is a third-generation anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitor (TKI) with high central nervous system penetration and activity against resistance mutations. Although its clinical efficacy as first-line treatment for ALK-positive advanced non-small cell lung cancer (NSCLC) has been demonstrated, its economic value within the Italian healthcare system remains to be fully established. This study evaluated the cost-effectiveness of lorlatinib compared with alectinib as first-line therapy in Italy.MethodsA partitioned survival model with three health states (progression-free, progressed disease, and death) was developed from the Italian National Health Service and societal perspectives over a 30-year time horizon. Clinical efficacy inputs were derived from the CROWN trial and indirect treatment comparisons using network meta-analysis. Costs (2026 euros) included drug acquisition, subsequent treatments, healthcare resource use, adverse events, end-of-life care, and societal costs. Health outcomes were expressed as life-years (LYs) and quality-adjusted life-years (QALYs). Deterministic, probabilistic, and scenario analyses were conducted to assess uncertainty.ResultsIn the base case, lorlatinib was dominant over alectinib, providing higher benefits (+2.01 LYs; +1.66 QALYs) at lower costs (-€19,210 per patient). This finding was robust across pricing scenarios. Probabilistic sensitivity analysis showed an almost 98,40% probability of cost-effectiveness at Italian willingness-to-pay thresholds.ConclusionsFrom both NHS and societal perspectives, lorlatinib represents a cost-saving and clinically superior first-line treatment option compared with alectinib for patients with ALK-positive advanced NSCLC in Italy.
Abstract licence: CC BY-NC-ND
Zhang H, Hu S, Liu Y, et al.
2026
BackgroundWith multiple first-line treatment options now available for advanced ALK-positive non-small cell lung cancer (NSCLC), clinicians and patients face significant challenges in selecting the optimal therapeutic strategy. This study aims to evaluate the cost-effectiveness of five tyrosine kinase inhibitors (TKIs) as first-line therapies from the perspective of the Chinese healthcare system.MethodsUsing crizotinib as a common comparator, we performed indirect comparisons across five ALK-TKIs by reconstructing survival data and applying fractional polynomial models to estimate time-varying hazard ratios. A partitioned survival model was developed to assess cost-effectiveness. Deterministic sensitivity analysis (DSA) and probabilistic sensitivity analysis (PSA) were conducted to evaluate model robustness. Primary outcomes included total costs, quality-adjusted life years (QALYs), and incremental cost-effectiveness ratios (ICERs). The willingness-to-pay (WTP) threshold was set at $27,906.00/QALY.ResultsCompared to crizotinib, the ICERs for lorlatinib, alectinib, ensartinib, brigatinib, and iruplinalkib were $4,674.43/QALY, $5,361.28/QALY, $199,751.00/QALY, -$29,623.06/QALY, and $4,652.70/QALY, respectively. Iruplinalkib yielded the highest QALY gain, while brigatinib was associated with the lowest total cost. DSA identified utility values and drug prices as key drivers of the ICERs. At a WTP threshold of $27,906/QALY, PSA indicated that iruplinalkib had the highest probability (75.70%) of being cost-effective.ConclusionFor patients with advanced ALK-positive NSCLC in China, lorlatinib, alectinib, brigatinib, and iruplinalkib are cost-effective compared to crizotinib, with the exception of ensartinib. Among these, iruplinalkib is the most cost-effective TKI for first-line treatment, followed by lorlatinib.
Abstract licence: CC BY-NC-ND
A. Shaw, T. Bauer, F. de Marinis, et al.
The New England journal of medicine, 2020
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
24 hours
Mechanism
Non-small cell lung cancer (NSCLC) accounts for up to 85% of lung cancer cases w…
Food interactions
4 warnings
Human targets
11 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1.2 hours
Half-life
24 hours
Protein binding
66%
Volume of distribution
305 L
Metabolism
21%
Elimination
100 mg
Clearance
11 L/h
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L39905]
In the EU, it is indicated for the treatment of adult patients with ALK-positive advanced NSCLC not previously treated with an ALK inhibitor, or whose disease has progressed after using either [alectinib] or [ceritinib], or [crizotinib] and at least one other ALK inhibitor.
[L13580]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 539 interactions
There are no data on the presence of lorlatinib or its metabolites in either human or animal milk or its effects on the breastfed infant or on milk production [FDA Label]. Because of the potential for serious adverse reactions in breastfed infants, instruct women not to breastfeed during treatment with lorlatinib and for 7 days after the final dose [FDA Label].
Advise female patients of reproductive potential to use effective non-hormonal contraception during treatment with lorlatinib and for at least 6 months after the final dose [FDA Label]. Advise females of reproductive potential to use a non-hormonal method of contraception, because lorlatinib can render hormonal contraceptives ineffective [FDA Label].
Based on genotoxicity findings, advise males with female partners of reproductive potential to use effective contraception during treatment with lorlatinib and for at least 3 months after the final dose [FDA Label].
Based on findings from animal studies, use of lorlatinib may transiently impair male fertility [FDA Label].
The safety and effectiveness of lorlatinib in pediatric patients have not been established [FDA Label].
Of the 295 patients in Study B7461001 who received 100 mg lorlatinib orally once daily, 18% of patients were aged 65 years or older [FDA Label].
Although data are limited, no clinically important differences in safety or efficacy were observed between patients aged 65 years or older and younger patients [FDA Label].
No dose adjustment is recommended for patients with mild hepatic impairment (total bilirubin ≤ upper limit of normal ULN with AST > ULN or total bilirubin >1 to 1.5 × ULN with any AST) [FDA Label]. The recommended dose of lorlatinib has not been established for patients with moderate or severe hepatic impairment [FDA Label].
No dose adjustment is recommended for patients with mild or moderate renal impairment (creatinine clearance [CLcr] 30 to 89 mL/min estimated by Cockcroft-Gault) [FDA Label]. The recommended dose of lorlatinib has not been established for patients with severe renal impairment [FDA Label].
Carcinogenicity studies have not been conducted with lorlatinib [FDA Label].
Lorlatinib was aneugenic in an in vitro assay in human lymphoblastoid TK6 cells and positive for micronuclei formation in vivo in the bone marrow of rats. Lorlatinib was not mutagenic in an in vitro bacterial reverse mutation (Ames) assay [FDA Label].
Dedicated fertility studies were not conducted with lorlatinib [FDA Label]. Findings in male reproductive organs occurred in repeat-dose toxicity studies and included lower testicular, epididymal, and prostate weights; testicular tubular degeneration/atrophy; prostatic atrophy; and/or epididymal inflammation at 15 mg/kg/day and 7 mg/kg/day in rats and dogs, respectively (approximately 8 and 2 times, respectively, the human exposure at the recommended dose of 100 mg based on AUC) [FDA Label].
The effects on male reproductive organs were reversible [FDA Label].
Distended abdomen, skin rash, and increased cholesterol and triglycerides occurred in animals [FDA Label]. These findings were accompanied by hyperplasia and dilation of the bile ducts in the liver and acinar atrophy of the pancreas in rats at 15 mg/kg/day and in dogs at 2 mg/kg/day (approximately 8 and 0.5 times, respectively, the human exposure at the recommended dose of 100 mg based on AUC) [FDA Label]. All effects were reversible within the recovery period [FDA Label].
Subsequnetly, lorlatinib is a kinase inhibitor with in vitro activity against ALK and number of other tyrosine kinase receptor related targets including ROS1, TYK1, FER, FPS, TRKA, TRKB, TRKC, FAK, FAK2, and ACK [FDA Label]. Lorlatinib demonstrated in vitro activity against multiple mutant forms of the ALK enzyme, including some mutations detected in tumors at the time of disease progression on crizotinib and other ALK inhibitors [FDA Label]. Moreover, lorlatinib possesses the capability to cross the blood-brain barrier, allowing it to reach and treat progressive or worsening brain metastases as well [L4848][A40078]. The overall antitumor activity of lorlatinib in in-vivo models appears to be dose-dependent and correlated with the inhibition of ALK phosphorylation [FDA Label].
Although many ALK-positive metastatic NSCLC patients respond to initial tyrosine kinase therapies, such patients also often experience tumor progression [A40081]. Various clinical trials performed with lorlatinib, however, have demonstrated its utility to effect tumor regression in ALK-positive metastatic NSCLC patients who experience tumor progression despite current use or having already used various first and second-generation tyrosine kinase inhibitors like crizotinib, alectinib, or ceritinib [A40086].
In 295 patients who received lorlatinib at the recommended dosage of 100 mg once daily and had an ECG measurement in the same Study B7461001, the maximum mean change from baseline for their PR interval was 16.4 ms (2-sided 90% upper confidence interval CI 19.4 ms) [FDA Label]. Among the 284 patients with PR interval <200 ms at baseline, 14% had PR interval prolongation ≥200 ms after starting use with lorlatinib [FDA Label]. The prolongation of PR interval occurred in a concentration-dependent manner and atrioventricular block occurred in 1% of patients [FDA Label].
Finally, in 275 patients who received lorlatinib at the recommended dosage in the activity-estimating portion of Study B7461001, no large mean increases from baseline in the QTcF interval (i.e., >20 ms) were detected [FDA Label].
How the body processes this drug — absorption, distribution, metabolism, and elimination
The mean absolute bioavailability is 81% (90% CI 75.7%, 86.2%) after oral administration compared to intravenous administration [FDA Label].
Administration of lorlatinib with a high fat, high-calorie meal (approximately 1000 calories with 150 calories from protein, 250 calories from carbohydrate, and 500 to 600 calories from fat) had no clinically meaningful effect on lorlatinib pharmacokinetics [FDA Label].
Proteins and enzymes this drug interacts with in the body
Plays a role in the regulation of mast cell degranulation. Plays a role in the regulation of cell differentiation and promotes neurite outgrowth in response to NGF signaling. Plays a role in cell scattering and cell migration in response to HGF-induced activation of EZR.
Phosphorylates BCR and down-regulates BCR kinase activity. Phosphorylates HCLS1/HS1, PECAM1, STAT3 and TRIM28
PMID:1281417 PMID:15488758 PMID:17196528 PMID:1849459 PMID:1850821 PMID:22649032 PMID:27445338 PMID:8325889
Can also bind and be activated by NTF3/neurotrophin-3. However, NTF3 only supports axonal extension through NTRK1 but has no effect on neuron survival (By similarity).
Upon dimeric NGF ligand-binding, undergoes homodimerization, autophosphorylation and activation .
PMID:1281417
Recruits, phosphorylates and/or activates several downstream effectors including SHC1, FRS2, SH2B1, SH2B2 and PLCG1 that regulate distinct overlapping signaling cascades driving cell survival and differentiation. Through SHC1 and FRS2 activates a GRB2-Ras-MAPK cascade that regulates cell differentiation and survival. Through PLCG1 controls NF-Kappa-B activation and the transcription of genes involved in cell survival.
Through SHC1 and SH2B1 controls a Ras-PI3 kinase-AKT1 signaling cascade that is also regulating survival. In absence of ligand and activation, may promote cell death, making the survival of neurons dependent on trophic factors
PMID:15494731 PMID:7574684
Upon ligand-binding, undergoes homodimerization, autophosphorylation and activation .
PMID:15494731
Recruits, phosphorylates and/or activates several downstream effectors including SHC1, FRS2, SH2B1, SH2B2 and PLCG1 that regulate distinct overlapping signaling cascades.
Through SHC1, FRS2, SH2B1, SH2B2 activates the GRB2-Ras-MAPK cascade that regulates for instance neuronal differentiation including neurite outgrowth. Through the same effectors controls the Ras-PI3 kinase-AKT1 signaling cascade that mainly regulates growth and survival. Through PLCG1 and the downstream protein kinase C-regulated pathways controls synaptic plasticity.
Thereby, plays a role in learning and memory by regulating both short term synaptic function and long-term potentiation. PLCG1 also leads to NF-Kappa-B activation and the transcription of genes involved in cell survival. Hence, it is able to suppress anoikis, the apoptosis resulting from loss of cell-matrix interactions.
May also play a role in neutrophin-dependent calcium signaling in glial cells and mediate communication between neurons and glia
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC L01ED05
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)
Lorlatinib
Additional database identifiers
Drugs Product Database (DPD)
23119
ChemSpider
32813339
BindingDB
50018830
PDB
5P8
ZINC
ZINC000098208524
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18889
GeneCards
STYK1
UniProt Accession
STYK1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3657
GeneCards
FES
Guide to Pharmacology
2023
UniProt Accession
FES_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8031
GenAtlas
NTRK1
GeneCards
NTRK1
GenBank Gene Database
M23102
GenBank Protein Database
339918
Guide to Pharmacology
1817
UniProt Accession
NTRK1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8032
GeneCards
NTRK2
GenBank Gene Database
U12140
GenBank Protein Database
530791
Guide to Pharmacology
1818
UniProt Accession
NTRK2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8033
GeneCards
NTRK3
Guide to Pharmacology
1819
UniProt Accession
NTRK3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9611
GenAtlas
PTK2
GeneCards
PTK2
GenBank Gene Database
L13616
Guide to Pharmacology
2180
UniProt Accession
FAK1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9612
GenAtlas
PTK2B
GeneCards
PTK2B
GenBank Gene Database
U33284
GenBank Protein Database
988305
Guide to Pharmacology
2181
UniProt Accession
FAK2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:19297
GenAtlas
TNK2
GeneCards
TNK2
GenBank Gene Database
L13738
GenBank Protein Database
8850245
Guide to Pharmacology
2246
UniProt Accession
ACK1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10261
GeneCards
ROS1
Guide to Pharmacology
1840
UniProt Accession
ROS1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:427
GenAtlas
ALK
GeneCards
ALK
GenBank Gene Database
U62540
GenBank Protein Database
2454168
Guide to Pharmacology
1839
UniProt Accession
ALK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3655
GeneCards
FER
Guide to Pharmacology
2022
UniProt Accession
FER_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: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: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:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2621
GeneCards
CYP2C19
GenBank Gene Database
M61854
GenBank Protein Database
181344
Guide to Pharmacology
1328
UniProt Accession
CP2CJ_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12535
GeneCards
UGT1A3
GenBank Gene Database
M84127
GenBank Protein Database
340135
UniProt Accession
UD13_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_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