Alectinib 150mg capsules
Requires a prescription from a doctor or prescriber
Alectinib is a second generation oral drug that selectively inhibits the activity of anaplastic lymphoma kinase (ALK) tyrosine kinase.
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).
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Safety monitoring data
Yellow Card reports
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Suspected adverse reactions reported for Alectinib
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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 Alectinib
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2 branded products available
MHRA licensed products
View all licensed products for Alectinib on the MHRA register
Alecensa 150mg capsules
WHO defined daily dose (DDD)
1.2 gram
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
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(10)
Alectinib for untreated ALK-positive advanced non-small-cell lung cancer (TA536)
Alectinib for adjuvant treatment of ALK-positive non-small-cell lung cancer (TA1014)
Alectinib for previously treated anaplastic lymphoma kinase-positive advanced non-small-cell lung cancer (terminated appraisal) (TA438)
Brigatinib for ALK-positive advanced non-small-cell lung cancer that has not been previously treated with an ALK inhibitor (TA670)
Lorlatinib for ALK-positive advanced non-small-cell lung cancer that has not been treated with an ALK inhibitor (TA1103)
Lorlatinib for previously treated ALK-positive advanced non-small-cell lung cancer (TA628)
Brigatinib for treating ALK-positive advanced non-small-cell lung cancer after crizotinib (TA571)
Lung cancer: diagnosis and management (NG122)
Ceritinib for untreated ALK-positive non-small-cell lung cancer (TA500)
Atezolizumab in combination for treating metastatic non-squamous non-small-cell lung cancer (TA584)
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. 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: 23 · Randomised trials: 4 · 2014–2026
Showing the 50 most relevant studies, sorted by most relevant.
Toyoaki Hida, Hiroshi Nokihara, Masashi Kondo, et al.
The Lancet, 2017
- Crizotinib
- Anaplastic Lymphoma Kinase
- Antineoplastic Agents
Daniel Samacá-Samacá, L. Prieto-Pinto, A. Pérez, et al.
Lung Cancer Management, 2023
Liang Shi, Shuhong Gao, L. Tong, et al.
Frontiers in Oncology, 2023
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
Yi‐Long Wu, Rafał Dziadziuszko, Jin Seok Ahn, et al.
New England Journal of Medicine, 2024
- Tyrosine Kinase Inhibitors
- Antineoplastic Agents
- Carbazoles
Koichi Andō, Kaho Akimoto, Hiroki Sato, et al.
Cancers, 2020
Lida Wang, Zhixin Sheng, Junying Zhang, et al.
Journal of Chemotherapy, 2021
- Carcinoma, Non-Small-Cell Lung
- Lung Neoplasms
- Network Meta-Analysis
Koichi Andō, Ryo Manabe, Yasunari Kishino, et al.
Cancers, 2021
Junsheng Fan, Zengfei Xia, Xiaoli Zhang, et al.
OncoTargets and Therapy, 2018
Tung Hoang, Seung‐Kwon Myung, Thu Thi Pham, et al.
Cancers, 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
33 hr
Mechanism
Alectinib is a second generation oral drug that selectively inhibits the activit…
Food interactions
3 warnings
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
4 hours
Half-life
33 hr
Protein binding
99%
Volume of distribution
4016 L
Metabolism
Elimination
98%
Clearance
81.9L/h
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Approved under accelerated approval in 2015, alectinib is indicated for use in patients who have progressed on or were not tolerant of crizotinib, which is associated with the development of resistance.
[L51008]
It is also indicated as an adjuvant treatment in adult patients following tumor resection of ALK-positive non-small cell lung cancer.
[L51008]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 566 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
In vitro studies suggest that alectinib is not a substrate for P-gp while M4 is.
Proteins and enzymes this drug interacts with in the body
PMID:11121404 PMID:11387242 PMID:16317043 PMID:17274988 PMID:30061385 PMID:34646012 PMID:34819673
Also acts as a key thinness protein involved in the resistance to weight gain: in hypothalamic neurons, controls energy expenditure acting as a negative regulator of white adipose tissue lipolysis and sympathetic tone to fine-tune energy homeostasis (By similarity). Following activation by ALKAL2 ligand at the cell surface, transduces an extracellular signal into an intracellular response .
PMID:30061385 PMID:33411331 PMID:34646012 PMID:34819673
In contrast, ALKAL1 is not a potent physiological ligand for ALK .
PMID:34646012
Ligand-binding to the extracellular domain induces tyrosine kinase activation, leading to activation of the mitogen-activated protein kinase (MAPK) pathway .
PMID:34819673
Phosphorylates almost exclusively at the first tyrosine of the Y-x-x-x-Y-Y motif .
PMID:15226403 PMID:16878150
Induces tyrosine phosphorylation of CBL, FRS2, IRS1 and SHC1, as well as of the MAP kinases MAPK1/ERK2 and MAPK3/ERK1 .
PMID:15226403 PMID:16878150
ALK activation may also be regulated by pleiotrophin (PTN) and midkine (MDK) .
PMID:11278720 PMID:11809760 PMID:12107166 PMID:12122009
PTN-binding induces MAPK pathway activation, which is important for the anti-apoptotic signaling of PTN and regulation of cell proliferation .
PMID:11278720 PMID:11809760 PMID:12107166
MDK-binding induces phosphorylation of the ALK target insulin receptor substrate (IRS1), activates mitogen-activated protein kinases (MAPKs) and PI3-kinase, resulting also in cell proliferation induction .
PMID:12122009
Drives NF-kappa-B activation, probably through IRS1 and the activation of the AKT serine/threonine kinase .
PMID:15226403 PMID:16878150
Recruitment of IRS1 to activated ALK and the activation of NF-kappa-B are essential for the autocrine growth and survival signaling of MDK PMID:15226403 PMID:16878150
Proteins that transport this drug across cell membranes
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
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 L01ED03
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)
Alectinib
Additional database identifiers
Drugs Product Database (DPD)
22813
ChemSpider
26326738
BindingDB
50362781
PDB
EMH
ZINC
ZINC000066166864
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:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_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
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q21099132), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.