Ponatinib 30mg tablets
Requires a prescription from a doctor or prescriber
Ponatinib is a novel Bcr-Abl tyrosine kinase inhibitor that is especially effective against the T315I mutation for the treatment of chronic myeloid leukemia.
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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 Ponatinib
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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 Ponatinib
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2 branded products available
MHRA licensed products
View all licensed products for Ponatinib on the MHRA register
Ponatinib 30mg tablets
WHO defined daily dose (DDD)
45 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
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(5)
Ponatinib for treating chronic myeloid leukaemia and acute lymphoblastic leukaemia (TA451)
Asciminib for treating chronic myeloid leukaemia after 2 or more tyrosine kinase inhibitors (TA813)
Obecabtagene autoleucel for treating relapsed or refractory B-cell precursor acute lymphoblastic leukaemia (TA1116)
Brexucabtagene autoleucel for treating relapsed or refractory B-cell acute lymphoblastic leukaemia in people 26 years and over (TA893)
Inotuzumab ozogamicin for treating relapsed or refractory B-cell acute lymphoblastic leukaemia (TA541)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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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: 15 · Randomised trials: 3 · 2018–2026
Showing the 50 most relevant studies, sorted by most relevant.
J. Cortes, J. Apperley, E. Lomaia, et al.
Blood, 2021
E. Jabbour, H. Kantarjian, Ibrahim Aldoss, et al.
JAMA, 2024
M. Raza, Huzaifa Fayyaz Khwaja, H. Arshad, et al.
Critical reviews in oncology/hematology, 2025
- Philadelphia Chromosome
- Imidazoles
- Pyridazines
Kong J, Jang J, Kong JH, et al.
2026
- Imidazoles
- Pyridazines
- Antineoplastic Agents
Ponatinib, a third-generation BCR::ABL1 inhibitor, has antileukemic activity but is associated with cardiovascular toxicity, for which transcriptome-level responses remain incompletely characterized. Here, we defined a ponatinib-associated transcriptomic signature and examined its mechanistic implications using two public RNA sequencing (RNA-Seq) datasets: GSE186341 (11 cancer cell lines treated with kinase inhibitors) and GSE217421 (induced pluripotent stem cell (iPSC)-derived cardiomyocytes treated with approved drugs). Principal component analysis (PCA) and k-means clustering were used to define expression-based subgroups of vehicle-treated (DMSO) controls. DESeq2, followed by fixed-effect meta-analysis, estimated subgroup-specific treatment effects and pooled effect estimates across subgroups. In GSE186341, we identified 2639 meta-analytic differentially expressed genes (meta-DEGs). Among these, 81 genes were also differentially expressed in GSE217421 after ponatinib treatment, identifying an overlapping gene set across datasets. In contrast, imatinib showed no overlap with these 81 genes under the same cross-dataset analysis framework. Cardiotoxicity-relevant functions were represented by directionally consistent genes linked to cardiac repolarization-associated ion handling (KCNN3), insulin-responsive metabolic regulation (FOXO1, HK2), cyclic adenosine monophosphate (cAMP)-responsive stress signaling (RAPGEF3), and mitochondrial homeostasis and redox regulation (MCL1, GCH1). Collectively, these results define a ponatinib-associated transcriptomic signature and nominate cross-dataset transcript-level candidates for subsequent mechanistic and experimental validation in ponatinib-associated cardiotoxicity.
Abstract licence: CC BY
F. Tan, Tracy L. Putoczki, S. Stylli, et al.
OncoTargets and therapy, 2019
E. Jabbour, V. Oehler, Paul B. Koller, et al.
JAMA oncology, 2024
Jordi Cortés, Dong-Wook Kim, J. Pinilla-Ibarz, et al.
Blood, 2018
E. Jabbour, N. Short, F. Ravandi, et al.
The Lancet. Haematology, 2018
C. Eide, M. Zabriskie, Samantha L Savage Stevens, et al.
Cancer cell, 2019
E. Jabbour, N. Short, N. Jain, et al.
The Lancet. Haematology, 2022
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
28 days
Mechanism
Ponatinib is a multi-target kinase inhibitor.
Food interactions
3 warnings
Human targets
15 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
6 hours
Half-life
45 mg
[L52425]…
Protein binding
99%
[L52425]
Volume of distribution
45 mg
[L52425]…
Metabolism
64%
Elimination
87%
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L52425]
It can also be used as a monotherapy where no other kinase inhibitors are indicated or where there is a T315I-positive mutation.
[L52425]
Ponatinib is indicated in the treatment of chronic myleloid leukemia (CML) with resistance or intolerance to at least 2 kinase inhibitors.
[L52425]
It can also be used for accelerated or blast phase CML where no other kinase inhibitors are indicated.
[L52425]
Finally, it is also indicated for T315I-positive CML in the chronic, accelerated, or blast phase.
[L52425]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1362 interactions
[L52425]
How the body processes this drug — absorption, distribution, metabolism, and elimination
The aqueous solubility of ponatinib is pH dependent, with higher pH resulting in lower solubility.
When 45 mg of ponatinib is given to cancer patients, the pharmacokinetic parameters are as follows:
Cmax = 73 ng/mL;
AUC = 1253 ng•hr/mL;
[L52425]
[L52425]
[L52425]
Ponatinib is a weak substrate for P-gp and ABCG2.
[L52425]
[L52425]
Ponatinib is also metabolized by esterases and/or amidases.
[L52425]
[L52425]
Proteins and enzymes this drug interacts with in the body
Involved in the regulation of cell adhesion and motility through phosphorylation of key regulators of these processes such as BCAR1, CRK, CRKL, DOK1, EFS or NEDD9 .
PMID:22810897
Phosphorylates multiple receptor tyrosine kinases and more particularly promotes endocytosis of EGFR, facilitates the formation of neuromuscular synapses through MUSK, inhibits PDGFRB-mediated chemotaxis and modulates the endocytosis of activated B-cell receptor complexes. Other substrates which are involved in endocytosis regulation are the caveolin (CAV1) and RIN1. Moreover, ABL1 regulates the CBL family of ubiquitin ligases that drive receptor down-regulation and actin remodeling.
Phosphorylation of CBL leads to increased EGFR stability. Involved in late-stage autophagy by regulating positively the trafficking and function of lysosomal components. ABL1 targets to mitochondria in response to oxidative stress and thereby mediates mitochondrial dysfunction and cell death.
In response to oxidative stress, phosphorylates serine/threonine kinase PRKD2 at 'Tyr-717' .
PMID:28428613
ABL1 is also translocated in the nucleus where it has DNA-binding activity and is involved in DNA-damage response and apoptosis. Many substrates are known mediators of DNA repair: DDB1, DDB2, ERCC3, ERCC6, RAD9A, RAD51, RAD52 or WRN. Activates the proapoptotic pathway when the DNA damage is too severe to be repaired.
Phosphorylates TP73, a primary regulator for this type of damage-induced apoptosis. Phosphorylates the caspase CASP9 on 'Tyr-153' and regulates its processing in the apoptotic response to DNA damage. Phosphorylates PSMA7 that leads to an inhibition of proteasomal activity and cell cycle transition blocks.
ABL1 also acts as a regulator of multiple pathological signaling cascades during infection. Several known tyrosine-phosphorylated microbial proteins have been identified as ABL1 substrates. This is the case of A36R of Vaccinia virus, Tir (translocated intimin receptor) of pathogenic E.coli and possibly Citrobacter, CagA (cytotoxin-associated gene A) of H.pylori, or AnkA (ankyrin repeat-containing protein A) of A.phagocytophilum.
Pathogens can highjack ABL1 kinase signaling to reorganize the host actin cytoskeleton for multiple purposes, like facilitating intracellular movement and host cell exit. Finally, functions as its own regulator through autocatalytic activity as well as through phosphorylation of its inhibitor, ABI1. Regulates T-cell differentiation in a TBX21-dependent manner (By similarity).
Positively regulates chemokine-mediated T-cell migration, polarization, and homing to lymph nodes and immune-challenged tissues, potentially via activation of NEDD9/HEF1 and RAP1 (By similarity). Phosphorylates TBX21 on tyrosine residues leading to an enhancement of its transcriptional activator activity (By similarity)
PMID:17116687 PMID:1903516 PMID:7479768
The central Dbl homology (DH) domain functions as guanine nucleotide exchange factor (GEF) that modulates the GTPases CDC42, RHOA and RAC1.
Promotes the conversion of CDC42, RHOA and RAC1 from the GDP-bound to the GTP-bound form .
PMID:23940119 PMID:7479768
The amino terminus contains an intrinsic kinase activity .
PMID:1657398
Functions as an important negative regulator of neuronal RAC1 activity (By similarity). Regulates macrophage functions such as CSF1-directed motility and phagocytosis through the modulation of RAC1 activity .
PMID:17116687
Plays a major role as a RHOA GEF in keratinocytes being involved in focal adhesion formation and keratinocyte differentiation PMID:23940119
Activates the AKT1 signaling pathway by phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase. Activated KIT also transmits signals via GRB2 and activation of RAS, RAF1 and the MAP kinases MAPK1/ERK2 and/or MAPK3/ERK1. Promotes activation of STAT family members STAT1, STAT3, STAT5A and STAT5B.
Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate. KIT signaling is modulated by protein phosphatases, and by rapid internalization and degradation of the receptor. Activated KIT promotes phosphorylation of the protein phosphatases PTPN6/SHP-1 and PTPRU, and of the transcription factors STAT1, STAT3, STAT5A and STAT5B.
Promotes phosphorylation of PIK3R1, CBL, CRK (isoform Crk-II), LYN, MAPK1/ERK2 and/or MAPK3/ERK1, PLCG1, SRC and SHC1
PMID:20064382 PMID:20616503 PMID:20702524 PMID:21357690 PMID:21454698 PMID:24560924 PMID:28846097 PMID:28846099 PMID:28953886 PMID:31118272
In contrast to most receptor tyrosine kinases, RET requires not only its cognate ligands but also coreceptors, for activation .
PMID:21994944 PMID:23333276 PMID:28846097 PMID:28846099 PMID:28953886
GDNF ligands (GDNF, NRTN, ARTN, PSPN and GDF15) first bind their corresponding GDNFR coreceptors (GFRA1, GFRA2, GFRA3, GFRA4 and GFRAL, respectively), triggering RET autophosphorylation and activation, leading to activation of downstream signaling pathways, including the MAPK- and AKT-signaling pathways .
PMID:21994944 PMID:23333276 PMID:24560924 PMID:25242331 PMID:28846097 PMID:28846099 PMID:28953886
Acts as a dependence receptor via the GDNF-GFRA1 signaling: in the presence of the ligand GDNF in somatotrophs within pituitary, promotes survival and down regulates growth hormone (GH) production, but triggers apoptosis in absence of GDNF .
PMID:20616503 PMID:21994944
Required for the molecular mechanisms orchestration during intestine organogenesis via the ARTN-GFRA3 signaling: involved in the development of enteric nervous system and renal organogenesis during embryonic life, and promotes the formation of Peyer's patch-like structures, a major component of the gut-associated lymphoid tissue (By similarity). Mediates, through interaction with GDF15-receptor GFRAL, GDF15-induced cell-signaling in the brainstem which triggers an aversive response, characterized by nausea, vomiting, and/or loss of appetite in response to various stresses .
PMID:28846097 PMID:28846099 PMID:28953886
Modulates cell adhesion via its cleavage by caspase in sympathetic neurons and mediates cell migration in an integrin (e.g. ITGB1 and ITGB3)-dependent manner .
PMID:20702524 PMID:21357690
Also active in the absence of ligand, triggering apoptosis through a mechanism that requires receptor intracellular caspase cleavage .
PMID:21357690
Triggers the differentiation of rapidly adapting (RA) mechanoreceptors .
PMID:20064382
Involved in the development of the neural crest (By similarity).
Regulates nociceptor survival and size (By similarity). Phosphorylates PTK2/FAK1 PMID:21454698
Required for post-natal hematopoiesis. After birth, activates or inhibits angiogenesis, depending on the context. Inhibits angiogenesis and promotes vascular stability in quiescent vessels, where endothelial cells have tight contacts.
In quiescent vessels, ANGPT1 oligomers recruit TEK to cell-cell contacts, forming complexes with TEK molecules from adjoining cells, and this leads to preferential activation of phosphatidylinositol 3-kinase and the AKT1 signaling cascades. In migrating endothelial cells that lack cell-cell adhesions, ANGT1 recruits TEK to contacts with the extracellular matrix, leading to the formation of focal adhesion complexes, activation of PTK2/FAK and of the downstream kinases MAPK1/ERK2 and MAPK3/ERK1, and ultimately to the stimulation of sprouting angiogenesis. ANGPT1 signaling triggers receptor dimerization and autophosphorylation at specific tyrosine residues that then serve as binding sites for scaffold proteins and effectors.
Signaling is modulated by ANGPT2 that has lower affinity for TEK, can promote TEK autophosphorylation in the absence of ANGPT1, but inhibits ANGPT1-mediated signaling by competing for the same binding site. Signaling is also modulated by formation of heterodimers with TIE1, and by proteolytic processing that gives rise to a soluble TEK extracellular domain. The soluble extracellular domain modulates signaling by functioning as decoy receptor for angiopoietins.
TEK phosphorylates DOK2, GRB7, GRB14, PIK3R1; SHC1 and TIE1
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
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
ATC L01EA05
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)
Ponatinib
Additional database identifiers
Drugs Product Database (DPD)
22576
ChemSpider
24747381
BindingDB
50322535
PDB
0LI
ZINC
ZINC000036701290
HUGO Gene Nomenclature Committee (HGNC)
HGNC:76
GenAtlas
ABL1
GeneCards
ABL1
GenBank Gene Database
X16416
GenBank Protein Database
28237
Guide to Pharmacology
1923
UniProt Accession
ABL1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1014
GeneCards
BCR
UniProt Accession
BCR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6342
GenAtlas
KIT
GeneCards
KIT
GenBank Gene Database
X06182
GenBank Protein Database
34085
Guide to Pharmacology
1805
UniProt Accession
KIT_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9967
GenAtlas
RET
GeneCards
RET
GenBank Gene Database
X12949
Guide to Pharmacology
2185
UniProt Accession
RET_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11724
GenAtlas
TEK
GeneCards
TEK
GenBank Gene Database
L06139
Guide to Pharmacology
1842
UniProt Accession
TIE2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3765
GenAtlas
FLT3
GeneCards
FLT3
GenBank Gene Database
U02687
GenBank Protein Database
409573
Guide to Pharmacology
1807
UniProt Accession
FLT3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3688
GenAtlas
FGFR1
GeneCards
FGFR1
GenBank Gene Database
X51803
GenBank Protein Database
31368
Guide to Pharmacology
1808
UniProt Accession
FGFR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3689
GenAtlas
FGFR2
GenBank Gene Database
X52832
GenBank Protein Database
31374
Guide to Pharmacology
1809
UniProt Accession
FGFR2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3690
GenAtlas
FGFR3
GeneCards
FGFR3
GenBank Gene Database
M58051
GenBank Protein Database
182569
Guide to Pharmacology
1810
UniProt Accession
FGFR3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3691
GenAtlas
FGFR4
GeneCards
FGFR4
GenBank Gene Database
X57205
GenBank Protein Database
31372
Guide to Pharmacology
1811
UniProt Accession
FGFR4_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:11283
GenAtlas
SRC
GeneCards
SRC
GenBank Gene Database
AL133293
GenBank Protein Database
10635153
Guide to Pharmacology
2206
UniProt Accession
SRC_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6735
GeneCards
LYN
GenBank Gene Database
M16038
GenBank Protein Database
307144
Guide to Pharmacology
2060
UniProt Accession
LYN_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6307
GenAtlas
KDR
GeneCards
KDR
GenBank Gene Database
AF035121
GenBank Protein Database
2655412
Guide to Pharmacology
1813
UniProt Accession
VGFR2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8803
GenAtlas
PDGFRA
GeneCards
PDGFRA
GenBank Gene Database
M21574
GenBank Protein Database
189734
Guide to Pharmacology
1803
UniProt Accession
PGFRA_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:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_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:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_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
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q198728), 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.