Momelotinib 150mg tablets
Requires a prescription from a doctor or prescriber
Momelotinib is a Janus Kinase 1 (JAK1) and 2 (JAK2) inhibitor.
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Suspected adverse reactions reported for Momelotinib
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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.
EudraVigilance
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Suspected adverse reactions reported for Momelotinib
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1 branded products available
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Omjjara 150mg 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.
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(2)
Momelotinib for treating myelofibrosis-related splenomegaly or symptoms (TA957)
Fedratinib for treating disease-related splenomegaly or symptoms in myelofibrosis (TA1018)
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
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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: 6 · Randomised trials: 7 · 2016–2025
Showing the 50 most relevant studies, sorted by most relevant.
R. Mesa, J. Kiladjian, J. Catalano, et al.
Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2017
C. Harrison, A. Vannucchi, U. Platzbecker, et al.
The Lancet. Haematology, 2018
M. Aldalal'ah, J. Al-Nusair, Nora Al-Khateeb, et al.
Blood, 2024
S. Verstovsek, Ruben A. Mesa, V MNSSVKR GUPTA, et al.
Blood Advances, 2023
- Anemia
- Thrombocytopenia
- Primary Myelofibrosis
Malte Asshoff, V. Petzer, M. Warr, et al.
Blood, 2017
Wu Ye, Xia Wu, Xue Zheng, et al.
2020
Abstract Background The meta-analysis compared the efficacy and safety of momelotinib, ruxolitinib and pacitinib in patients with myeloproliferative neoplasms(MPN), which includes essential thrombocythemia, polycythemia vera and primary myelofibrosis. Methods We searched multiple databases and collected relevant studies before Dec. 20,2019. According to predefined criteria, we included eight qualified phase 3 randomized controlled trials with 2125 patients in the meta-analysis. Statistical analysis used StataMP14 and Indirect Treatment Comparisons software. The meta-analysis is registered with PROSPERO, number CRD42020164271. Results The relative risk (95%confidence interval) of momelotinib vs ruxolitinib, ruxolitinib vs pacritinib and momelotinib vs pacritinib by indirect-comparison are as follows: The RR(95%CI) for ≥ 35% reduction in spleen volume from baseline at week 24/32 as determined by magnetic resonance imaging or computed tomography were 0.93(95%CI0.69-1.25), 10.87(95%CI2.52-46.79) and 10.09(95%CI2.27- 44.74); The RR(95%CI) for ≥ 50% reduction in total symptom score from baseline at week 24–32 assessed using the modified Myelofibrosis Symptom Assessment Form were 1.61(95%CI0.25-10.15), 4.40(95%CI2.13-9.09) and 7.12 (95%CI0.91-55.41); The RR(95%CI) for the risk of anemia were 0.60(95%CI0.20-1.85), 0.80(95%CI0.56-1.14) and 0.48 (95%CI0.15-1.56); The RR(95%CI) for thrombocytopenia were 0.69(95%CI0.50-0.96), 1.33(95%CI0.77-2.30) and 0.92(95%CI0.48-1.74); The RR (95%CI) for the risk of fatigue were 1.07(95%CI0.71-1.59), 0.82(95%CI0.49-1.37) and 0.88(95%CI0.46-1.68); The RR(95%CI) for the risk of diarrhea were 1.32(95%CI0.58-3.01), 0.11(95%CI0.03-0.46) and 0.39(95%CI0.15-1.02); The RR(95%CI) for abdominal pain were 0.95(95%CI0.61-1.48), 0.83(95%CI0.30-2.25) and 0.78(95%CI0.26-2.35). The RR(95CI) for the improvement of transfusion-independent of pacritinib vs ruxolitinib was 6.36 (95%CI0.79-50.98). Conclusions Excluding the improvement of transfusion-independent and the risk of thrombocytopenia, pacritinib had relatively poorer efficacy and higher risk of adverse events compared with momelotinib or ruxolitinib. Momelotinib had similar or better efficacy and similar or lower risk of adverse events than ruxolitinib while excluding the risk of diarrhea. In general, momelotinib has the best potential therapeutic value in patients with MPN among the three drugs, but further clinical studies are needed to prove it.
Abstract licence: CC BY 4.0
S. Verstovsek, A. Gerds, A. Vannucchi, et al.
Lancet, 2023
- Anemia
- Primary Myelofibrosis
- Janus Kinase Inhibitors
Shimoda K, Komatsu N, Matsumura I, et al.
2024
- Benzamides
- Nitriles
- Pyrazoles
Anna Rita Migliaccio
Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature, 2019
S. Verstovsek, Ruben A. Mesa, V MNSSVKR GUPTA, et al.
Blood, 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
Not available
Mechanism
One of the molecular pathways that have been implicated in the pathogenesis of M…
Food interactions
1 warning
Human targets
6 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
97%
[A261561]…
Half-life
[L48186]
Protein binding
91%
[L48186]
Volume of distribution
984 L
[L48186]
Metabolism
36%
Elimination
69%
Clearance
103 L/h
[L48186]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L48186]
In Canada, momelotinib is indicated for the treatment of splenomegaly and/or disease-related symptoms, in adult patients with
intermediate or high-risk primary myelofibrosis (MF), post polycythemia vera myelofibrosis or post essential thrombocythemia MF who have moderate to severe anemia.
[L52635]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 246 interactions
Further management should be as clinically indicated. Hemodialysis is not expected to enhance the elimination of momelotinib.
[L48186]
Momelotinib is an adenosine triphosphate-competitive inhibitor of wild-type JAK1 and JAK2 as well as mutant JAK2V617F, which contribute to the signalling of several cytokines and growth factors that are important for hematopoiesis and immune function. Momelotinib and its major human circulating metabolite, M21, have higher inhibitory activity for JAK2 compared to other members of the JAK family - JAK3 and tyrosine kinase 2 (TYK2). Momelotinib and M21 additionally inhibit activin A receptor type 1 (ACVR1), also known as activin receptor-like kinase 2 (ALK2), which produces subsequent inhibition of liver hepcidin expression and increased iron availability, resulting in increased red blood cell production. Dysregulated JAK signalling may also contribute to inflammation and hyperactivation of ACVR1.[L48186] Suppression of hepcidin by momelotinib increases circulating iron and hemoglobin, and stimulates erythropoiesis in the bone marrow.[A261571]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A261561]
The mean (%CV) steady-state Cmax is 479 ng/mL (61%), and the mean (%CV) AUC is 3,288 ng x h/mL (60%) at the maximum recommended dosage. Momelotinib exposure (i.e., Cmax and AUC) increases dose proportionally from 100 mg to 300 mg (0.5 to 1.5 times the maximum recommended dosage), but less than dose-proportional at doses from 400 mg to 800 mg (two to four times the maximum recommended dosage). There is no clinically significant accumulation.
The Tmax at steady state is two hours (Q1: 1 hour; Q3: 3 hours) post-dose.
[L48186]
No clinically significant differences in momelotinib pharmacokinetics were observed following administration of either a high-fat meal (800 kcal; 50% fat) or low-fat meal (400 kcal; 20% fat) in healthy subjects.
[L48186]
[L48186]
[L48186]
[L48186]
[A261551][L48186]
M21 is a major metabolite in humans that retains approximately 40% of the pharmacological activity of the parent. The mean ratio of M21 to momelotinib for AUC ranged from 1.4 to 2.1.
[L48186]
Momelotinib can undergo amide hydrolysis, N-dealkylation, nitrile hydrolysis, nitrile oxidation, and glucuronidation.
[A261546]
[A261551][L48186]
[L48186]
Proteins and enzymes this drug interacts with in the body
PMID:16239216 PMID:28111307 PMID:32750333 PMID:7615558 PMID:8232552
Kinase partner for the interleukin (IL)-2 receptor PMID:11909529 as well as interleukin (IL)-10 receptor .
PMID:12133952
Kinase partner for the type I interferon receptor IFNAR2 .
PMID:16239216 PMID:28111307 PMID:32750333 PMID:7615558 PMID:8232552
In response to interferon-binding to IFNAR1-IFNAR2 heterodimer, phosphorylates and activates its binding partner IFNAR2, creating docking sites for STAT proteins .
PMID:7759950
Directly phosphorylates STAT proteins but also activates STAT signaling through the transactivation of other JAK kinases associated with signaling receptors PMID:16239216 PMID:32750333 PMID:8232552
PMID:15690087 PMID:7615558 PMID:9657743 PMID:15899890
Following ligand-binding to cell surface receptors, phosphorylates specific tyrosine residues on the cytoplasmic tails of the receptor, creating docking sites for STATs proteins .
PMID:15690087 PMID:9618263
Subsequently, phosphorylates the STATs proteins once they are recruited to the receptor.
Phosphorylated STATs then form homodimer or heterodimers and translocate to the nucleus to activate gene transcription. For example, cell stimulation with erythropoietin (EPO) during erythropoiesis leads to JAK2 autophosphorylation, activation, and its association with erythropoietin receptor (EPOR) that becomes phosphorylated in its cytoplasmic domain .
PMID:9657743
Then, STAT5 (STAT5A or STAT5B) is recruited, phosphorylated and activated by JAK2. Once activated, dimerized STAT5 translocates into the nucleus and promotes the transcription of several essential genes involved in the modulation of erythropoiesis.
Part of a signaling cascade that is activated by increased cellular retinol and that leads to the activation of STAT5 (STAT5A or STAT5B) .
PMID:21368206
In addition, JAK2 mediates angiotensin-2-induced ARHGEF1 phosphorylation .
PMID:20098430
Plays a role in cell cycle by phosphorylating CDKN1B .
PMID:21423214
Cooperates with TEC through reciprocal phosphorylation to mediate cytokine-driven activation of FOS transcription. In the nucleus, plays a key role in chromatin by specifically mediating phosphorylation of 'Tyr-41' of histone H3 (H3Y41ph), a specific tag that promotes exclusion of CBX5 (HP1 alpha) from chromatin .
PMID:19783980
Up-regulates the potassium voltage-gated channel activity of KCNA3 PMID:25644777
Following ligand binding to cell surface receptors, phosphorylates specific tyrosine residues on the cytoplasmic tails of the receptor, creating docking sites for STATs proteins. Subsequently, phosphorylates the STATs proteins once they are recruited to the receptor. Phosphorylated STATs then form homodimer or heterodimers and translocate to the nucleus to activate gene transcription.
For example, upon IL2R activation by IL2, JAK1 and JAK3 molecules bind to IL2R beta (IL2RB) and gamma chain (IL2RG) subunits inducing the tyrosine phosphorylation of both receptor subunits on their cytoplasmic domain. Then, STAT5A and STAT5B are recruited, phosphorylated and activated by JAK1 and JAK3. Once activated, dimerized STAT5 translocates to the nucleus and promotes the transcription of specific target genes in a cytokine-specific fashion
PMID:10542297 PMID:10995743 PMID:7657660 PMID:7813427 PMID:8232552
Plays both structural and catalytic roles in numerous interleukins and interferons (IFN-alpha/beta) signaling .
PMID:10542297
Associates with heterodimeric cytokine receptor complexes and activates STAT family members including STAT1, STAT3, STAT4 or STAT6 .
PMID:10542297 PMID:7638186
The heterodimeric cytokine receptor complexes are composed of (1) a TYK2-associated receptor chain (IFNAR1, IL12RB1, IL10RB or IL13RA1), and (2) a second receptor chain associated either with JAK1 or JAK2 .
PMID:10542297 PMID:25762719 PMID:7526154 PMID:7813427
In response to cytokine-binding to receptors, phosphorylates and activates receptors (IFNAR1, IL12RB1, IL10RB or IL13RA1), creating docking sites for STAT members .
PMID:7526154 PMID:7657660
In turn, recruited STATs are phosphorylated by TYK2 (or JAK1/JAK2 on the second receptor chain), form homo- and heterodimers, translocate to the nucleus, and regulate cytokine/growth factor responsive genes .
PMID:10542297 PMID:25762719 PMID:7657660
Negatively regulates STAT3 activity by promototing phosphorylation at a specific tyrosine that differs from the site used for signaling PMID:29162862
PMID:20628059 PMID:22977237
As a type I receptor, forms heterotetrameric receptor complexes with the type II receptors AMHR2, ACVR2A or ACVR2B .
PMID:17911401
Upon binding of ligands such as BMP7 or GDF2/BMP9 to the heteromeric complexes, type II receptors transphosphorylate ACVR1 intracellular domain .
PMID:25354296
In turn, ACVR1 kinase domain is activated and subsequently phosphorylates SMAD1/5/8 proteins that transduce the signal .
PMID:9748228
In addition to its role in mediating BMP pathway-specific signaling, suppresses TGFbeta/activin pathway signaling by interfering with the binding of activin to its type II receptor .
PMID:17911401
Besides canonical SMAD signaling, can activate non-canonical pathways such as p38 mitogen-activated protein kinases/MAPKs (By similarity). May promote the expression of HAMP, potentially via its interaction with BMP6 (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
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:10358072 PMID:15159445 PMID:17412826
Shows broad substrate specificity, can transport both organic anions such as bile acid taurocholate (cholyltaurine) and conjugated steroids (dehydroepiandrosterone 3-sulfate, 17-beta-glucuronosyl estradiol, and estrone 3-sulfate), as well as eicosanoids (prostaglandin E2, thromboxane B2, leukotriene C4, and leukotriene E4), and thyroid hormones (T4/L-thyroxine, and T3/3,3',5'-triiodo-L-thyronine) .
PMID:10358072 PMID:10601278 PMID:10873595 PMID:11159893 PMID:12196548 PMID:12568656 PMID:15159445 PMID:15970799 PMID:16627748 PMID:17412826 PMID:19129463 PMID:26979622
Can take up bilirubin glucuronides from plasma into the liver, contributing to the detoxification-enhancing liver-blood shuttling loop .
PMID:22232210
Involved in the clearance of endogenous and exogenous substrates from the liver .
PMID:10358072 PMID:10601278
Transports coproporphyrin I and III, by-products of heme synthesis, and may be involved in their hepatic disposition .
PMID:26383540
May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable). Can transport HMG-CoA reductase inhibitors (also known as statins), such as pravastatin and pitavastatin, a clinically important class of hypolipidemic drugs .
PMID:10601278 PMID:15159445 PMID:15970799
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drug methotrexate .
PMID:23243220
May also transport antihypertension agents, such as the angiotensin-converting enzyme (ACE) inhibitor prodrug enalapril, and the highly selective angiotensin II AT1-receptor antagonist valsartan, in the liver .
PMID:16624871 PMID:16627748
Shows a pH-sensitive substrate specificity towards prostaglandin E2 and T4 which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions PMID:19129463
PMID:10779507 PMID:15159445 PMID:17412826
Shows broad substrate specificity, can transport both organic anions such as bile acid taurocholate (cholyltaurine) and conjugated steroids (17-beta-glucuronosyl estradiol, dehydroepiandrosterone sulfate (DHEAS), and estrone 3-sulfate), as well as eicosanoid leukotriene C4, prostaglandin E2 and L-thyroxine (T4) .
PMID:10779507 PMID:11159893 PMID:12568656 PMID:15159445 PMID:17412826 PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions .
PMID:19129463
Shows a pH-sensitive substrate specificity towards sulfated steroids, taurocholate and T4 which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Involved in the clearance of bile acids and organic anions from the liver .
PMID:22232210
Can take up bilirubin glucuronides from plasma into the liver, contributing to the detoxification-enhancing liver-blood shuttling loop .
PMID:22232210
Transports coproporphyrin I and III, by-products of heme synthesis, and may be involved in their hepatic disposition .
PMID:26383540
May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable). Can transport HMG-CoA reductase inhibitors (also known as statins) such as pitavastatin, a clinically important class of hypolipidemic drugs .
PMID:15159445
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drugs methotrexate and paclitaxel .
PMID:23243220
May also transport antihypertension agents, such as the angiotensin-converting enzyme (ACE) inhibitor prodrug enalapril, and the highly selective angiotensin II AT1-receptor antagonist valsartan, in the liver PMID:16624871 PMID:16627748
ATC L01EJ04
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)
Momelotinib
Additional database identifiers
Drugs Product Database (DPD)
24021
ChemSpider
24676202
BindingDB
50311017
PDB
C87
ZINC
ZINC000043199890
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6190
GeneCards
JAK1
Guide to Pharmacology
2047
UniProt Accession
JAK1_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:6193
GenAtlas
JAK3
GeneCards
JAK3
GenBank Gene Database
U57096
Guide to Pharmacology
2049
UniProt Accession
JAK3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12440
GeneCards
TYK2
GenBank Gene Database
X54637
GenBank Protein Database
37504
Guide to Pharmacology
2269
UniProt Accession
TYK2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:171
GenAtlas
ACVR1
GeneCards
ACVR1
GenBank Gene Database
L02911
GenBank Protein Database
338219
Guide to Pharmacology
1785
UniProt Accession
ACVR1_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: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:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_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:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_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:12530
GeneCards
UGT1A1
GenBank Gene Database
M57899
GenBank Protein Database
184473
Guide to Pharmacology
2990
UniProt Accession
UD11_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12541
GeneCards
UGT1A9
GenBank Gene Database
S55985
GenBank Protein Database
7690346
UniProt Accession
UD19_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
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10959
GenAtlas
SLCO1B1
GeneCards
SLCO1B1
GenBank Gene Database
AF060500
GenBank Protein Database
5051630
Guide to Pharmacology
1220
UniProt Accession
SO1B1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10961
GeneCards
SLCO1B3
GenBank Gene Database
AJ251506
GenBank Protein Database
9187497
Guide to Pharmacology
1221
UniProt Accession
SO1B3_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
Linked open data from Wikidata (Q252602), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.