Pemigatinib 4.5mg tablets
Prescription only
Requires a prescription from a doctor or prescriber
Tablet
4.5mg
Oral
Pemigatinib is a small molecule kinase inhibitor with antitumour activity.
Active ingredients:
Pemigatinib
1 safety notice
Safety information for pregnancy and breastfeeding
Pregnancy
In animal studies, pemigatinib caused fetal harm and embryo-fetal death in pregnant rats.
Breastfeeding
FDA advises nursing women to avoid breastfeeding when receiving pemigatinib.
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
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Source: MHRA Products DatabaseOGL 3.0
Updated 3 months ago(16 Jan 2026)Safety monitoring data
Yellow Card reports
MHRA
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 Pemigatinib
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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
EMA
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 Pemigatinib
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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
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1 products
MHRA licensed products
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Pemazyre 4.5mg tablets
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Erdafitinib 5mg tablets
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Pemigatinib 9mg tablets
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Same therapeutic group
Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
Clinical guidelines and formulary information
British National Formulary
Pemigatinib
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(4)
Pemigatinib for treating relapsed or refractory advanced cholangiocarcinoma with FGFR2 fusion or rearrangement (TA722)
TA722
Technology appraisal
Updated Aug 2021Futibatinib for previously treated advanced cholangiocarcinoma with FGFR2 fusion or rearrangement (TA1005)
TA1005
Technology appraisal
Updated Sept 2024Ivosidenib for treating advanced cholangiocarcinoma with an IDH1 R132 mutation after 1 or more systemic treatments (TA948)
TA948
Technology appraisal
Updated Jan 2024Erdafitinib for treating unresectable or metastatic urothelial cancer with FGFR3 alterations after a PD-1 or PD-L1 inhibitor (TA1062)
TA1062
Technology appraisal
Updated May 2025Source: 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 & product information
Official product databases and supply status monitoring
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. emc (electronic medicines compendium) is operated by Datapharm Ltd. Shortage information sourced from NHS Specialist Pharmacy Service (SPS), sps.nhs.uk.
Codes for healthcare professionals and prescribing systems
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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 codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
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Searching UK clinical trials...
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.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
Not available
Mechanism
Fibroblast growth factor receptor (FGFR) is a receptor tyrosine kinase involved…
Food interactions
3 warnings
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
13.5 mg
Following administration of a single oral dose of 13.5 mg pemigatinib, the median Tmax was 1.13…
Half-life
13.5 mg
Following administration of a single oral dose of 13.5 mg pemigatinib, the geometric mean elimination half-life (t½) of pemigatinib was 15.4…
Protein binding
90.6%
The in vitro serum protein binding of pemigatinib was 90.6% at drug concentrations ranging from 1 to 10 µM.
[L13050]
[L13050]
Volume of distribution
235 L
The apparent volume of distribution was 235 L (60.8% CV) following a single oral dose of 13.5 mg pemigatinib.
[L13050]
[L13050]
Metabolism
Pemigatinib is predominantly metabolized by the CYP3A4 enzyme in vitro.
[L13050]…
[L13050]…
Elimination
11 mg
Following oral administration of a single radiolabeled dose of 11 mg pemigatinib, about 82.4%…
Clearance
13.5 mg
Following administration of a single oral dose of 13.5 mg pemigatinib, the geometric mean apparent clearance (CL/F) was 10.6 L/h (54% CV).
[L13050]
[L13050]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Pemigatinib is a small molecule kinase inhibitor with antitumour activity. It works by inhibiting fibroblast growth factor receptors (FGFRs), which are receptor tyrosine kinases that activate signalling pathways in tumour cells.[A193719] FGFRs gained attention as potential therapeutic targets in selected cancers, as FGFR gene alterations were observed in a wide variety of cancers including those of the urinary bladder, breast, ovary, prostate, endometrium, lung, and stomach.[A198984] Deregulated FGFR signalling pathway can lead the development of oncogenes and tumour-promoting physiological processes, such as cancer cell proliferation, enhanced angiogenesis, and evasion of cell death.[A193716]
In April 2020, pemigatinib was approved by the FDA for the treatment of unresectable locally advanced or metastatic cholangiocarcinoma in previously treated adult patients with a fibroblast growth factor receptor 2 (FGFR2) gene fusion or other rearrangements as detected by an FDA-approved test.[L13068] Cholangiocarcinoma is the most common primary malignancy affecting the biliary tract and the second most common primary hepatic malignancy. This malignancy accounts for 15% to 20% of primary hepatobiliary malignancies, which account for 13% of overall cancer-related global mortality. With increasing research on the pathogenesis of cholangiocarcinoma and potential therapeutic targets for anticancer drug treatment, recent studies show that up to 45% of patients with intrahepatic cholangiocarcinoma exhibited gene rearrangements resulting in oncogenic fibroblast growth factor 2 (FGFR2) fusion proteins.[A198963] The FDA-approved indication for pemigatinib was granted under accelerated approval based on the overall response rate and duration of response in pre-marketing clinical trials. Pemigatinib is marketed under the brand name Pemazyre, and it is available as oral tablets.[L13050]
In April 2020, pemigatinib was approved by the FDA for the treatment of unresectable locally advanced or metastatic cholangiocarcinoma in previously treated adult patients with a fibroblast growth factor receptor 2 (FGFR2) gene fusion or other rearrangements as detected by an FDA-approved test.[L13068] Cholangiocarcinoma is the most common primary malignancy affecting the biliary tract and the second most common primary hepatic malignancy. This malignancy accounts for 15% to 20% of primary hepatobiliary malignancies, which account for 13% of overall cancer-related global mortality. With increasing research on the pathogenesis of cholangiocarcinoma and potential therapeutic targets for anticancer drug treatment, recent studies show that up to 45% of patients with intrahepatic cholangiocarcinoma exhibited gene rearrangements resulting in oncogenic fibroblast growth factor 2 (FGFR2) fusion proteins.[A198963] The FDA-approved indication for pemigatinib was granted under accelerated approval based on the overall response rate and duration of response in pre-marketing clinical trials. Pemigatinib is marketed under the brand name Pemazyre, and it is available as oral tablets.[L13050]
Properties:
solid
Avg. mass: 487.51 Da
DrugBank indication
Pemigatinib is indicated for the treatment of unresectable locally advanced or metastatic cholangiocarcinoma in previously-treated adult patients with a fibroblast growth factor receptor 2 (FGFR2) fusion or other rearrangement as detected by an FDA-approved test.
[L13050]
It is also indicated for the treatment of adults with relapsed or refractory myeloid/lymphoid neoplasms (MLNs) with FGFR1 rearrangement.
[L43005]
[L13050]
It is also indicated for the treatment of adults with relapsed or refractory myeloid/lymphoid neoplasms (MLNs) with FGFR1 rearrangement.
[L43005]
Also known as(69)
INCB054828
Pemigatinib
2.7.10.1
Basic fibroblast growth factor receptor 1
bFGF-R-1
BFGFR
CEK
FGFBR
Dosage forms(6)
Tablet (Oral) — 13.5 mg
Tablet (Oral) — 13.5 mg/1
Tablet (Oral) — 4.5 mg/1
Tablet (Oral) — 4.5 mg
Tablet (Oral) — 9 mg/1
Tablet (Oral) — 9 mg
Molecular properties(19)
Drug interactions(157)
Known interactions with other medications. Always consult a healthcare professional.
Pitolisant
Unknown severity
The serum concentration of Pemigatinib can be decreased when it is combined with Pitolisant.
Metreleptin
Moderate
The metabolism of Pemigatinib can be increased when combined with Metreleptin.
Cenobamate
Unknown severity
The serum concentration of Pemigatinib can be decreased when it is combined with Cenobamate.
The metabolism of Tucatinib can be decreased when combined with Pemigatinib.
Bexarotene
Moderate
The metabolism of Pemigatinib can be increased when combined with Bexarotene.
The metabolism of Pemigatinib can be increased when combined with Bosentan.
The metabolism of Pemigatinib can be increased when combined with Nafcillin.
The metabolism of Pemigatinib can be increased when combined with Efavirenz.
The metabolism of Pemigatinib can be increased when combined with Modafinil.
Etravirine
Moderate
The metabolism of Pemigatinib can be increased when combined with Etravirine.
The metabolism of Pemigatinib can be increased when combined with Avasimibe.
The metabolism of Pemigatinib can be increased when combined with Echinacea.
Dexamethasone acetate
Moderate
The metabolism of Pemigatinib can be increased when combined with Dexamethasone acetate.
Cyclosporine
Moderate
The metabolism of Pemigatinib can be decreased when combined with Cyclosporine.
Fluvoxamine
Moderate
The metabolism of Pemigatinib can be decreased when combined with Fluvoxamine.
Fluconazole
Moderate
The metabolism of Pemigatinib can be decreased when combined with Fluconazole.
Erythromycin
Moderate
The metabolism of Pemigatinib can be decreased when combined with Erythromycin.
Ziprasidone
Moderate
The metabolism of Pemigatinib can be decreased when combined with Ziprasidone.
Isradipine
Moderate
The metabolism of Pemigatinib can be decreased when combined with Isradipine.
The metabolism of Pemigatinib can be decreased when combined with Diltiazem.
The metabolism of Pemigatinib can be decreased when combined with Clozapine.
Haloperidol
Unknown severity
The serum concentration of Haloperidol can be increased when it is combined with Pemigatinib.
Ciprofloxacin
Moderate
The metabolism of Pemigatinib can be decreased when combined with Ciprofloxacin.
Nicardipine
Moderate
The metabolism of Pemigatinib can be decreased when combined with Nicardipine.
The metabolism of Pemigatinib can be decreased when combined with Verapamil.
Aprepitant
Moderate
The metabolism of Pemigatinib can be decreased when combined with Aprepitant.
The metabolism of Pemigatinib can be decreased when combined with Isoniazid.
Tioconazole
Moderate
The metabolism of Pemigatinib can be decreased when combined with Tioconazole.
Primaquine
Moderate
The metabolism of Pemigatinib can be decreased when combined with Primaquine.
Miconazole
Moderate
The metabolism of Pemigatinib can be decreased when combined with Miconazole.
The metabolism of Pemigatinib can be decreased when combined with Danazol.
Fusidic acid
Moderate
The metabolism of Pemigatinib can be decreased when combined with Fusidic acid.
Zimelidine
Moderate
The metabolism of Pemigatinib can be decreased when combined with Zimelidine.
Dronedarone
Moderate
The metabolism of Pemigatinib can be decreased when combined with Dronedarone.
Milnacipran
Moderate
The metabolism of Pemigatinib can be decreased when combined with Milnacipran.
Simeprevir
Moderate
The metabolism of Pemigatinib can be decreased when combined with Simeprevir.
Isavuconazonium
Moderate
The metabolism of Pemigatinib can be decreased when combined with Isavuconazonium.
Desvenlafaxine
Moderate
The metabolism of Pemigatinib can be decreased when combined with Desvenlafaxine.
Nilvadipine
Moderate
The metabolism of Pemigatinib can be decreased when combined with Nilvadipine.
Seproxetine
Moderate
The metabolism of Pemigatinib can be decreased when combined with Seproxetine.
Linagliptin
Moderate
The metabolism of Pemigatinib can be decreased when combined with Linagliptin.
Luliconazole
Moderate
The metabolism of Pemigatinib can be decreased when combined with Luliconazole.
The metabolism of Pemigatinib can be decreased when combined with Indalpine.
Netupitant
Moderate
The metabolism of Pemigatinib can be decreased when combined with Netupitant.
Barnidipine
Moderate
The metabolism of Pemigatinib can be decreased when combined with Barnidipine.
Benidipine
Moderate
The metabolism of Pemigatinib can be decreased when combined with Benidipine.
Venetoclax
Moderate
The metabolism of Pemigatinib can be decreased when combined with Venetoclax.
Isavuconazole
Moderate
The metabolism of Pemigatinib can be decreased when combined with Isavuconazole.
Fosnetupitant
Moderate
The metabolism of Pemigatinib can be decreased when combined with Fosnetupitant.
Berotralstat
Moderate
The metabolism of Pemigatinib can be decreased when combined with Berotralstat.
Showing 50 of 157 interactions
Food & lifestyle interactions
Avoid Grapefruit
Avoid grapefruit products. Grapefruit may increase drug levels and adverse effects.
Advice
Take at the same time every day.
Advice
Take with or without food. A high-fat or high-calorie meal does not have clinically significant effects on drug concentrations.
Toxicity & overdose
There is limited information on the LD50 value and overdose profile of pemigatinib.
In animal studies, pemigatinib caused fetal harm and embryo-fetal death in pregnant rats. FDA advises nursing women to avoid breastfeeding when receiving pemigatinib. Physeal and cartilage dysplasia were present in multiple bones of rats and non-human primates with pemigatinib exposures lower than the human exposure at the clinical dose of 13.5 mg.
[L13050]
In animal studies, pemigatinib caused fetal harm and embryo-fetal death in pregnant rats. FDA advises nursing women to avoid breastfeeding when receiving pemigatinib. Physeal and cartilage dysplasia were present in multiple bones of rats and non-human primates with pemigatinib exposures lower than the human exposure at the clinical dose of 13.5 mg.
[L13050]
How it works
Mechanism of action
Fibroblast growth factor receptor (FGFR) is a receptor tyrosine kinase involved in activating signalling pathways that promote cell proliferation, survival, and migration, as well as growth arrest and cellular differentiation.[A193716] The initiation of the FGFR signalling pathway requires the binding of its natural ligand, fibroblast growth factor (FGF). Once FGF binds to the extracellular ligand-binding domain of the receptor, FGFRs dimerize and autophosphorylate the tyrosine residue in the intracellular tyrosine-kinase domain, leading to the activation of the tyrosine kinase.[A193719] Downstream cascades involve phosphorylation of multiple intracellular signalling proteins, such as phosphatidylinositol 3 kinase (PI3K)-AKT and RAS/mitogen-activated protein kinase (MAPK), and phospholipase Cγ, which activates the protein kinase C pathway.[A193716][A193719] FGFR-mediated pathway ultimately promotes cell growth, differentiation, survival, angiogenesis, and organogenesis, depending on cell type. Expressed in different isoforms in various tissues and cell lines, FGFRs are not constitutively active in normal cells.[A193719] However, FGFR1, FGFR2, or FGFR3 alterations in certain tumours can lead to constitutive FGFR activation and aberrant FGFR signalling, supporting the proliferation and survival of malignant cells.[L13050]
Pemigatinib inhibits FGFR1, FGFR2, and FGFR3, blocking their signalling pathways and decreasing cell viability in cancer cell lines with activating FGFR amplification and fusions that resulted in constitutive activation of FGFR signalling.[L13050] Genetic alterations in FGFR1, FGFR2, and FGFR3 (such as amplification, missense, or fusion mutations in the coding region) leading to constitutive activation of FGFR signalling pathways are observed in various tumours.[A193719][A198984] However, alterations in FGFR genes are demonstrated in selected patients and do not always imply oncogene development. Therefore, it is imperative that fusion or rearrangement of FGFRs are demonstrated through tests prior to initiation of drug therapy.[A193716]
Pemigatinib inhibits FGFR1, FGFR2, and FGFR3, blocking their signalling pathways and decreasing cell viability in cancer cell lines with activating FGFR amplification and fusions that resulted in constitutive activation of FGFR signalling.[L13050] Genetic alterations in FGFR1, FGFR2, and FGFR3 (such as amplification, missense, or fusion mutations in the coding region) leading to constitutive activation of FGFR signalling pathways are observed in various tumours.[A193719][A198984] However, alterations in FGFR genes are demonstrated in selected patients and do not always imply oncogene development. Therefore, it is imperative that fusion or rearrangement of FGFRs are demonstrated through tests prior to initiation of drug therapy.[A193716]
Pharmacodynamics
Pemigatinib is a small molecule kinase inhibitor that exerts anti-tumour activity through inhibition of fibroblast growth factor receptors (FGFRs). [A193716] With an IC50 of less than 2 nM, pemigatinib displays potent inhibition of FGFR1, FGFR2, and FGFR3. In mouse xenograft models of human tumours with FGFR1, FGFR2, or FGFR3 alterations, pemigatinib exhibited potent anti-tumour activity by suppressing the growth of xenografted tumour models. It also showed efficacy against a patient-derived xenograft model of cholangiocarcinoma that expressed an oncogenic FGFR2 Transformer-2 beta homolog (TRA2b) fusion protein.[A193716][L13050] Pemigatinib also inhibited FGFR4 in vitro, however at a concentration approximately 100 times higher than those that inhibit FGFR1, 2, and 3.[L13050]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Following administration of a single oral dose of 13.5 mg pemigatinib, the median Tmax was 1.13 (0.50-6.00) hours. The steady state was reached within 4 days following repeated once daily dosing, with the median drug accumulation ratio of 1.63 (range 0.63 to 3.28). Steady-state concentration of pemigatinib increased in a dose-proportional manner over the dose range of 1 to 20 mg, which is about 0.07 to 1.5 times the recommended dose.
The mean steady-state AUC and Cmax were 2620 nM x h (54% CV) and 236 nM, respectively.
[L13050]
The mean steady-state AUC and Cmax were 2620 nM x h (54% CV) and 236 nM, respectively.
[L13050]
Half-life
Following administration of a single oral dose of 13.5 mg pemigatinib, the geometric mean elimination half-life (t½) of pemigatinib was 15.4 (51.6% CV) hours.
[L13050]
[L13050]
Protein binding
The in vitro serum protein binding of pemigatinib was 90.6% at drug concentrations ranging from 1 to 10 µM.
[L13050]
[L13050]
Volume of distribution
The apparent volume of distribution was 235 L (60.8% CV) following a single oral dose of 13.5 mg pemigatinib.
[L13050]
[L13050]
Metabolism
Pemigatinib is predominantly metabolized by the CYP3A4 enzyme in vitro.
[L13050]
Its specific metabolic pathway and resulting metabolites have not yet been characterized.
[L13050]
Its specific metabolic pathway and resulting metabolites have not yet been characterized.
Route of elimination
Following oral administration of a single radiolabeled dose of 11 mg pemigatinib, about 82.4% of the dose was recovered in feces. Of this recovered drug, about 1.4% of the dose was unchanged parent compound. About 12.6% of the dose was recovered in urine, where 1% of the dose was unchanged.
[L13050]
[L13050]
Clearance
Following administration of a single oral dose of 13.5 mg pemigatinib, the geometric mean apparent clearance (CL/F) was 10.6 L/h (54% CV).
[L13050]
[L13050]
Drug targets(4)
Proteins and enzymes this drug interacts with in the body
Fibroblast growth factor receptor 1
FGFR1
inhibitor
Specific functionATP binding
Cellular location
Cell membrane
General function & pharmacology
Tyrosine-protein kinase that acts as a cell-surface receptor for fibroblast growth factors and plays an essential role in the regulation of embryonic development, cell proliferation, differentiation and migration. Required for normal mesoderm patterning and correct axial organization during embryonic development, normal skeletogenesis and normal development of the gonadotropin-releasing hormone (GnRH) neuronal system. Phosphorylates PLCG1, FRS2, GAB1 and SHB.
Ligand binding leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate. Phosphorylation of FRS2 triggers recruitment of GRB2, GAB1, PIK3R1 and SOS1, and mediates activation of RAS, MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway.
Promotes phosphorylation of SHC1, STAT1 and PTPN11/SHP2. In the nucleus, enhances RPS6KA1 and CREB1 activity and contributes to the regulation of transcription. FGFR1 signaling is down-regulated by IL17RD/SEF, and by FGFR1 ubiquitination, internalization and degradation
Ligand binding leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate. Phosphorylation of FRS2 triggers recruitment of GRB2, GAB1, PIK3R1 and SOS1, and mediates activation of RAS, MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway.
Promotes phosphorylation of SHC1, STAT1 and PTPN11/SHP2. In the nucleus, enhances RPS6KA1 and CREB1 activity and contributes to the regulation of transcription. FGFR1 signaling is down-regulated by IL17RD/SEF, and by FGFR1 ubiquitination, internalization and degradation
Fibroblast growth factor receptor 2
FGFR2
inhibitor
Specific functionATP binding
Cellular location
Cell membrane
General function & pharmacology
Tyrosine-protein kinase that acts as a cell-surface receptor for fibroblast growth factors and plays an essential role in the regulation of cell proliferation, differentiation, migration and apoptosis, and in the regulation of embryonic development. Required for normal embryonic patterning, trophoblast function, limb bud development, lung morphogenesis, osteogenesis and skin development. Plays an essential role in the regulation of osteoblast differentiation, proliferation and apoptosis, and is required for normal skeleton development.
Promotes cell proliferation in keratinocytes and immature osteoblasts, but promotes apoptosis in differentiated osteoblasts. Phosphorylates PLCG1, FRS2 and PAK4. Ligand binding leads to the activation of several signaling cascades.
Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate. Phosphorylation of FRS2 triggers recruitment of GRB2, GAB1, PIK3R1 and SOS1, and mediates activation of RAS, MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway. FGFR2 signaling is down-regulated by ubiquitination, internalization and degradation.
Mutations that lead to constitutive kinase activation or impair normal FGFR2 maturation, internalization and degradation lead to aberrant signaling. Over-expressed FGFR2 promotes activation of STAT1.
Promotes cell proliferation in keratinocytes and immature osteoblasts, but promotes apoptosis in differentiated osteoblasts. Phosphorylates PLCG1, FRS2 and PAK4. Ligand binding leads to the activation of several signaling cascades.
Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate. Phosphorylation of FRS2 triggers recruitment of GRB2, GAB1, PIK3R1 and SOS1, and mediates activation of RAS, MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway. FGFR2 signaling is down-regulated by ubiquitination, internalization and degradation.
Mutations that lead to constitutive kinase activation or impair normal FGFR2 maturation, internalization and degradation lead to aberrant signaling. Over-expressed FGFR2 promotes activation of STAT1.
Fibroblast growth factor receptor 3
FGFR3
inhibitor
Specific functionATP binding
Cellular location
Cell membrane
General function & pharmacology
Tyrosine-protein kinase that acts as a cell-surface receptor for fibroblast growth factors and plays an essential role in the regulation of cell proliferation, differentiation and apoptosis. Plays an essential role in the regulation of chondrocyte differentiation, proliferation and apoptosis, and is required for normal skeleton development. Regulates both osteogenesis and postnatal bone mineralization by osteoblasts.
Promotes apoptosis in chondrocytes, but can also promote cancer cell proliferation. Required for normal development of the inner ear. Phosphorylates PLCG1, CBL and FRS2.
Ligand binding leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate. Phosphorylation of FRS2 triggers recruitment of GRB2, GAB1, PIK3R1 and SOS1, and mediates activation of RAS, MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway.
Plays a role in the regulation of vitamin D metabolism. Mutations that lead to constitutive kinase activation or impair normal FGFR3 maturation, internalization and degradation lead to aberrant signaling. Over-expressed or constitutively activated FGFR3 promotes activation of PTPN11/SHP2, STAT1, STAT5A and STAT5B.
Secreted isoform 3 retains its capacity to bind FGF1 and FGF2 and hence may interfere with FGF signaling
Promotes apoptosis in chondrocytes, but can also promote cancer cell proliferation. Required for normal development of the inner ear. Phosphorylates PLCG1, CBL and FRS2.
Ligand binding leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate. Phosphorylation of FRS2 triggers recruitment of GRB2, GAB1, PIK3R1 and SOS1, and mediates activation of RAS, MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway.
Plays a role in the regulation of vitamin D metabolism. Mutations that lead to constitutive kinase activation or impair normal FGFR3 maturation, internalization and degradation lead to aberrant signaling. Over-expressed or constitutively activated FGFR3 promotes activation of PTPN11/SHP2, STAT1, STAT5A and STAT5B.
Secreted isoform 3 retains its capacity to bind FGF1 and FGF2 and hence may interfere with FGF signaling
Fibroblast growth factor receptor 4
FGFR4
inhibitor
Specific functionATP binding
Cellular location
Cell membrane
General function & pharmacology
Tyrosine-protein kinase that acts as a cell-surface receptor for fibroblast growth factors and plays a role in the regulation of cell proliferation, differentiation and migration, and in regulation of lipid metabolism, bile acid biosynthesis, glucose uptake, vitamin D metabolism and phosphate homeostasis. Required for normal down-regulation of the expression of CYP7A1, the rate-limiting enzyme in bile acid synthesis, in response to FGF19. Phosphorylates PLCG1 and FRS2.
Ligand binding leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate. Phosphorylation of FRS2 triggers recruitment of GRB2, GAB1, PIK3R1 and SOS1, and mediates activation of RAS, MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway.
Promotes SRC-dependent phosphorylation of the matrix protease MMP14 and its lysosomal degradation. FGFR4 signaling is down-regulated by receptor internalization and degradation; MMP14 promotes internalization and degradation of FGFR4. Mutations that lead to constitutive kinase activation or impair normal FGFR4 inactivation lead to aberrant signaling
Ligand binding leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate. Phosphorylation of FRS2 triggers recruitment of GRB2, GAB1, PIK3R1 and SOS1, and mediates activation of RAS, MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway.
Promotes SRC-dependent phosphorylation of the matrix protease MMP14 and its lysosomal degradation. FGFR4 signaling is down-regulated by receptor internalization and degradation; MMP14 promotes internalization and degradation of FGFR4. Mutations that lead to constitutive kinase activation or impair normal FGFR4 inactivation lead to aberrant signaling
Metabolizing enzymes(1)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
CYP3A4Cytochrome P450 3A4
substrate
Transporters(4)
Proteins that transport this drug across cell membranes
ATP-dependent translocase ABCB1
ABCB1
substrate
inhibitor
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Translocates drugs and phospholipids across the membrane .
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: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
Broad substrate specificity ATP-binding cassette transporter ABCG2
ABCG2
substrate
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Broad substrate specificity ATP-dependent transporter of the ATP-binding cassette (ABC) family that actively extrudes a wide variety of physiological compounds, dietary toxins and xenobiotics from cells .
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: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
Solute carrier family 22 member 2
SLC22A2
inhibitor
Specific functionacetylcholine transmembrane transporter activity
Cellular location
Basolateral cell membrane
General function & pharmacology
Electrogenic voltage-dependent transporter that mediates the transport of a variety of organic cations such as endogenous bioactive amines, cationic drugs and xenobiotics .
PMID:9260930 PMID:9687576
Functions as a Na(+)-independent, bidirectional uniporter .
PMID:21128598 PMID:9687576
Cation cellular uptake or release is driven by the electrochemical potential, i.e. membrane potential and concentration gradient .
PMID:15212162 PMID:9260930 PMID:9687576
However, may also engage electroneutral cation exchange when saturating concentrations of cation substrates are reached (By similarity). Predominantly expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow .
PMID:15783073
Implicated in monoamine neurotransmitters uptake such as histamine, dopamine, adrenaline/epinephrine, noradrenaline/norepinephrine, serotonin and tyramine, thereby supporting a physiological role in the central nervous system by regulating interstitial concentrations of neurotransmitters .
PMID:16581093 PMID:17460754 PMID:9687576
Also capable of transporting dopaminergic neuromodulators cyclo(his-pro), salsolinol and N-methyl-salsolinol, thereby involved in the maintenance of dopaminergic cell integrity in the central nervous system .
PMID:17460754
Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium .
PMID:15817714
Also transports guanidine and endogenous monoamines such as vitamin B1/thiamine, creatinine and N-1-methylnicotinamide (NMN) .
PMID:12089365 PMID:15212162 PMID:17072098 PMID:24961373 PMID:9260930
Mediates the uptake and efflux of quaternary ammonium compound choline .
PMID:9260930
Mediates the bidirectional transport of polyamine agmatine and the uptake of polyamines putrescine and spermidine .
PMID:12538837 PMID:21128598
Able to transport non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) .
PMID:11907186
Also involved in the uptake of xenobiotic 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) .
PMID:12395288 PMID:16394027
May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable)
PMID:9260930 PMID:9687576
Functions as a Na(+)-independent, bidirectional uniporter .
PMID:21128598 PMID:9687576
Cation cellular uptake or release is driven by the electrochemical potential, i.e. membrane potential and concentration gradient .
PMID:15212162 PMID:9260930 PMID:9687576
However, may also engage electroneutral cation exchange when saturating concentrations of cation substrates are reached (By similarity). Predominantly expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow .
PMID:15783073
Implicated in monoamine neurotransmitters uptake such as histamine, dopamine, adrenaline/epinephrine, noradrenaline/norepinephrine, serotonin and tyramine, thereby supporting a physiological role in the central nervous system by regulating interstitial concentrations of neurotransmitters .
PMID:16581093 PMID:17460754 PMID:9687576
Also capable of transporting dopaminergic neuromodulators cyclo(his-pro), salsolinol and N-methyl-salsolinol, thereby involved in the maintenance of dopaminergic cell integrity in the central nervous system .
PMID:17460754
Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium .
PMID:15817714
Also transports guanidine and endogenous monoamines such as vitamin B1/thiamine, creatinine and N-1-methylnicotinamide (NMN) .
PMID:12089365 PMID:15212162 PMID:17072098 PMID:24961373 PMID:9260930
Mediates the uptake and efflux of quaternary ammonium compound choline .
PMID:9260930
Mediates the bidirectional transport of polyamine agmatine and the uptake of polyamines putrescine and spermidine .
PMID:12538837 PMID:21128598
Able to transport non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) .
PMID:11907186
Also involved in the uptake of xenobiotic 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) .
PMID:12395288 PMID:16394027
May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable)
Multidrug and toxin extrusion protein 1
SLC47A1
inhibitor
Specific functionantiporter activity
Cellular location
Cell membrane
General function & pharmacology
Multidrug efflux pump that functions as a H(+)/organic cation antiporter .
PMID:16330770 PMID:17509534
Plays a physiological role in the excretion of cationic compounds including endogenous metabolites, drugs, toxins through the kidney and liver, into urine and bile respectively .
PMID:16330770 PMID:17495125 PMID:17509534 PMID:17582384 PMID:18305230 PMID:19158817 PMID:21128598 PMID:24961373
Mediates the efflux of endogenous compounds such as creatinine, vitamin B1/thiamine, agmatine and estrone-3-sulfate .
PMID:16330770 PMID:17495125 PMID:17509534 PMID:17582384 PMID:18305230 PMID:19158817 PMID:21128598 PMID:24961373
May also contribute to regulate the transport of cationic compounds in testis across the blood-testis-barrier (Probable)
PMID:16330770 PMID:17509534
Plays a physiological role in the excretion of cationic compounds including endogenous metabolites, drugs, toxins through the kidney and liver, into urine and bile respectively .
PMID:16330770 PMID:17495125 PMID:17509534 PMID:17582384 PMID:18305230 PMID:19158817 PMID:21128598 PMID:24961373
Mediates the efflux of endogenous compounds such as creatinine, vitamin B1/thiamine, agmatine and estrone-3-sulfate .
PMID:16330770 PMID:17495125 PMID:17509534 PMID:17582384 PMID:18305230 PMID:19158817 PMID:21128598 PMID:24961373
May also contribute to regulate the transport of cationic compounds in testis across the blood-testis-barrier (Probable)
Scientific references(4)
Casadei C., Dizman N., Schepisi G., Cursano M.C., Basso U., Santini D., Pal S.K., De Giorgi U.
Targeted therapies for advanced bladder cancer: new strategies with FGFR inhibitors.
Therapeutics Advanced Medicine Oncology
2019 Nov 2511:1758835919890285. doi: 10.1177/1758835919890285. eCollection 2019
Liu P.C.C., Koblish H., Wu L., Bowman K., Diamond S., DiMatteo D., Zhang Y., Hansbury M., Rupar M., Wen X., Collier P., Feldman P., Klabe R., Burke K.A., Soloviev M., Gardiner C., He X., Volgina A., Covington M., Ruggeri B., Wynn R., Burn T.C., Scherle P., Yeleswaram S., Yao W., Huber R., Hollis G.
INCB054828 (pemigatinib), a potent and selective inhibitor of fibroblast growth factor receptors 1, 2, and 3, displays activity against genetically defined tumor models.
PLoS One
2020 Apr 2115(4):e0231877. doi: 10.1371/journal.pone.0231877. eCollection 2020
Blechacz B.
Cholangiocarcinoma: Current Knowledge and New Developments.
Gut Liver
2017 Jan 1511(1):13-26. doi: 10.5009/gnl15568
Roskoski R Jr
The role of fibroblast growth factor receptor (FGFR) protein-tyrosine kinase inhibitors in the treatment of cancers including those of the urinary bladder.
Pharmacology Research
2020 Jan151:104567. doi: 10.1016/j.phrs.2019.104567. Epub 2019 Nov 23
ATC classification(1 code)
ATC L01EN02
Affected organisms(1)
Humans and other mammals
Protein Data Bank entries(1)
Commercial products(12)
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)
Pemigatinib
Additional database identifiers
Drugs Product Database (DPD)
23643
ChemSpider
68007304
BindingDB
301310
PDB
8ZF
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:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_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:10966
GeneCards
SLC22A2
GenBank Gene Database
X98333
GenBank Protein Database
2281942
Guide to Pharmacology
1020
UniProt Accession
S22A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:25588
GeneCards
SLC47A1
GenBank Gene Database
AK001709
GenBank Protein Database
7023138
Guide to Pharmacology
1216
UniProt Accession
S47A1_HUMAN
Patent information
4 active patents
11628162
United States
Approved 18 Apr 2023 · Expires 30 Aug 2040
14y 5m
11466004
United States
Approved 11 Oct 2022 · Expires 3 May 2039
13y 1m
9611267
United States
Approved 4 Apr 2017 · Expires 30 Jan 2035
8y 10m
10131667
United States
Approved 20 Nov 2018 · Expires 12 Jun 2033
7y 2m
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated about 1 month ago(4 Mar 2026)