Erdafitinib 5mg tablets
Prescription only
Requires a prescription from a doctor or prescriber
Tablet
5mg
Oral
Cytotoxic drugs
Active ingredients:
Erdafitinib
1 safety notice
Safety information for pregnancy and breastfeeding
Pregnancy
Based on the mechanism of action and findings in animal reproduction studies, erdafitinib can cause fetal harm when administered to a pregnant woman.
There are no available data on erdafitinib use in pregnant women to inform a drug-associated risk.
Oral administration of erdafitinib to pregnant rats during organogenesis caused malformations and embryo- fetal death at maternal exposures that were less than the human exposures at the maximum recommended human dose based on AUC.
Advise pregnant women and females of reproductive potential of the potential risk to the fetus.[L49731]
There are no data on the presence of erdafitinib in human milk, or the effects of erdafitinib on the breastfed child, or on milk production.
There are no data on the presence of erdafitinib in human milk, or the effects of erdafitinib on the breastfed child, or on milk production.
Because of the potential for serious adverse reactions from erdafitinib in a breastfed child, advise lactating women not to breastfeed during treatment with erdafitinib and for one month following the last dose.[L49731]
Pregnancy testing is recommended for females of reproductive potential prior to initiating treatment with erdafitinib.[L49731]
Erdafitinib can cause fetal harm when administered to a pregnant woman [FDA Label].
Pregnancy testing is recommended for females of reproductive potential prior to initiating treatment with erdafitinib.[L49731]
Erdafitinib can cause fetal harm when administered to a pregnant woman [FDA Label].
Breastfeeding
Because of the potential for serious adverse reactions from erdafitinib in a breastfed child, advise lactating women not to breastfeed during treatment with erdafitinib and for one month following the last dose.[L49731]
Pregnancy testing is recommended for females of reproductive potential prior to initiating treatment with erdafitinib.[L49731]
Erdafitinib can cause fetal harm when administered to a pregnant woman [FDA Label].
Pregnancy testing is recommended for females of reproductive potential prior to initiating treatment with erdafitinib.[L49731]
Erdafitinib can cause fetal harm when administered to a pregnant woman [FDA Label].
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
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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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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 Erdafitinib
About EudraVigilance
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.
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Clinical guidelines and formulary information
British National Formulary
Erdafitinib
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(2)
Erdafitinib for treating unresectable or metastatic urothelial cancer with FGFR3 alterations after a PD-1 or PD-L1 inhibitor (TA1062)
TA1062
Technology appraisal
Updated May 2025Bladder cancer: diagnosis and management (NG2)
NG2
NICE guideline
Updated Feb 2015Source: 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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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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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
59 hours
Mechanism
Fibroblast growth factor receptor (FGFR) is a transmembrane protein that is expr…
Food interactions
3 warnings
Human targets
10 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
8 mg
Following administration of erdafitinib 8 mg once daily, the mean (coefficient of variation [CV%]) steady-state maximum observed plasma concentration…
Half-life
59 hours
The mean effective half-life documented for erdafitinib is 59 hours, although it has also been observed between 50 to 60 hours.
[L45648][A177115]
[L45648][A177115]
Protein binding
99.8%
The protein binding recorded for erdafitinib is approximately 99.8%,…
Volume of distribution
26 to 29 L
The mean apparent volume of distribution determined for erdafitinib is about 26 to 29 L in patients.
[A177115][L45648]
[A177115][L45648]
Metabolism
39%
Erdafitinib is primarily metabolized by the cytochrome CYP2C9 and CYP3A4 isoenzymes in humans to form the O-demethylated major metabolite..
[L45648,…
[L45648,…
Elimination
69%
After administering a single oral dose of radiolabeled erdafitinib, about 69% of the dose was recovered in feces (19% as unchanged) and 19% in urine (13% as unchanged).
[L45648]…
[L45648]…
Clearance
0.362 L/h
The mean total apparent clearance (CL/F) documented for erdafitinib is about 0.362…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
In early April of 2019, the US FDA approved Janssen Pharmaceutical Companies' brand name Balversa (erdafitinib) as the first-ever fibroblast growth factor receptor (FGFR) kinase inhibitor indicated for patients with locally advanced or metastatic urothelial carcinoma, with susceptible FGFR3 or FGFR2 genetic alterations, that has progressed during or following platinum-containing chemotherapy, including within 12 months of neoadjuvant or adjuvant platinum-containing chemotherapy. [L5956][L5959] At the same time, the FDA also approved the therascreen FGFR RGQ RT-PCR Kit (Qiagen) for utilization as a companion diagnostic with erdafitinib for selecting patients for the indicated therapy [L5956][L5959].
Erdafitinib is the first personalized treatment targeting susceptible FGFR genetic alterations for patients with metastatic bladder cancer, which demonstrates the development of more personalized and precise medicines tailoring to a patient's specific genetic mutation.[L5956][L5959] Considering urothelial cancer is statistically the fourth most common kind of cancer in the world, the introduction of erdafitinib offers a much-needed new option in the ever-expanding therapeutic tool kit to treat such a prevalent medical condition.F4372
Erdafitinib is the first personalized treatment targeting susceptible FGFR genetic alterations for patients with metastatic bladder cancer, which demonstrates the development of more personalized and precise medicines tailoring to a patient's specific genetic mutation.[L5956][L5959] Considering urothelial cancer is statistically the fourth most common kind of cancer in the world, the introduction of erdafitinib offers a much-needed new option in the ever-expanding therapeutic tool kit to treat such a prevalent medical condition.F4372
Properties:
View FDA drug labelsolid
Avg. mass: 446.56 Da
DrugBank indication
Erdafitinib is a pan-fibroblast growth factor receptor (FGFR) tyrosine kinase inhibitor that is indicated for the treatment of adult patients with locally advanced or metastatic urothelial carcinoma that has susceptible FGFR3 or FGFR2 genetic alterations and has progressed during or following at least one line of prior platinum-containing chemotherapy including within 12 months of neoadjuvant or adjuvant platinum-containing chemotherapy.
[A177109][A177112][A177115][L45648]
The selection of patients for the treatment of locally advanced or metastatic urothelial carcinoma with erdafitinib should be based on the presence of susceptible FGFR genetic alterations in tumor specimens as detected by an FDA-approved companion diagnostic like the FDA-approved therascreen FGFR RGQ RT-PCR Kit as developed by QIAGEN.
[L45648]
This above indication is approved under accelerated approval by the FDA based on tumor response rate. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.
[L45648]
[A177109][A177112][A177115][L45648]
The selection of patients for the treatment of locally advanced or metastatic urothelial carcinoma with erdafitinib should be based on the presence of susceptible FGFR genetic alterations in tumor specimens as detected by an FDA-approved companion diagnostic like the FDA-approved therascreen FGFR RGQ RT-PCR Kit as developed by QIAGEN.
[L45648]
This above indication is approved under accelerated approval by the FDA based on tumor response rate. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.
[L45648]
Also known as(124)
Erdafitinib
2.7.10.1
Basic fibroblast growth factor receptor 1
bFGF-R-1
BFGFR
CEK
FGFBR
FGFR-1
Dosage forms(13)
Tablet (Oral) — 3 mg
Tablet (Oral) — 3.000 mg
Tablet (Oral) — 4 mg
Tablet (Oral) — 5 mg
Tablet, film coated (Oral) — 3 mg/1
Tablet, film coated (Oral) — 4 mg/1
Tablet, film coated (Oral) — 5 mg/1
Tablet, film coated (Oral) — 3 mg
Molecular properties(18)
Drug interactions(880)
Known interactions with other medications. Always consult a healthcare professional.
Armodafinil
Moderate
The metabolism of Erdafitinib can be increased when combined with Armodafinil.
The serum concentration of Bosutinib can be increased when it is combined with Erdafitinib.
Colchicine
Unknown severity
The serum concentration of Colchicine can be increased when it is combined with Erdafitinib.
The serum concentration of Edoxaban can be increased when it is combined with Erdafitinib.
Ledipasvir
Unknown severity
The serum concentration of Ledipasvir can be increased when it is combined with Erdafitinib.
The serum concentration of Naloxegol can be increased when it is combined with Erdafitinib.
The serum concentration of Pazopanib can be increased when it is combined with Erdafitinib.
Prucalopride
Unknown severity
The serum concentration of Prucalopride can be increased when it is combined with Erdafitinib.
Ranolazine
Unknown severity
The serum concentration of Ranolazine can be increased when it is combined with Erdafitinib.
The excretion of Silodosin can be decreased when combined with Erdafitinib.
The serum concentration of Rifaximin can be increased when it is combined with Erdafitinib.
Metreleptin
Moderate
The metabolism of Erdafitinib can be increased when combined with Metreleptin.
Crizotinib
Moderate
The metabolism of Erdafitinib can be decreased when combined with Crizotinib.
Doxorubicin
Unknown severity
The serum concentration of Doxorubicin can be increased when it is combined with Erdafitinib.
Betrixaban
Unknown severity
The serum concentration of Betrixaban can be increased when it is combined with Erdafitinib.
The excretion of Tipiracil can be decreased when combined with Erdafitinib.
Pitolisant
Unknown severity
The serum concentration of Erdafitinib can be decreased when it is combined with Pitolisant.
Varenicline
Unknown severity
The excretion of Varenicline can be decreased when combined with Erdafitinib.
Solriamfetol
Unknown severity
The serum concentration of Solriamfetol can be increased when it is combined with Erdafitinib.
The serum concentration of Prazosin can be increased when it is combined with Erdafitinib.
Ranitidine
Unknown severity
The serum concentration of Ranitidine can be increased when it is combined with Erdafitinib.
Choline salicylate
Unknown severity
The serum concentration of Choline salicylate can be increased when it is combined with Erdafitinib.
The serum concentration of Choline can be increased when it is combined with Erdafitinib.
The serum concentration of Metformin can be increased when it is combined with Erdafitinib.
Norepinephrine
Unknown severity
The serum concentration of Norepinephrine can be increased when it is combined with Erdafitinib.
The serum concentration of Reserpine can be increased when it is combined with Erdafitinib.
Pramipexole
Unknown severity
The serum concentration of Pramipexole can be increased when it is combined with Erdafitinib.
Lamivudine
Unknown severity
The serum concentration of Lamivudine can be increased when it is combined with Erdafitinib.
Amantadine
Unknown severity
The serum concentration of Amantadine can be increased when it is combined with Erdafitinib.
The serum concentration of Dopamine can be increased when it is combined with Erdafitinib.
The serum concentration of Memantine can be increased when it is combined with Erdafitinib.
The serum concentration of Histamine can be increased when it is combined with Erdafitinib.
The serum concentration of Agmatine can be increased when it is combined with Erdafitinib.
Nafamostat
Unknown severity
The serum concentration of Nafamostat can be increased when it is combined with Erdafitinib.
Dabigatran etexilate
Unknown severity
The serum concentration of Dabigatran etexilate can be increased when it is combined with Erdafitinib.
The serum concentration of Erdafitinib can be increased when it is combined with Felbamate.
The metabolism of Erdafitinib can be increased when combined with Lesinurad.
The serum concentration of Warfarin can be increased when it is combined with Erdafitinib.
Oritavancin
Moderate
The metabolism of Erdafitinib can be increased when combined with Oritavancin.
Esketamine
Moderate
The metabolism of Erdafitinib can be increased when combined with Esketamine.
The metabolism of Erdafitinib can be increased when combined with Genistein.
Asunaprevir
Moderate
The metabolism of Erdafitinib can be increased when combined with Asunaprevir.
Topiramate
Moderate
The metabolism of Erdafitinib can be increased when combined with Topiramate.
The metabolism of Erdafitinib can be increased when combined with Rifabutin.
Rufinamide
Moderate
The metabolism of Erdafitinib can be increased when combined with Rufinamide.
Glycerol phenylbutyrate
Moderate
The metabolism of Erdafitinib can be increased when combined with Glycerol phenylbutyrate.
Eslicarbazepine acetate
Moderate
The metabolism of Erdafitinib can be increased when combined with Eslicarbazepine acetate.
The metabolism of Erdafitinib can be increased when combined with Sarilumab.
Troglitazone
Unknown severity
The serum concentration of Erdafitinib can be increased when it is combined with Troglitazone.
Sulfinpyrazone
Unknown severity
The serum concentration of Erdafitinib can be increased when it is combined with Sulfinpyrazone.
Showing 50 of 880 interactions
Food & lifestyle interactions
Avoid Grapefruit
Exercise caution with grapefruit products. Grapefruit inhibits CYP3A4 metabolism, which may increase the serum concentration of erdafitinib.
Advice
Exercise caution with St. John's Wort. This herb induces the CYP3A metabolism of erdafitinib and may reduce its serum concentration.
Advice
Take with or without food. No clinically meaningful differences with erdafitinib pharmacokinetics were observed following administration of a high-fat and high-calorie meal (800 calories to 1,000 calories with approximately 50% of total caloric content of the meal from fat) in healthy subjects.
Toxicity & overdose
Based on the mechanism of action and findings in animal reproduction studies, erdafitinib can cause fetal harm when administered to a pregnant woman. There are no available data on erdafitinib use in pregnant women to inform a drug-associated risk. Oral administration of erdafitinib to pregnant rats during organogenesis caused malformations and embryo- fetal death at maternal exposures that were less than the human exposures at the maximum recommended human dose based on AUC.
Advise pregnant women and females of reproductive potential of the potential risk to the fetus.
[L49731]
There are no data on the presence of erdafitinib in human milk, or the effects of erdafitinib on the breastfed child, or on milk production. Because of the potential for serious adverse reactions from erdafitinib in a breastfed child, advise lactating women not to breastfeed during treatment with erdafitinib and for one month following the last dose.
[L49731]
Pregnancy testing is recommended for females of reproductive potential prior to initiating treatment with erdafitinib.
[L49731]
Erdafitinib can cause fetal harm when administered to a pregnant woman [FDA Label]. Advise females of reproductive potential to use effective contraception during treatment with erdafitinib and for one month after the last dose.
[L49731]
Advise male patients with female partners of reproductive potential to use effective contraception during treatment with erdafitinib and for one month after the last dose.
[L49731]
Based on findings from animal studies, erdafitinib may impair fertility in females of reproductive potential.
[L49731]
Safety and effectiveness of erdafitinib in pediatric patients have not been established.
[L49731]
No overall differences in safety or effectiveness were observed between these patients and younger patients in the use of erdafitinib.
[L49731]
Erdafitinib plasma concentrations were predicted to be higher in patients with the CYP2C9*3/*3 genotype.
Monitor for increased adverse reactions in patients who are known or suspected to have CYP2C9*3/*3 genotype.
[L49731]
Carcinogenicity studies have not been conducted with erdafitinib.
[L49731]
Erdafitinib was not mutagenic in a bacterial reverse mutation (Ames) assay and was not clastogenic in an in vitro micronucleus or an in vivo rat bone marrow micronucleus assay.
[L49731]
Fertility studies in animals have not been conducted with erdafitinib. In the 3-month repeat-dose toxicity study, erdafitinib showed effects on female reproductive organs (necrosis of the ovarian corpora lutea) in rats at an exposure less than the human exposure (AUC) at maximum recommended human dose.
[L49731]
Advise pregnant women and females of reproductive potential of the potential risk to the fetus.
[L49731]
There are no data on the presence of erdafitinib in human milk, or the effects of erdafitinib on the breastfed child, or on milk production. Because of the potential for serious adverse reactions from erdafitinib in a breastfed child, advise lactating women not to breastfeed during treatment with erdafitinib and for one month following the last dose.
[L49731]
Pregnancy testing is recommended for females of reproductive potential prior to initiating treatment with erdafitinib.
[L49731]
Erdafitinib can cause fetal harm when administered to a pregnant woman [FDA Label]. Advise females of reproductive potential to use effective contraception during treatment with erdafitinib and for one month after the last dose.
[L49731]
Advise male patients with female partners of reproductive potential to use effective contraception during treatment with erdafitinib and for one month after the last dose.
[L49731]
Based on findings from animal studies, erdafitinib may impair fertility in females of reproductive potential.
[L49731]
Safety and effectiveness of erdafitinib in pediatric patients have not been established.
[L49731]
No overall differences in safety or effectiveness were observed between these patients and younger patients in the use of erdafitinib.
[L49731]
Erdafitinib plasma concentrations were predicted to be higher in patients with the CYP2C9*3/*3 genotype.
Monitor for increased adverse reactions in patients who are known or suspected to have CYP2C9*3/*3 genotype.
[L49731]
Carcinogenicity studies have not been conducted with erdafitinib.
[L49731]
Erdafitinib was not mutagenic in a bacterial reverse mutation (Ames) assay and was not clastogenic in an in vitro micronucleus or an in vivo rat bone marrow micronucleus assay.
[L49731]
Fertility studies in animals have not been conducted with erdafitinib. In the 3-month repeat-dose toxicity study, erdafitinib showed effects on female reproductive organs (necrosis of the ovarian corpora lutea) in rats at an exposure less than the human exposure (AUC) at maximum recommended human dose.
[L49731]
How it works
Mechanism of action
Fibroblast growth factor receptor (FGFR) is a transmembrane protein that is expressed ubiquitously in normal tissues and is involved in various endogenous bio-physiological processes including the homeostasis of phosphate and vitamin D, cell proliferation, cell anti-apoptotic signaling, and cell migration in a variety of cell types.[A177109] Concurrently, genetic mutations such as gene amplification, point mutations, and chromosomal translocations of all four FGFR genes (FGFR1, FGFR2, FGFR3, and FGFR4) or deregulation of FGFR pathways have been implicated in the pathogenesis of various cancers, including urothelial cancer, as they promote cell proliferation, migration, angiogenesis, and anti-apoptosis.[A177109][L45648]
Erdafitinib is an oral selective pan-FGFR kinase inhibitor that binds to and inhibits the enzymatic activity of expressed FGFR1, FGFR2, FGFR3, and FGFR4 based on in vitro data.[L45648][A177109][A177115] In particular, erdafitinib demonstrates inhibition of FGFR phosphorylation and signaling as well as decreased cell viability in cell lines expressing FGFR genetic alterations.[A177109][A177115][L45648] Erdafitinib demonstrated antitumor activity in FGFR-expressing cell lines and xenograft models derived from tumor types, including bladder cancer.[A177109][A177115][L45648]
Erdafitinib is an oral selective pan-FGFR kinase inhibitor that binds to and inhibits the enzymatic activity of expressed FGFR1, FGFR2, FGFR3, and FGFR4 based on in vitro data.[L45648][A177109][A177115] In particular, erdafitinib demonstrates inhibition of FGFR phosphorylation and signaling as well as decreased cell viability in cell lines expressing FGFR genetic alterations.[A177109][A177115][L45648] Erdafitinib demonstrated antitumor activity in FGFR-expressing cell lines and xenograft models derived from tumor types, including bladder cancer.[A177109][A177115][L45648]
Pharmacodynamics
Upon administration, it was observed that erdafitinib increased serum phosphate levels as a consequence of FGFR inhibition. Erdafitinib should be increased to the maximum recommended dose to achieve target serum phosphate levels of 5.5– 7.0 mg/dL in early cycles with continuous daily dosing.[A177109][A177115][L45648]
Subsequently, in erdafitinib clinical trials, the use of drugs that could increase serum phosphate levels, such as potassium phosphate supplements, vitamin D supplements, antacids, phosphate-containing enemas or laxatives, and medications known to have phosphate as an excipient were prohibited unless no alternatives existed.[A177109][A177115][L45648] To manage phosphate elevation, phosphate binders were utilized. Additionally, the concomitant use of agents that can alter serum phosphate levels before the initial erdafitinib dose increase period based on serum phosphate levels was also avoided.[A177109][A177115][L45648]
Furthermore, based on the evaluation of QTc interval in an open-label, dose escalation, and dose expansion study in 187 patients with cancer, erdafitinib had no large effect (i.e., > 20 ms) on the QTc interval.[L45648]
Subsequently, in erdafitinib clinical trials, the use of drugs that could increase serum phosphate levels, such as potassium phosphate supplements, vitamin D supplements, antacids, phosphate-containing enemas or laxatives, and medications known to have phosphate as an excipient were prohibited unless no alternatives existed.[A177109][A177115][L45648] To manage phosphate elevation, phosphate binders were utilized. Additionally, the concomitant use of agents that can alter serum phosphate levels before the initial erdafitinib dose increase period based on serum phosphate levels was also avoided.[A177109][A177115][L45648]
Furthermore, based on the evaluation of QTc interval in an open-label, dose escalation, and dose expansion study in 187 patients with cancer, erdafitinib had no large effect (i.e., > 20 ms) on the QTc interval.[L45648]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Following administration of erdafitinib 8 mg once daily, the mean (coefficient of variation [CV%]) steady-state maximum observed plasma concentration (Cmax), area under the curve (AUCtau), and minimum observed plasma concentration (Cmin) were 1,399 ng/mL (51%), 29,268 ng·h/mL (60%), and 936 ng/mL (65%), respectively.
[L45648]
Following single and repeated once-daily dosing, erdafitinib exposure (maximum observed plasma concentration [Cmax] and area under the plasma concentration-time curve AUC) increased proportionally across the dose range of 0.5 to 12 mg (0.06 to 1.3 times the maximum approved recommended dose).
[L45648]
Steady-state was achieved after 2 weeks with once-daily dosing and the mean accumulation ratio was 4-fold.
[L45648]
The median time to achieve peak plasma concentration (tmax) was 2.5 hours (range: 2 to 6 hours).
[L45648]
No clinically meaningful differences with erdafitinib pharmacokinetics were observed following the administration of a high-fat and high-calorie meal (800 calories to 1,000 calories with approximately 50% of the total caloric content of the meal from fat) in healthy subjects.
[L45648]
[L45648]
Following single and repeated once-daily dosing, erdafitinib exposure (maximum observed plasma concentration [Cmax] and area under the plasma concentration-time curve AUC) increased proportionally across the dose range of 0.5 to 12 mg (0.06 to 1.3 times the maximum approved recommended dose).
[L45648]
Steady-state was achieved after 2 weeks with once-daily dosing and the mean accumulation ratio was 4-fold.
[L45648]
The median time to achieve peak plasma concentration (tmax) was 2.5 hours (range: 2 to 6 hours).
[L45648]
No clinically meaningful differences with erdafitinib pharmacokinetics were observed following the administration of a high-fat and high-calorie meal (800 calories to 1,000 calories with approximately 50% of the total caloric content of the meal from fat) in healthy subjects.
[L45648]
Half-life
The mean effective half-life documented for erdafitinib is 59 hours, although it has also been observed between 50 to 60 hours.
[L45648][A177115]
[L45648][A177115]
Protein binding
The protein binding recorded for erdafitinib is approximately 99.8%, and it was determined to be primarily bound to alpha-1-acid glycoprotein.
[L45648]
[L45648]
Volume of distribution
The mean apparent volume of distribution determined for erdafitinib is about 26 to 29 L in patients.
[A177115][L45648]
[A177115][L45648]
Metabolism
Erdafitinib is primarily metabolized by the cytochrome CYP2C9 and CYP3A4 isoenzymes in humans to form the O-demethylated major metabolite..
[L45648][L45653]
The contribution of CYP2C9 and CYP3A4 in the total clearance of erdafitinib is estimated to be 39% and 20% respectively.
[L45648]
Unchanged erdafitinib was ultimately the predominant drug-related moiety found in the plasma - no circulating metabolites were observed.
[L45648]
[L45648][L45653]
The contribution of CYP2C9 and CYP3A4 in the total clearance of erdafitinib is estimated to be 39% and 20% respectively.
[L45648]
Unchanged erdafitinib was ultimately the predominant drug-related moiety found in the plasma - no circulating metabolites were observed.
[L45648]
Route of elimination
After administering a single oral dose of radiolabeled erdafitinib, about 69% of the dose was recovered in feces (19% as unchanged) and 19% in urine (13% as unchanged).
[L45648]
[L45648]
Clearance
The mean total apparent clearance (CL/F) documented for erdafitinib is about 0.362 L/h, while the oral clearance has been observed to be approximately 0.26 L/h .
[L45648][A177115]
[L45648][A177115]
Drug targets(10)
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
Proto-oncogene tyrosine-protein kinase receptor Ret
RET
substrate
Specific functionATP binding
Cellular location
Cell membrane
General function & pharmacology
Receptor tyrosine-protein kinase involved in numerous cellular mechanisms including cell proliferation, neuronal navigation, cell migration, and cell differentiation in response to glia cell line-derived growth family factors (GDNF, NRTN, ARTN, PSPN and GDF15) .
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
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
Metabolizing enzymes(2)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
CYP2C9Cytochrome P450 2C9
substrate
CYP3A4Cytochrome P450 3A4
substrate
inhibitor
inducer
Transporters(2)
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
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)
Carriers(1)
Proteins that carry this drug through the body
Alpha-1-acid glycoprotein 2
ORM2
binder
Cellular location
Secreted
General function & pharmacology
Functions as a transport protein in the blood stream. Binds various hydrophobic ligands in the interior of its beta-barrel domain. Also binds synthetic drugs and influences their distribution and availability.
Appears to function in modulating the activity of the immune system during the acute-phase reaction
Appears to function in modulating the activity of the immune system during the acute-phase reaction
Scientific references(3)
Nishina T., Takahashi S., Iwasawa R., Noguchi H., Aoki M., Doi T.
Safety, pharmacokinetic, and pharmacodynamics of erdafitinib, a pan-fibroblast growth factor receptor (FGFR) tyrosine kinase inhibitor, in patients with advanced or refractory solid tumors.
Invest New Drugs
2018 Jun36(3):424-434. doi: 10.1007/s10637-017-0514-4. Epub 2017 Sep 30
Perera T.P.S., Jovcheva E., Mevellec L., Vialard J., De Lange D., Verhulst T., Paulussen C., Van De Ven K., King P., Freyne E., Rees D.C., Squires M., Saxty G., Page M., Murray C.W., Gilissen R., Ward G., Thompson N.T., Newell D.R., Cheng N., Xie L., Yang J., Platero S.J., Karkera J.D., Moy C., Angibaud P., Laquerre S., Lorenzi M.V.
Discovery and Pharmacological Characterization of JNJ-42756493 (Erdafitinib), a Functionally Selective Small-Molecule FGFR Family Inhibitor.
Molecular Cancer Therapeutics
2017 Jun16(6):1010-1020. doi: 10.1158/1535-7163.MCT-16-0589. Epub 2017 Mar 24
Tabernero J., Bahleda R., Dienstmann R., Infante J.R., Mita A., Italiano A., Calvo E., Moreno V., Adamo B., Gazzah A., Zhong B., Platero S.J., Smit J.W., Stuyckens K., Chatterjee-Kishore M., Rodon J., Peddareddigari V., Luo F.R., Soria J.C.
Phase I Dose-Escalation Study of JNJ-42756493, an Oral Pan-Fibroblast Growth Factor Receptor Inhibitor, in Patients With Advanced Solid Tumors.
Journal of Clinical Oncology
2015 Oct 2033(30):3401-8. doi: 10.1200/JCO.2014.60.7341. Epub 2015 Aug 31
ATC classification(1 code)
ATC L01EN01
Affected organisms(1)
Humans and other mammals
Experimental properties(1)
Protein Data Bank entries(1)
Commercial products(18)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Erdafitinib
Additional database identifiers
Drugs Product Database (DPD)
23382
ChemSpider
35308353
BindingDB
50525939
PDB
5SF
ZINC
ZINC000168520308
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:9967
GenAtlas
RET
GeneCards
RET
GenBank Gene Database
X12949
Guide to Pharmacology
2185
UniProt Accession
RET_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2433
GenAtlas
CSF1R
GeneCards
CSF1R
GenBank Gene Database
M25786
GenBank Protein Database
553224
Guide to Pharmacology
1806
UniProt Accession
CSF1R_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:8804
GenAtlas
PDGFRB
GeneCards
PDGFRB
GenBank Gene Database
J03278
GenBank Protein Database
189732
Guide to Pharmacology
1804
UniProt Accession
PGFRB_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: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:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_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:8498
GenAtlas
ORM1
GeneCards
ORM1
GenBank Gene Database
X02544
GenBank Protein Database
757907
UniProt Accession
A1AG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8499
GeneCards
ORM2
GenBank Gene Database
BC015964
GenBank Protein Database
16359000
UniProt Accession
A1AG2_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:10966
GeneCards
SLC22A2
GenBank Gene Database
X98333
GenBank Protein Database
2281942
Guide to Pharmacology
1020
UniProt Accession
S22A2_HUMAN
Patent information
8 active patents
11077106
United States
Approved 3 Aug 2021 · Expires 2 Feb 2038
11y 10m
10478494
United States
Approved 19 Nov 2019 · Expires 13 Aug 2036
10y 4m
10898482
United States
Approved 26 Jan 2021 · Expires 9 Feb 2036
9y 10m
11684620
United States
Approved 27 Jun 2023 · Expires 9 Feb 2036
9y 10m
12037644
United States
Approved 16 Jul 2024 · Expires 18 Oct 2035
9y 6m
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)