Palifermin 6.25mg powder for solution for injection vials
Palifermin is a recombinant human keratinocyte growth factor (KGF).
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
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Suspected adverse reactions reported for Palifermin
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1 branded products available
WHO defined daily dose (DDD)
4.2 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
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Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(1)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 8 · Randomised trials: 4 · Trials: 7 · 2005–2027
Showing the 50 most relevant studies, sorted by most relevant.
Braguês R, Marvão MF, Correia P, et al.
2024
Children undergoing antineoplastic treatment often present severe side effects due to the dosage and duration of treatments, with oral mucositis emerging as one of the most prevalent and painful inflammatory conditions. There is a growing body of evidence on therapeutic interventions such as cryotherapy, low-level laser therapy, and natural compounds for this condition. The aim of this systematic review was to identify and compare therapies for the management of cancer treatment-induced oral mucositis in pediatric patients. From 2655 articles obtained in initial searches, 39 articles were considered in this systematic review, after applying inclusion/exclusion criteria. Low-level laser therapy, palifermin, honey, and zinc demonstrated reductions in oral mucositis incidence, duration, severity, and pain reported by the patient. Although there are several therapies in place for the prevention and treatment of oral mucositis in children, evidence of their efficacy is still inconclusive to establish accurate clinical protocols.
Abstract licence: CC BY
Villa JF, Strang A, Owolabi A, et al.
2025
ObjectiveOral mucositis (OM) is a debilitating complication of cancer therapies, affecting up to 85% of patients undergoing bone marrow transplantation and nearly all receiving head and neck radiotherapy. Characterized by mucosal inflammation, ulceration, and severe pain, OM significantly impairs oral intake, speech, and quality of life. These disruptions, compounded by complications such as infection, bleeding, and increased healthcare costs, often necessitate treatment delays or modifications, negatively impacting cancer prognosis. Recent insights into nociceptive and neuropathic mechanisms of OM-related pain have led to the development of innovative management strategies. Given the debilitating nature of OM in cancer patients and the critical need for effective pain control, this review aims to examine pharmacological advancements targeting the complex nature of OM-related pain, including agents such as lidocaine, doxepin, benzydamine, methylene blue, opioids, gabapentin, palifermin, caphosol, and ketamine.MethodsA literature search was conducted in the PUBMED, COCHRANE, and MEDLINE databases, covering studies from 2000 to 2024. Studies focusing on OM pathogenesis and pain management strategies were screened. Inclusion criteria encompassed randomized controlled trials, meta-analyses, and systematic reviews involving adult patients treated with lidocaine, doxepin, benzydamine, methylene blue, opioids, gabapentin, palifermin, caphosol, or ketamine for OM-associated pain.ConclusionOM pain arises from nociceptive and neuropathic pathways involving inflammatory cytokines and neuropeptides. Current interventions, including topical and systemic agents, have shown promise, yet variability in treatment protocols and limited high-quality evidence hinder standardized practices. This review highlights the clinical applicability of emerging therapies, such as avasopasem manganese, which has demonstrated efficacy in mitigating OM progression. Ongoing clinical trials targeting novel pathways that modulate mucosal inflammatory response and limit disease severity offer hope for improved pain relief. Addressing the multifaceted nature of OM-associated pain is essential for enhancing quality of life and optimizing cancer treatment outcomes. Further research is needed to establish robust, evidence-based guidelines for OM pain management.
Abstract licence: CC BY-NC
Patel P, Robinson PD, Baggott C, et al.
2021
- Practice Guidelines as Topic
- Oropharynx
- Neoplasms
PurposeTo update the 2015 clinical practice guideline for the prevention of oral mucositis in pediatric cancer or hematopoietic stem cell transplant (HSCT) patients.MethodsWe performed seven systematic reviews of mucositis prevention. Three reviews included randomized controlled trials (RCTs) conducted in pediatric and adult patients evaluating cryotherapy, keratinocyte growth factor (KGF) or photobiomodulation therapy with a focus on efficacy. Three reviews included studies of any design conducted in pediatric patients evaluating these same interventions with a focus on adverse events and feasibility. One review included all RCTs of any intervention for mucositis prevention in pediatric patients. Primary outcome was severe oral mucositis.ResultsWe included 107 unique studies of cryotherapy (22 RCTs and 4 pediatric studies); KGF (15 RCTs and 12 pediatric studies); photobiomodulation therapy (29 RCTs and 8 pediatric studies) and any intervention (31 pediatric RCTs). Effects on severe mucositis reduction from RCTs were cryotherapy risk ratio (RR) 0.49 and 95% confidence interval (CI) 0.31-0.76; palifermin RR 0.81 and 95% CI 0.69-0.95 and photobiomodulation therapy RR 0.40 and 95% CI 0.27-0.60. Cryotherapy was not feasible in young children while photobiomodulation therapy was feasible across age groups. Palifermin was associated with adverse effects.ConclusionsCryotherapy should be used for older cooperative pediatric patients who will receive short infusions of melphalan or 5-fluorouracil. Intraoral photobiomodulation therapy (620-750 nm spectrum) should be used in pediatric patients undergoing autologous or allogeneic HSCT and for pediatric head and neck carcinoma patients undergoing radiotherapy. Palifermin should not be used routinely in pediatric cancer or HSCT patients.
Abstract licence: CC BY-NC-ND
John Coutsouvelis, Carmela Corallo, Andrew Spencer, et al.
Critical Reviews in Oncology/Hematology, 2022
- Neoplasms
- Hematologic Neoplasms
- Stomatitis
Hamid Reza Mozaffari, Mehrdad Payandeh, Mazaher Ramezani, et al.
Współczesna Onkologia, 2017
M. Adil, S. Sriram, M. Azharuddin, et al.
Value in Health, 2019
Lucchese A, Matarese G, Manuelli M, et al.
2016
- Oral Ulcer
- Stomatitis
- Radiation Injuries
Gholizadeh N, Mehdipoor M, Sajadi H, et al.
2016
Alessandra Lucchese, Giovanni Matarese, Luis Huanca Ghislanzoni, et al.
Leukemia & Lymphoma, 2015
- Stomatitis
- Protective Agents
- Transplantation Conditioning
N. Blijlevens, S. Sonis
Annals of Oncology, 2007
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
4.5 hours
Mechanism
Palifermin has been shown to protect oral and intestinal epithelia from the effe…
Food interactions
None known
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Half-life
4.5 hours
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Palifermin was granted FDA approval on 15 December 2004.[L17933]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 132 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
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.
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
Plays essential roles in vascularization. Critical for normal heart development and for regulating the vascular response to injury. Also required for avascular cartilage development
ATC V03AF08
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)
Palifermin
Additional database identifiers
Drugs Product Database (DPD)
17147
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: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:5273
GenAtlas
HSPG2
GeneCards
HSPG2
GenBank Gene Database
X62515
GenBank Protein Database
29470
UniProt Accession
PGBM_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72