Amifostine 375mg powder for solution for infusion vials
A phosphorothioate proposed as a radiation-protective agent.
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Suspected adverse reactions reported for Amifostine
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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 Amifostine
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1 branded products available
WHO defined daily dose (DDD)
1.7 gram
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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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: 20 · Randomised trials: 18 · 1996–2026
Showing the 50 most relevant studies, sorted by most relevant.
D. Brizel, Todd H. Wasserman, M. Henke, et al.
Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2000
G. Kemp, P. Rose, J. Lurain, et al.
Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 1996
Dosia Antonadou, Nikos Coliarakis, Maria Synodinou, et al.
International Journal of Radiation Oncology*Biology*Physics, 2001
Mercadante V, Smith DK, Abdalla-Aslan R, et al.
2025
- Xerostomia
- Salivary Glands
- Neoplasms
PurposeThis systematic review aimed to assess the updated literature for the prevention of salivary gland hypofunction and xerostomia induced by non-surgical cancer therapies.MethodsElectronic databases of MEDLINE/PubMed, EMBASE, and Cochrane Library were searched for randomized controlled trials (RCT) that investigated interventions to prevent salivary gland hypofunction and/or xerostomia. Literature search began from the 2010 systematic review publications from the Multinational Association of Supportive Care in Cancer/International Society of Oral Oncology (MASCC/ISOO) up to February 2024. Two independent reviewers extracted information regarding study design, study population, cancer treatment modality, interventions, outcome measures, methods, results, risk of bias (RoB version 2), and conclusions for each article.ResultsA total of 51 publications addressing preventive interventions were included. Eight RCTs on tissue-sparing radiation modalities were included showing significant lower prevalence of xerostomia, with unclear effect on salivary gland hypofunction. Three RCTs on preventive acupuncture showed reduced prevalence of xerostomia but not of salivary gland hypofunction. Two RCTs on muscarinic agonist stimulation with bethanechol suggested a preventive effect on saliva flow rate and xerostomia in patients undergoing head and neck radiation or radioactive iodine therapy. Two studies on submandibular gland transfer showed higher salivary flow rates compared to pilocarpine and lower prevalence of xerostomia compared to no active intervention. There is insufficient evidence on the effectiveness of vitamin E, amifostine, photobiomodulation, and miscellaneous preventive interventions.ConclusionThis systematic review continues to support the potential of tissue-sparing tecniques and intensity-modulated radiation therapy (IMRT) to preserve salivary gland function in patients with head and neck cancer, with limited evidence on other preventive strategies, including acupuncture and bethanecol. Preventive focus should be on optimized and new approaches developed to further reduce radiation dose to the parotid, the submandibular, and minor salivary glands. As these glands are major contributors to moistening of the oral cavity, limiting the radiation dose to the salivary glands through various modalities has demonstrated reduction in prevalence and severity of salivary gland hypofunction and xerostomia. There remains no evidence on preventive approaches for checkpoint inhibitors and other biologicals due to the lack of RCTs.
Abstract licence: CC BY
Shrateh ON, Habib A, Ur Rehman Shamsi H, et al.
2026
- Head and Neck Neoplasms
- Xerostomia
- Radiation Injuries
Radiation-induced xerostomia is a frequent and debilitating complication in patients undergoing radiotherapy for head and neck cancer. This study aimed to compare the effectiveness of available treatment modalities in preventing or managing radiation-induced xerostomia and associated complications in head and neck cancer patients. A detailed search of PubMed and Google Scholar was conducted. Only randomised controlled trials (RCTs) involving radiotherapy-treated head and neck cancer patients were included. The interventions that were analysed encompassed pharmacological agents (for example, pilocarpine, and amifostine), antioxidants, herbal formulations, acupuncture, low-level laser therapy (LLLT), and regenerative approaches. Primary outcomes included severity of xerostomia, rates of salivary flow, mucositis, oral pain, dysphagia, and fatigue. Thirty-one randomised clinical trials met the inclusion criteria. Pooled analysis showed no significant reduction in severity of xerostomia at weeks 3, 4, or 6, or 6 months. Stimulated salivary flow did not significantly improve (mean difference (MD): 0.22; p = 0.15), while unstimulated salivary flow showed a significant benefit (MD: 0.13; 95% CI: 0.09 to 0.17; p < 0.00001). A significant reduction in the severity of oral pain was also noted (MD: -2.25; p < 0.0001). No significant differences were found for the incidence or duration of mucositis, dysphagia, or fatigue. Considerable heterogeneity was observed across the studies and no single intervention demonstrated consistent efficacy in managing radiation-induced xerostomia. Some therapies have shown promise in improving unstimulated salivary flow and reducing oral pain; however, the overall evidence remains inconclusive. To address this persistent clinical challenge, future trials should adopt standardised outcome measures, assess combination therapies, and investigate novel regenerative strategies.
Abstract licence: CC BY-NC-ND
Reddy PD, Rumde P, Helou V, et al.
2026
ObjectiveTo review and evaluate treatments for radiation-induced fibrosis (RIF) following head and neck cancer (HNC) therapy.Data sourcesMedline, Embase.com, Web of Science, and Cochrane Library.Review methodsA systematic review was conducted on the management of HNC RIF using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Descriptive synthesis was conducted to summarize treatment efficacy.ResultsAfter initial screening of 4078 titles and abstracts, 147 full-text articles were reviewed, with eight meeting inclusion criteria. Pharmacological interventions included pentoxifylline-tocopherol, pravastatin, amifostine, and topical superoxide dismutase (SOD). Pentoxifylline-tocopherol, pravastatin, and amifostine demonstrated variable fibrosis improvement rates across studies. In one uncontrolled trial, 83% of patients receiving pentoxifylline-tocopherol achieved ≥50% reduction in measured fibrotic surface area, and pravastatin reduced fibrosis thickness by ≥30% in 35.7% of patients. Procedural interventions included lipotransfer and microcurrent therapy, with lipotransfer associated with physical improvements in 97% of patients (n = 38) and microcurrent therapy enhancing cervical mobility in 92% of patients (n = 26).ConclusionImprovements in HNC fibrosis after current treatments ranged widely across studies; however, substantial heterogeneity in study design and outcome measurement limits definitive conclusions regarding comparative effectiveness.
Abstract licence: CC BY
Lou S, Li X, Shi L
2026
BackgroundRadiation-induced oral mucositis (RIOM) affects over 80% of head and neck tumor patients receiving radiotherapy. Although four routine drugs are used for RIOM prevention, direct comparative evidence across multiple clinical outcomes remains insufficient. This study aims to compare the effects of different pharmacological interventions on RIOM in patients with head and neck tumors via a network meta-analysis of RIOM.MethodsWe conducted systematic searches in PubMed, EMBASE, and the Cochrane Library for RCTs published up to August 31, 2025. The search only included articles in English. We selected studies that reported on the severity of RIOM, the duration of RIOM, the severity of xerostomia, and the severity of dysphagia as primary outcomes. Secondary outcomes included the use of analgesics, weight loss, the use of feeding tubes, and treatment interruptions. We used the Risk-of-Bias 2 (RoB2) tool to assess the risk of bias in the included studies and performed a network meta-analysis by using Stata 17.0 software.ResultsA total of 29 RCTs involving 2,276 patients were included. Glutamine significantly reduced the risk of RIOM compared with amifostine [odds ratio (OR) =0.13, 95% confidence interval (CI): 0.03-0.51] and cytokine (OR =0.31, 95% CI: 0.10-0.99). Compared with amifostine, cytokine (OR: 10.28, 95% CI: 1.09, 96.79), glutamine (OR: 11.09, 95% CI: 1.10, 112.24), and placebo (OR: 12.54, 95% CI: 1.41, 111.20) all significantly increased the number of cases with dysphagia. Glutamine reduced the number of patients requiring feeding tubes and the incidence of treatment interruptions. However, no significant differences were found in the duration of RIOM, the number of reported ≥ grade II xerostomia cases, the number of patients using analgesics, or weight loss.ConclusionsGlutamine is recommended as the preferred pharmacological intervention for preventing and alleviating RIOM in head and neck cancer patients, particularly in reducing the risks of severe RIOM, incidence of feeding tube, and treatment interruptions. Additionally, amifostine significantly reduced the risk of dysphagia. Based on the current evidence, glutamine appears to offer the most favorable risk-benefit profile among the evaluated interventions. Future research should adopt well-designed, unified RCTs with adequate samples to revalidate whether these measures are truly effective and safe.
Abstract licence: CC BY-NC-ND
Ndlovu B, Joorst L, Matthys C, et al.
2026
- Skin
- Plants, Medicinal
- Radiation-Protective Agents
Background and purposeTherapeutic exposure to ionizing radiation (IR) is fundamental to radiotherapy; however, radiation-induced skin toxicity remains a common and dose-limiting adverse effect. Although synthetic radioprotectors such as amifostine reduce radiation-mediated damage through free radical scavenging and DNA repair enhancement, their clinical application is constrained by significant side effects. Natural products, particularly antioxidant-rich medicinal plants, represent a promising complementary strategy for protecting skin tissue against radiation-induced oxidative and genotoxic injury. Despite this potential, plant-based radioprotective agents remain underexplored, particularly in Africa, a region with extensive traditional use of plants for skin disorders. A systematic review was performed to identify studies examining radiation-induced skin damage and the protective effects of African medicinal plants. A total of 26 studies met the inclusion criteria and were included in this review.ConclusionsThe literature demonstrates that therapeutic IR exposure induces oxidative stress, DNA damage and inflammatory responses in skin cells. This review identifies five African medicinal plants with reported radioprotective properties. However, only one species, Aloe arborescens, has been specifically evaluated for skin protection. The reported radioprotective effects were primarily attributed to antioxidant activity and modulation of cellular repair pathways. This systematic review identifies a significant research gap regarding African medicinal plants for skin radioprotection, despite their traditional use and documented biological activities. This review highlights the potential of these plants as adjunctive agents to mitigate radiation-induced skin toxicity, strengthening the rationale for further translational research in radiotherapy and photomedicine. Additionally, further research is warranted to validate these findings and to explore their potential translation into clinical applications.
Abstract licence: CC BY-NC-ND
Ezerioha CE, Uahomo PO, Chidi-Ezerioha PA, et al.
2026
BackgroundChemotherapy-induced toxicity remains a major cause of treatment discontinuation, reduced quality of life, and long-term morbidity in cancer survivors. Established chemoprotective agents (dexrazoxane, mesna, and amifostine) are limited by narrow indications (dexrazoxane: only anthracycline cardiotoxicity), significant adverse effects (amifostine: hypotension in 62%), and lack of efficacy against common toxicities such as peripheral neuropathy.ObjectiveThis focused review evaluates emerging chemoprotective strategies with preclinical or early clinical data published between 2015 and 2025, with an emphasis on agents that address unmet clinical needs.MethodsThis is a critical narrative review, not a systematic review. A literature search was conducted in PubMed, Scopus, and ClinicalTrials.gov (2015-2025) using keywords including "chemoprotection," "nanoparticle," "curcumin," "resveratrol," "dual COX-2/TNF-α inhibitor," "Nrf2 modulator," and "chemotherapy-induced peripheral neuropathy." Articles were selected based on relevance to chemoprotection, mechanistic clarity, and availability of preclinical or clinical data.ResultsThree major emerging categories were identified: (i) Nanoformulated natural products such as curcumin, resveratrol, luteolin, and naringenin encapsulated in polymeric, lipid, or cyclodextrin-based nanocarriers, demonstrate improved bioavailability and enhanced efficacy in preclinical models though chemoprotection-specific clinical data remain limited (ii) Dual COX-2/TNF-α inhibitors (e.g., NO-donating aspirin). simultaneously suppress inflammatory and oncogenic signaling (NF-κB, β-catenin, STAT3) and have shown polyp burden reduction in familial adenomatous polyposis, though cardiovascular safety concerns persist. (iii) Nrf2 pathway modulators, including sulforaphane (activator) and brusatol (inhibitor), present a paradox: activation protects normal tissues but may also shield tumors. Physical strategies (limb hypothermia) and repurposed drugs (metformin) offer additional avenues but need Phase III validation. Emerging mechanistic frontiers including ferroptosis inhibition, pyroptosis modulation, and neuroimmune targeting represent additional promising directions.ConclusionNanoformulation is the most technologically mature strategy for overcoming bioavailability barriers. Dual inhibitors offer pleiotropic benefits but require safer designs. Nrf2 modulators demand careful patient stratification. Future trials must incorporate biomarker-driven enrollment and standardized chemoprotection endpoints. Comparative analysis across categories reveals that strategies with simpler mechanisms and well-defined surrogate endpoints have advanced furthest clinically, highlighting the importance of rigorous trial design and validated biomarkers for successful translation.
Abstract licence: CC BY
J. Kouvaris, V. Kouloulias, L. Vlahos
The oncologist, 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
11 found
Half-life
8 minutes
Mechanism
The thiol metabolite is responsible for most of the cytoprotective and radioprotective properties of amifostine.
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Half-life
8 minutes
Metabolism
Elimination
10-second
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 307 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC V03AF05
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)
Amifostine
Additional database identifiers
Drugs Product Database (DPD)
57
ChemSpider
2056
ZINC
ZINC000021992285
HUGO Gene Nomenclature Committee (HGNC)
HGNC:441
GenAtlas
ALPPL2
GeneCards
ALPG
GenBank Gene Database
J03252
GenBank Protein Database
178428
UniProt Accession
PPBN_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:438
GeneCards
ALPL
GenBank Gene Database
X14174
GenBank Protein Database
28738
UniProt Accession
PPBT_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