Temoporfin 3mg/3ml solution for injection vials
Requires a prescription from a doctor or prescriber
Temoporfin is a photosensitizing agent used in the treatment of squamous cell carcinoma of the head and neck [FDA Label].
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Safety monitoring data
Yellow Card reports
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Suspected adverse reactions reported for Temoporfin
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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.
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Suspected adverse reactions reported for Temoporfin
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1 branded products available
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Foscan 3mg/3ml solution for injection vials
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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Codes for healthcare professionals and prescribing systems
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NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 4 · Randomised trials: 2 · 2000–2026
Showing the 50 most relevant studies, sorted by most relevant.
Mathias O. Senge, Johan C. Brandt
Photochemistry and Photobiology, 2011
N. Dragicevic-Curic, D. Scheglmann, V. Albrecht, et al.
Journal of controlled release : official journal of the Controlled Release Society, 2008
Truls Hauge, Truls Hauge, Petra Weber Hauge, et al.
Photodiagnosis and photodynamic therapy, 2016
Ming Chen, Xiangli Liu, A. Fahr
International journal of pharmaceutics, 2011
Kuwatani M, Sakamoto N
2023
To overcome the poor prognosis of cholangiocarcinoma (CCA), highly targeted therapies, such as antibody-drug conjugates (ADCs), photodynamic therapy (PDT) with/without systemic chemotherapy, and experimental photoimmunotherapy (PIT), have been developed. Three preclinical trials have investigated the use of ADCs targeting specific antigens, namely HER2, MUC1, and glypican-1 (GPC1), for CCA. Trastuzumab emtansine demonstrated higher antiproliferative activity in CCA cells expressing higher levels of HER2. Similarly, "staphylococcal enterotoxin A-MUC1 antibody" and "anti-GPC1 antibody-monomethyl auristatin F" conjugates showed anticancer activity. PDT is effective in areas where appropriate photosensitizers and light coexist. Its mechanism involves photosensitizer excitation and subsequent reactive oxygen species production in cancer cells upon irradiation. Hematoporphyrin derivatives, temoporfin, phthalocyanine-4, talaporfin, and chlorine e6 derivatives have mainly been used clinically and preclinically in bile duct cancer. Currently, new forms of photosensitizers with nanotechnology and novel irradiation catheters are being developed. PIT is the most novel anti-cancer therapy developed in 2011 that selectively kills targeted cancer cells using a unique photosensitizer called "IR700" conjugated with an antibody specific for cancer cells. PIT is currently in the early stages of development for identifying appropriate CCA cell targets and irradiation devices. Future human and artificial intelligence collaboration has potential for overcoming challenges related to identifying universal CCA cell targets. This could pave the way for highly targeted therapies for CCA, such as ADC, PDT, and PIT.
Abstract licence: CC BY
Basak Fındık, Ege Su Uyar, Antonio Monari, et al.
2025
N. Dragicevic-Curic, D. Scheglmann, V. Albrecht, et al.
Colloids and surfaces. B, Biointerfaces, 2009
N. Dragicevic-Curic, S. Gräfe, B. Gitter, et al.
International journal of pharmaceutics, 2010
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
65 h
Mechanism
Temoporfin is excited from ground state to the first excited singlet state by th…
Food interactions
None known
Human targets
None mapped
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
2-4 h
[L1128]…
Half-life
65 h
[L1128]…
Protein binding
85-88%
Volume of distribution
0.34-0.46 L/kg
[L1128]
Temoporfin is known to distribute into the tissues and preferentially collects in tumour tissue.…
Metabolism
Elimination
Clearance
3.9-4.1 mL
[L1128]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 42 of 42 interactions
[L1128]
Systemic toxicity presented as reduced red blood cell and platelet counts and increased white blood cell counts and liver and spleen weights. Skin inflammation, pycnotic spermatocytes and increased extramedullary haematopoiesis in spleen and the lymph nodes was also observed. Under low-light conditions mild phototoxicity was observed only at high doses.
Severe phototoxicity has been seen in rats with repeated doses of up to 1 mg/kg/day under normal lighting .
[L1128]
This effect is less severe under low-light conditions.
Two weeks of repeated doses of 0.5-0.6 mg/kg/day resulted in inflammation of the injection site and skin in rats. At 0.3 mg/kg/day under low-light in rats, the only effect seen was an increase in white blood cell counts.
In beagle dogs recieving repeated doses of up to 3mg/kg/day under low-light conditions, reddening of the skin and injection site inflammation was seen .
[L1128]
Serious injection site damage was observed.
There is evidence that photodynamic therapy with Temoporfin activates macrophages and increases phagocytosis [A31548]. These activated macrophages also produce more tumour necrosis factor-α (TNF-α) and nitric oxide (NO). It is thought that this increase in macrophage activity contributes to the efficacy of therapy through phagocytosis of cancer cells and increased cell death signalling though TNF-α. The increase in NO production likely contributes to oxidative damage through reactive nitrogen species.
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L1128]
[L1128]
[A31545]
This makes up about 70% of the bound drug immediately after administration. The remainder is bound to plasma lipoproteins with 22% bound to high density lipoprotein (HDL), 4% bound to low density lipoprotein (LDL), and 4% bound to very low density lipoprotein (VLDL).
Within 24 hours after administration, Temoporfin undergoes redistribution to lipoproteins with about 73% bound to HDL, 8% bound to LDL, and 3% bound to VLDL. Only 17% remains bound to the unknown high density protein after redistribution.
[L1128]
Temoporfin is known to distribute into the tissues and preferentially collects in tumour tissue.
[L1128]
ATC L01XD05
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)
Temoporfin
DrugBank citations
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q7698204), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.