Temsirolimus 30mg/1.2ml solution for infusion vials and diluent
Requires a prescription from a doctor or prescriber
Temsirolimus is a derivative of sirolimus used in the treatment of renal cell carcinoma (RCC).
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Suspected adverse reactions reported for Temsirolimus
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Torisel 30mg/1.2ml concentrate for solution for infusion vials and diluent
WHO defined daily dose (DDD)
3.57 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 BNF/ATC 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.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(6)
Bevacizumab (first-line), sorafenib (first- and second-line), sunitinib (second-line) and temsirolimus (first-line) for the treatment of advanced and/or metastatic renal cell carcinoma (TA178)
Temsirolimus for the treatment of relapsed or refractory mantle cell lymphoma (terminated appraisal) (TA207)
Ibrutinib for treating relapsed or refractory mantle cell lymphoma (TA502)
Tivozanib for treating advanced renal cell carcinoma (TA512)
Sorafenib for treating advanced hepatocellular carcinoma (TA474)
Kidney cancer: diagnosis and management (NG256)
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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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
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 all 27 studies.
Reviews & meta-analyses: 5 · Randomised trials: 3 · 2007–2026
Showing all 27 studies, sorted by most relevant.
R. Mody, A. Naranjo, Collin Van Ryn, et al.
The Lancet. Oncology, 2017
- N-Myc Proto-Oncogene Protein
- Irinotecan
- Temozolomide
Zahra Goudarzi, Mehrdad Mostafavi, M. Salesi, et al.
Cost Effectiveness and Resource Allocation : C/E, 2023
OBJECTIVE: Renal cell carcinoma (RCC) is the most common type of kidney cancer. VEGF inhibitors and mTORs are the most common therapeutic options among the different classes of available treatments. In this study, the effectiveness of Everolimus was compared to Temsirolimus, and Everolimus plusLenvatinib in renal cell carcinoma patients by review of the international clinical evidence. MATERIALS AND METHODS: A systematic review was conducted and all relevant published clinical studies on the efficacy and cost-effectiveness of Everolimus, Temsirolimus, and Lenvatinib plus Everolimus were searched comprehensively in electronic databases including Pubmed, Scopus, Medline, Cochrane Library, and ISI web of science. The Q score and I2 test checked the Heterogeneity and publication bias test, respectively. Egger's test and Begg's test were used to checking publication bias. The hazard ratio (HR) of included studies and subclass analysis were estimated by fixed and random effect models. RESULTS: Out of 1816 found studies, ultimately, were included considering inclusion and exclusion criteria. None of these studies evaluated all three treatment strategies together and each study was about one strategy. Only one study was found for Everolimus plus Lenvatinib, so it was excluded from meta-analysis. Overall, data from 526 patients on Temsirolimus and 648 patients on Everolimus were included in Meta-Analysis. Accordingly, the efficacy of Everolimus and Temsirolimus was not statistically significant in assessed outcomes (PFS, TTSF, and death). However, Everlimus is superior to Temsirolimus in OS (Q = 3.61, p-value: 0.462, I2 = 0%). No heterogeneity or bias was detected. CONCLUSION: According to the results of this study, Everolimus could be related to an increase of OS versus Temsirolimus as a second line treatment of ORCC patients.
Abstract licence: CC BY
L. Mascarenhas, Yueh-Yun Chi, P. Hingorani, et al.
Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2019
- Neoplasm Recurrence, Local
- Bevacizumab
- Vinorelbine
Abha A. Gupta, Wei Xue, D. J. Harrison, et al.
The Lancet. Oncology, 2024
- Forkhead Box Protein O1
- Irinotecan
- Progression-Free Survival
M. Dreyling, W. Jurczak, M. Jerkeman, et al.
Lancet, 2016
- Adenine
- Antineoplastic Agents
- Neoplasm Staging
G. Hudes, M. Carducci, P. Tomczak, et al.
The New England journal of medicine, 2007
- Antineoplastic Agents
- Antineoplastic Combined Chemotherapy Protocols
- Carcinoma, Renal Cell
C. Aghajanian, V. Filiaci, D. Dizon, et al.
Gynecologic oncology, 2018
- Bevacizumab
- Antineoplastic Combined Chemotherapy Protocols
- Neoplasm Recurrence, Local
Y. Oh, Joo Hee Park, T. A. Djunadi, et al.
Frontiers in Endocrinology, 2024
- Adenocarcinoma
- Thiocarbamates
- Thyroid Neoplasms
Treating advanced thyroid cancer presents challenges due to its resistance to various treatment modalities, thereby limiting therapeutic options. To our knowledge, this study is the first to report the efficacy of temsirolimus in conjunction with dual immunotherapy of nivolumab/ipilimumab to treat heavily treated advanced PDTC. A 50-year-old female initially presented with a rapidly enlarging mass on her right neck. Subsequent diagnosis revealed poorly differentiated thyroid carcinoma, leading to a total thyroidectomy followed by post-operative radioablation therapy. After four years, an examination for persistent cough revealed a recurrence of the disease within multiple mediastinal nodes. Genetic analysis of blood samples uncovered somatic mutations in the tumor, specifically involving PTEN and TP53 . The disease progressed despite palliative radiation, lenvatinib, and nivolumab/ipilimumab therapy. Consequently, temsirolimus, functioning as an mTOR inhibitor, was introduced as an adjunct to the nivolumab/ipilimumab regimen. This combination approach yielded remarkable clinical improvement and disease control for a duration of approximately six months. Temsirolimus likely suppressed the aberrantly activated PI3K/AKT/mTOR signaling pathway, facilitated by the PTEN genetic alteration, thus engendering an effective treatment response. This synergy between targeted agents and immunotherapy presents a promising therapeutic strategy for advanced PDTC patients with limited treatment alternatives. In previous clinical trials, mTOR inhibitors have demonstrated the ability to maintain stable disease (SD) in 65% to 74% for advanced thyroid cancer patients, including those with PDTC. When combined with other targeted therapies, the observed SD or partial response rates range from 80% to 97%. Many of these trials primarily involved differentiated thyroid carcinoma, with diverse genetic mutations. Thyroid cancer patients with alterations in the PI3K/mTOR/Akt appeared to benefit most from mTOR inhibitors. However, no clear association between the efficacy of mTOR inhibitors and specific histologies or genetic mutations has been established. Future studies are warranted to elucidate these associations.
Abstract licence: CC BY
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
17.3 hr
Mechanism
Temsirolimus is an inhibitor of mTOR (mammalian target of rapamycin).
Food interactions
2 warnings
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
30 - 60 minutes
Half-life
17.3 hr
Protein binding
87%
Volume of distribution
172 L
Metabolism
Elimination
76%
Clearance
16.2 L/h
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1420 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:12087098 PMID:12150925 PMID:12150926 PMID:12231510 PMID:12718876 PMID:14651849 PMID:15268862 PMID:15467718 PMID:15545625 PMID:15718470 PMID:18497260 PMID:18762023 PMID:18925875 PMID:20516213 PMID:20537536 PMID:21659604 PMID:23429703 PMID:23429704 PMID:25799227 PMID:26018084 PMID:29150432 PMID:29236692 PMID:31112131 PMID:31601708 PMID:32561715 PMID:34519269 PMID:37751742
MTOR directly or indirectly regulates the phosphorylation of at least 800 proteins .
PMID:15268862 PMID:15467718 PMID:17517883 PMID:18372248 PMID:18497260 PMID:18925875 PMID:20516213 PMID:21576368 PMID:21659604 PMID:23429704 PMID:30171069 PMID:29236692 PMID:37751742
Functions as part of 2 structurally and functionally distinct signaling complexes mTORC1 and mTORC2 (mTOR complex 1 and 2) .
PMID:15268862 PMID:15467718 PMID:18497260 PMID:18925875 PMID:20516213 PMID:21576368 PMID:21659604 PMID:23429704 PMID:29424687 PMID:29567957 PMID:35926713
In response to nutrients, growth factors or amino acids, mTORC1 is recruited to the lysosome membrane and promotes protein, lipid and nucleotide synthesis by phosphorylating key regulators of mRNA translation and ribosome synthesis .
PMID:12087098 PMID:12150925 PMID:12150926 PMID:12231510 PMID:12718876 PMID:14651849 PMID:15268862 PMID:15467718 PMID:15545625 PMID:15718470 PMID:18497260 PMID:18762023 PMID:18925875 PMID:20516213 PMID:20537536 PMID:21659604 PMID:23429703 PMID:23429704 PMID:25799227 PMID:26018084 PMID:29150432 PMID:29236692 PMID:31112131 PMID:34519269
This includes phosphorylation of EIF4EBP1 and release of its inhibition toward the elongation initiation factor 4E (eiF4E) .
PMID:24403073 PMID:29236692
Moreover, phosphorylates and activates RPS6KB1 and RPS6KB2 that promote protein synthesis by modulating the activity of their downstream targets including ribosomal protein S6, eukaryotic translation initiation factor EIF4B, and the inhibitor of translation initiation PDCD4 .
PMID:12087098 PMID:12150925 PMID:18925875 PMID:29150432 PMID:29236692
Stimulates the pyrimidine biosynthesis pathway, both by acute regulation through RPS6KB1-mediated phosphorylation of the biosynthetic enzyme CAD, and delayed regulation, through transcriptional enhancement of the pentose phosphate pathway which produces 5-phosphoribosyl-1-pyrophosphate (PRPP), an allosteric activator of CAD at a later step in synthesis, this function is dependent on the mTORC1 complex .
PMID:23429703 PMID:23429704
Regulates ribosome synthesis by activating RNA polymerase III-dependent transcription through phosphorylation and inhibition of MAF1 an RNA polymerase III-repressor .
PMID:20516213
Activates dormant ribosomes by mediating phosphorylation of SERBP1, leading to SERBP1 inactivation and reactivation of translation .
PMID:36691768
In parallel to protein synthesis, also regulates lipid synthesis through SREBF1/SREBP1 and LPIN1 .
PMID:23426360
To maintain energy homeostasis mTORC1 may also regulate mitochondrial biogenesis through regulation of PPARGC1A (By similarity). In the same time, mTORC1 inhibits catabolic pathways: negatively regulates autophagy through phosphorylation of ULK1 .
PMID:32561715
Under nutrient sufficiency, phosphorylates ULK1 at 'Ser-758', disrupting the interaction with AMPK and preventing activation of ULK1 .
PMID:32561715
Also prevents autophagy through phosphorylation of the autophagy inhibitor DAP .
PMID:20537536
Also prevents autophagy by phosphorylating RUBCNL/Pacer under nutrient-rich conditions .
PMID:30704899
Prevents autophagy by mediating phosphorylation of AMBRA1, thereby inhibiting AMBRA1 ability to mediate ubiquitination of ULK1 and interaction between AMBRA1 and PPP2CA .
PMID:23524951 PMID:25438055
mTORC1 exerts a feedback control on upstream growth factor signaling that includes phosphorylation and activation of GRB10 a INSR-dependent signaling suppressor .
PMID:21659604
Among other potential targets mTORC1 may phosphorylate CLIP1 and regulate microtubules .
PMID:12231510
The mTORC1 complex is inhibited in response to starvation and amino acid depletion .
PMID:12150925 PMID:12150926 PMID:24403073 PMID:31695197
The non-canonical mTORC1 complex, which acts independently of RHEB, specifically mediates phosphorylation of MiT/TFE factors MITF, TFEB and TFE3 in the presence of nutrients, promoting their cytosolic retention and inactivation .
PMID:22343943 PMID:22576015 PMID:22692423 PMID:24448649 PMID:32612235 PMID:36608670 PMID:36697823
Upon starvation or lysosomal stress, inhibition of mTORC1 induces dephosphorylation and nuclear translocation of TFEB and TFE3, promoting their transcription factor activity .
PMID:22343943 PMID:22576015 PMID:22692423 PMID:24448649 PMID:32612235 PMID:36608670
The mTORC1 complex regulates pyroptosis in macrophages by promoting GSDMD oligomerization .
PMID:34289345
MTOR phosphorylates RPTOR which in turn inhibits mTORC1 (By similarity). As part of the mTORC2 complex, MTOR transduces signals from growth factors to pathways involved in proliferation, cytoskeletal organization, lipogenesis and anabolic output .
PMID:15268862 PMID:15467718 PMID:24670654 PMID:29424687 PMID:29567957 PMID:35926713
In response to growth factors, mTORC2 phosphorylates and activates AGC protein kinase family members, including AKT (AKT1, AKT2 and AKT3), PKC (PRKCA, PRKCB and PRKCE) and SGK1 .
PMID:15268862 PMID:15467718 PMID:21376236 PMID:24670654 PMID:29424687 PMID:29567957 PMID:35926713
In contrast to mTORC1, mTORC2 is nutrient-insensitive .
PMID:15467718
mTORC2 plays a critical role in AKT1 activation by mediating phosphorylation of different sites depending on the context, such as 'Thr-450', 'Ser-473', 'Ser-477' or 'Thr-479', facilitating the phosphorylation of the activation loop of AKT1 on 'Thr-308' by PDPK1/PDK1 which is a prerequisite for full activation .
PMID:15718470 PMID:21376236 PMID:24670654 PMID:29424687 PMID:29567957
mTORC2 also regulates the phosphorylation of SGK1 at 'Ser-422' .
PMID:18925875
mTORC2 may regulate the actin cytoskeleton, through phosphorylation of PRKCA, PXN and activation of the Rho-type guanine nucleotide exchange factors RHOA and RAC1A or RAC1B .
PMID:15268862
The mTORC2 complex also phosphorylates various proteins involved in insulin signaling, such as FBXW8 and IGF2BP1 (By similarity).
May also regulate insulin signaling by acting as a tyrosine protein kinase that catalyzes phosphorylation of IGF1R and INSR; additional evidence are however required to confirm this result in vivo .
PMID:26584640
Regulates osteoclastogenesis by adjusting the expression of CEBPB isoforms (By similarity). Plays an important regulatory role in the circadian clock function; regulates period length and rhythm amplitude of the suprachiasmatic nucleus (SCN) and liver clocks (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
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
ATC L01EG01
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)
Temsirolimus
Additional database identifiers
Drugs Product Database (DPD)
20180
ChemSpider
21468899
BindingDB
50343413
PDB
A4I
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3942
GenAtlas
FRAP1
GeneCards
MTOR
GenBank Gene Database
L34075
Guide to Pharmacology
2109
UniProt Accession
MTOR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_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:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2640
GeneCards
CYP3A7
GenBank Gene Database
D00408
GenBank Protein Database
220149
UniProt Accession
CP3A7_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
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q7699074), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.