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- tenoposide
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- Teniposide
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- Teniposide
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- the 22nd letter of the Roman alphabet (同)v
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- vanadium の化学記号
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2014/05/06 19:48:04」(JST)
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Teniposide
|
Systematic (IUPAC) name |
(5R,5aR,8aR,9S)-5,8,8a,9-Tetrahydro-5-(4-hydroxy-3,5-dimethoxyphenyl)-9-({4,6-O-[(R)-2-thienylmethylene]-β-D-glucopyranosyl}oxy)furo[3',4':6,7]naphtho[2,3-d]-1,3-dioxol-6(5aH)-one |
Clinical data |
AHFS/Drugs.com |
monograph |
MedlinePlus |
a692045 |
Pregnancy cat. |
D (AU) D (US) |
Legal status |
℞-only (US) |
Routes |
Intravenous |
Pharmacokinetic data |
Bioavailability |
n/a |
Protein binding |
>99% |
Metabolism |
Hepatic (CYP2C19-mediated) |
Half-life |
5 hours |
Excretion |
Renal and fecal |
Identifiers |
CAS number |
29767-20-2 Y |
ATC code |
L01CB02 |
PubChem |
CID 34698 |
DrugBank |
DB00444 |
ChemSpider |
31930 N |
UNII |
957E6438QA N |
KEGG |
D02698 Y |
ChEBI |
CHEBI:75988 N |
ChEMBL |
CHEMBL1200536 N |
Chemical data |
Formula |
C32H32O13S |
Mol. mass |
656.655 g/mol |
N (what is this?) (verify) |
Teniposide (Vumon, VM-26) is a chemotherapeutic medication[1] mainly used in the treatment of childhood acute lymphocytic leukemia (ALL). It is in a class of drugs known as podophyllotoxin derivatives and slows the growth of cancer cells in the body.
Contents
- 1 Mechanism of action
- 2 Administration
- 3 Side-effects
- 4 References
Mechanism of action
Teniposide causes dose-dependent single- and double-stranded breaks in DNA and DNA-protein cross-links. The mechanism of action appears to be related to the inhibition of type II topoisomerase activity since teniposide does not intercalate into DNA or bind strongly to DNA. The cytotoxic effects of teniposide are related to the relative number of double-stranded DNA breaks produced in cells, which are a reflection of the stabilization of a topoisomerase II-DNA intermediate.
Administration
The medication is injected though a vein and burns if it leaks under the skin. It is sometimes used in combination with other anticancer drugs.
Side-effects
Teniposide, when used with other chemotherapeutic agents for the treatment of ALL, results in severe myelosuppression. Other common side effects include gastrointestinal toxicity, hypersensitivity reactions, and alopecia.
References
- ^ Cragg, Gordon M.; Newman, David J. (2005). "Plants as a source of anti-cancer agents". Journal of Ethnopharmacology 100 (1–2): 72–9. doi:10.1016/j.jep.2005.05.011. PMID 16009521.
UpToDate Contents
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English Journal
- Can in-vitro chemoresponse assays help find new treatment regimens for malignant gliomas?
- Linz U, Ulus B, Neuloh G, Clusmann H, Oertel M, Nolte K, Weis J, Heussen N, Gilsbach JM.Author information aResearch Center Jülich (FZJ), Institute of Complex Systems, Jülich bDepartment of Neurosurgery cDepartment of Neuropathology dDepartment of Medical Statistics, RWTH Aachen University, Aachen, Germany.AbstractVarious in-vitro chemosensitivity and resistance assays (CSRAs) have been demonstrated to be helpful decision aids for non-neurological tumors. Here, we evaluated the performance characteristics of two CSRAs for glioblastoma (GB) cells. The chemoresponse of fresh GB cells from 30 patients was studied in vitro using the ATP tumor chemoresponse assay and the chemotherapy resistance assay (CTR-Test). Both assay platforms provided comparable results. Of seven different chemotherapeutic drugs and drug combinations tested in vitro, treosulfan plus cytarabine (TARA) was the most effective, followed by nimustine (ACNU) plus teniposide (VM26) and temozolomide (TMZ). Whereas ACNU/VM26 and TMZ have proven their clinical value for malignant gliomas in large randomized studies, TARA has not been successful in newly diagnosed gliomas. This seeming discrepancy between in vitro and clinical result might be explained by the pharmacological behavior of treosulfan. Our results show reasonable agreement between two cell-based CSRAs. They appear to confirm the clinical effectiveness of drugs used in GB treatment as long as pharmacological preconditions such as overcoming the blood-brain barrier are properly considered.
- Anti-cancer drugs.Anticancer Drugs.2014 Jan 13. [Epub ahead of print]
- Various in-vitro chemosensitivity and resistance assays (CSRAs) have been demonstrated to be helpful decision aids for non-neurological tumors. Here, we evaluated the performance characteristics of two CSRAs for glioblastoma (GB) cells. The chemoresponse of fresh GB cells from 30 patients was studie
- PMID 24423983
- Neurologic complications of chemotherapy and other newer and experimental approaches.
- Soffietti R1, Trevisan E2, Rudà R2.Author information 1Division of Neuro-Oncology, Department of Neuroscience, University and San Giovanni Battista Hospital, Turin, Italy. Electronic address: riccardo.soffietti@unito.it.2Division of Neuro-Oncology, Department of Neuroscience, University and San Giovanni Battista Hospital, Turin, Italy.AbstractNeurologic complications of conventional cytototxic agents as well as those from monoclonal antibodies and targeted therapies are increasingly observed in patients with cancer. The major categories are represented by alkylating agents (platinum compounds, ifosfamide, procarbazine, thiotepa), mitotic spindle inhibitors (vinca alkaloids, taxanes, etoposide, teniposide), proteasome inhibitors (bortezomib), antibiotics, antimetabolites, thalidomide, lenalidomide, topoisomerase inhibitors, interferon-α, hormones, bevacizumab, trastuzumab, and small tyrosine kinase inhibitors. Peripheral neuropathy is a common adverse effect of a number of chemotherapeutic drugs and often represents a critical factor limiting an adequate dose-intensity of chemotherapy. Regarding the central nervous system (CNS), it is vulnerable to many forms of toxicity from chemotherapeutic agents, including encephalopathy syndromes and confusional states, seizures, headache, cerebrovascular complications, visual loss, cerebellar syndromes, and myelopathy. For a given drug, the occurrence of CNS toxicity depends on several factors, including the total dose, route of administration, presence of structural brain lesions, exposure to prior or concurrent irradiation, and interactions with other drugs. However, many of the neurotoxic reactions are rare and idiosyncratic, and remain unpredictable. Several forms of neuroprotection and rehabilitation are being investigated. Last, the so-called "chemobrain" is an emerging issue, as it is a model of a subtle of and long-lasting damage to neuronal structures from some antineoplastic agents.
- Handbook of clinical neurology.Handb Clin Neurol.2014;121:1199-218. doi: 10.1016/B978-0-7020-4088-7.00080-8.
- Neurologic complications of conventional cytototxic agents as well as those from monoclonal antibodies and targeted therapies are increasingly observed in patients with cancer. The major categories are represented by alkylating agents (platinum compounds, ifosfamide, procarbazine, thiotepa), mitotic
- PMID 24365412
- Comparison of the clinical efficacy of temozolomide (TMZ) versus nimustine (ACNU)-based chemotherapy in newly diagnosed glioblastoma.
- Wang Y, Chen X, Zhang Z, Li S, Chen B, Wu C, Wang L, Zhang X, Wang J, Chen L, Jiang T.Author information Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, No.6 Tiantan Xili, Dongcheng District, Beijing, 100050, China.AbstractAlthough temozolomide (TMZ) replaced nitrosoureas as the standard initial chemotherapy for glioblastoma (GBM), no studies have compared TMZ with nimustine (ACNU), a nitrosourea agent widely used in central Europe and most Asian regions. One hundred thirty-five patients with GBM who underwent extensive tumor resection in our institution received both radiation and chemotherapy as initial treatment, 34 received TMZ and 101 ACNU-based (ACNU plus teniposide or cisplatin) chemotherapy. Efficacy analysis included overall survival (OS) and progression-free survival (PFS). The following prognostic factors were taken into account: age, performance status, extent of resection, and O(6)-methylguanine-DNA-methyltransferase (MGMT) gene status. The median OS was superior in the TMZ versus the ACNU group (p = 0.011), although MGMT gene silencing, which is associated with a striking survival benefit from alkylating agents, was more frequent in the ACNU group. In multivariate Cox analysis adjusting for the common prognostic factors, TMZ chemotherapy independently predicted a favorable outcome (p = 0.002 for OS, hazard ratio [HR], 0.45; p = 0.011 for PFS, HR, 0.56). Given that >40 % of patients in ACNU group did not receive the intensive chemotherapy cycles because of severe hematological and nonhematological toxicity, we performed a further subanalysis for patients who received at least 4 cycles of chemotherapy. Although a modest improvement in survival occurred in this ACNU subgroup, the efficacy was still inferior to that in the TMZ cohort. Our data suggest that the survival benefit of TMZ therapy is superior to that of an ACNU-based regimen in patients with extensive tumor resection, also shows greater tolerability.
- Neurosurgical review.Neurosurg Rev.2014 Jan;37(1):73-8. doi: 10.1007/s10143-013-0490-x. Epub 2013 Aug 3.
- Although temozolomide (TMZ) replaced nitrosoureas as the standard initial chemotherapy for glioblastoma (GBM), no studies have compared TMZ with nimustine (ACNU), a nitrosourea agent widely used in central Europe and most Asian regions. One hundred thirty-five patients with GBM who underwent extensi
- PMID 23912878
Japanese Journal
- オリイメック株式会社 フォーミングマシン「VM-26」の開発
- Jun and JNK kinase are activated in thymocytes in response to VM26 and radiation but not glucocorticoids.
- P-14 トポイソメラーゼII阻害活性を有するテルペノイド類の研究(ポスター発表の部)
- 野崎 浩,保井 敦,池田 正五,中山 充,高岡 大輔,筒井 研,筒井 公子
- 天然有機化合物討論会講演要旨集 (37), 349-354, 1995-09-01
- … Therefore, functional mechanism of them to topoisomerase II enzyme was different from those of conventional inhibitors such as VP-16 and VM-26. …
- NAID 110006679435
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- Teniposide (ten I POE side) Trade name: Vumon ® Other name: VM-26 Drug type: Teniposide is an anti-cancer ("antineoplastic" or "cytotoxic") chemotherapy drug. This medication is classified as an "topoisomerase II ...
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