Temsirolimus (CCI-779, NSC 683864)
Licensed by Pfizer 製品コードS1044
分子量(MW)：1030.29
Temsirolimus (CCI-779, NSC 683864) is a specific mTOR inhibitor with IC50 of 1.76 μM in a cell-free assay.
カスタマーフィードバック(4)
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mTOR inhibitors attenuate ganetespib-driven elevation of HSPs in multiple tumor cell types. A375 melanoma cells were treated with vehicle, ganetespib (25 nmol/L), BEZ235 (500 nmol/L), or temsirolimus (500 nmol/L), either alone or in combination, for 24 hours. The levels of HSP90α, HSP70, HSP27, and GAPDH were determined by immunoblotting.
Mol Cancer Res 2014 12, 703-13. Temsirolimus (CCI-779, NSC 683864) purchased from Selleck.
SCID mice with PC-9/Vec or PC-9/HGF tumors were administered as described in Figure. Four hours after final administration of erlotinib, tumors were harvested, and tumor cell angiogenesis (CD31) were determined by immunohistochemistry.
PLoS One 2013 8, e62104. Temsirolimus (CCI-779, NSC 683864) purchased from Selleck.
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SCID mice with PC-9/Vec or PC-9/HGF tumors were administered 25 mg/kg erlotinib once daily for 4 days or 50 mg/kg temsirolimus once from day 8. Four hours after final erlotinib administration, tumors were harvested, and the relative levels of proteins in the tumor lysates were determined by western blotting.
PLoS One 2013 8, e62104. Temsirolimus (CCI-779, NSC 683864) purchased from Selleck.
Breast cancer cells were pretreated with 100ng/ml EGF for 15 min and then treated with the indicated concentrations of Temsirolimus for 24 hours.
Dr. Zhang of Tianjin Medical University. Temsirolimus (CCI-779, NSC 683864) purchased from Selleck.
製品安全説明書
mTOR阻害剤の選択性比較
生物活性
| 製品説明 | Temsirolimus (CCI-779, NSC 683864) is a specific mTOR inhibitor with IC50 of 1.76 μM in a cell-free assay. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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| 体外試験 |
In the absence of FKBP12, Temsirolimus potently inhibits mTOR kinase activity with IC50 of 1.76 μM, similar to that of rapamycin with IC50 of 1.74 μM. Temsirolimus treatment at nanomolar concentrations (10 nM to <5 μM) displays a modest and selective antiproliferative activity via FKBP12-dependent mechanism, but can completely inhibit the proliferation of a broad panel of tumor cells at low micromolar concentrations (5-15 μM), involving FKBP12-independent suppression of mTOR signaling. Temsirolimus treatment at micromolar but not nanomolar concentrations (20 μM) causes a marked decline in global protein synthesis and disassembly of polyribosomes, accompanied by rapid increase in the phosphorylation of translation elongation factor eEF2 and the translation initiation factor eIF2A. [1] Temsirolimus inhibits the phosphorylation of ribosomal protein S6, more potently in PTEN-positive DU145 cells than in PTEN-negative PC-3 cells, and inhibits cell growth and clonogenic survival of both cells in a concentration-dependent manner. [2] Temsirolimus (100 ng/mL) potently inhibits proliferation and induces apoptosis in primary human lymphoblastic leukemia (ALL) cells. [3] |
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| 体内試験 | In the NOD/SCID xenograft models with human ALL, Temsirolimus treatment at 10 mg/kg/day produces a decrease in peripheral blood blasts and in splenomegaly [3] Administration of Temsirolimus (20 mg/kg i.p. 5 days/week) significantly delays the growth of DAOY xenografts by 160% after 1 week and 240% after 2 weeks, compared with controls. Single high-dose of Temsirolimus (100 mg/kg i.p) treatment induces 37% regression of tumor volume within 1 week. Temsirolimus treatment for 2 weeks also delays the growth of rapamycin-resistant U251 xenografts by 148%. [4] Inhibition of mTOR by Temsirolimus improves performance on four different behavioral tasks and decreases aggregate formation in a mouse model of Huntington disease. [5] Administration of Temsirolimus induces significant dose-dependent, antitumor responses against subcutaneous growth of 8226, OPM-2, and U266 xenografts with ED50 of 20 mg/kg and 2 mg/kg for 8226 and OPM-2, respectively, which are associated with inhibited proliferation and angiogenesis, induction of apoptosis, and reduction in tumor cell size. [6] |
お薦めの試験操作（参考用のみ）
| キナーゼ試験： |
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In vitro assay of mTOR catalytic activity: The Flag-tagged wild-type human mTOR (Flag-mTOR) DNA constructs are transiently transfected into HEK293 cells. Protein extraction and purification of Flag-mTOR are carried out 48 hours later. In vitro kinase assays of purified Flag-mTOR in the presence of various concentrations of Temsirolimus without FKBP12 are performed in 96-well plate and detected by dissociation-enhanced lanthanide fluorescent immunoassay (DELFIA) using His6-S6K1 as the substrate. Enzymes is first diluted in kinase assay buffer (10 mM Hepes (pH 7.4), 50 mM NaCl, 50 mM β-glycerophosphate, 10 mM MnCl2, 0.5 mM DTT, 0.25 μM microcystin LR, and 100 μg/mL BSA). To each well, 12 μL of the diluted enzyme is mixed briefly with 0.5 μL Temsirolimus. The kinase reaction is initiated by adding 12.5 μL kinase assay buffer containing ATP and His6-S6K to give a final reaction volume of 25 μL containing 800 ng/mL FLAG-mTOR, 100 μM ATP, and 1.25 μM His6-S6K. The reaction plate is incubated for 2 hours (linear at 1-6 hours) at room temperature with gentle shaking and then terminated by adding 25 μL Stop buffer (20 mM Hepes (pH 7.4), 20 mM EDTA, and 20 mM EGTA). The DELFIA detection of the phosphorylated (Thr-389) His6-S6K is performed at room temperature using a monoclonal anti-P(T389)-p70S6K antibody labeled with Europium-N1-ITC (Eu) (10.4 Eu per antibody). 45 μL of the terminated kinase reaction mixture is transferred to a MaxiSorp plate containing 55 μL PBS. The His6-S6K is allowed to attach for 2 hours after which the wells are aspirated and washed once with PBS. 100 μL of DELFIA buffer with 40 ng/mL Eu-P(T389)-S6K antibody is added. The antibody binding is continued for 1 hour with gentle agitation. The wells are then aspirated and washed four times with PBS containing 0.05% Tween 20 (PBST). 100 μL of DELFIA Enhancement solution is added to each well and the plates are read in a PerkinElmer Victor model plate reader. |
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溶解度 (25°C)
| 体外 | Ethanol | 75 mg/mL (72.79 mM) |
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| DMSO | 67 mg/mL (65.03 mM) | |
| Water | Insoluble | |
| 体内 |
左から（NMPから）右の順に溶剤を製品に加えます(文献ではなく、Selleckの実験によるデータ): 2% DMSO+30% PEG 300 +2% Tween 80+ddH2O 混合させたのち直ちに使用することを推奨します。 |
7mg/mL |
* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程で起きる正常な現象ですからご安心ください。
化学情報
| 分子量 | 1030.29 |
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| 化学式 | C56H87NO16 |
| CAS No. | 162635-04-3 |
| 保管 | 粉 |
| in solvent | |
| 別名 | N/A |
便利ツール
モル濃度計算器
求めたい質量、体積または濃度を計算してください。
質量 (g) = 濃度 (mol/L) x 体積 (L) x 分子量 (g/mol)
モル濃度計算器方程式
*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとMSDS/COA（製品ページで利用可能な）。
希釈計算器
貯蔵液を準備するために必要な希釈率を計算してください。Selleck希釈計算器は、以下の方程式に基づきます：
開始濃度 x 開始体積 = 最終濃度 x 最終体積
希釈の計算式
この方程式は、一般に略語を使われます：C1V1 = C2V2 ( 入力 出力 )
常に貯蔵液を準備するとき、小びんラベルとMSDS/COA（オンラインで利用できる）で見つかる製品のバッチに特有の分子量を使ってください。
分子量计算器
そのモル質量と元素組成を計算するために、合成物の化学式を入力してください：
チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2
モル濃度計算器
臨床試験
| NCT Number | Recruitment | Conditions | Sponsor/Collaborators | Start Date | Phases |
|---|---|---|---|---|---|
| NCT01010126 | Completed | Adult Hepatocellular Carcinoma|Advanced Adult Hepatocellular Carcinoma|Endometrial Serous Adenocarcinoma|Localized Non-Resectable Adult Liver Carcinoma|Lung Carcinoid Tumor|Malignant Pancreatic Gastrinoma|Malignant Pancreatic Glucagonoma|Malignant Pancreatic Insulinoma|Malignant Pancreatic Somatostatinoma|Metastatic Digestive System Neuroendocrine Tumor G1|Ovarian Carcinosarcoma|Ovarian Endometrioid Adenocarcinoma|Ovarian Seromucinous Carcinoma|Ovarian Serous Surface Papillary Adenocarcinoma|Pancreatic Alpha Cell Adenoma|Pancreatic Beta Cell Adenoma|Pancreatic Delta Cell Adenoma|Pancreatic G-Cell Adenoma|Pancreatic Polypeptide Tumor|Recurrent Adult Liver Carcinoma|Recurrent Digestive System Neuroendocrine Tumor G1|Recurrent Fallopian Tube Carcinoma|Recurrent Ovarian Carcinoma|Recurrent Pancreatic Neuroendocrine Carcinoma|Recurrent Primary Peritoneal Carcinoma|Recurrent Uterine Corpus Carcinoma|Regional Digestive System Neuroendocrine Tumor G1|Stage IIIA Fallopian Tube Cancer|Stage IIIA Ovarian Cancer|Stage IIIA Primary Peritoneal Cancer|Stage IIIA Uterine Corpus Cancer|Stage IIIB Fallopian Tube Cancer|Stage IIIB Ovarian Cancer|Stage IIIB Primary Peritoneal Cancer|Stage IIIB Uterine Corpus Cancer|Stage IIIC Fallopian Tube Cancer|Stage IIIC Ovarian Cancer|Stage IIIC Primary Peritoneal Cancer|Stage IIIC Uterine Corpus Cancer|Stage IV Fallopian Tube Cancer|Stage IV Ovarian Cancer|Stage IV Primary Peritoneal Cancer|Stage IVA Uterine Corpus Cancer|Stage IVB Uterine Corpus Cancer|Uterine Carcinosarcoma | National Cancer Institute (NCI) | September 8 2009 | Phase 2 |
| NCT00703625 | Completed | Resistant Solid Malignancies | Washington University School of Medicine | March 8 2008 | Phase 1 |
| NCT03158389 | Recruiting | Glioblastoma Adult | University Hospital Heidelberg|German Cancer Aid|German Cancer Research Center|National Center for Tumor Diseases Heidelberg | May 7 2018 | Phase 1|Phase 2 |
| NCT03297606 | Recruiting | Lymphoma Non-Hodgkin|Multiple Myeloma|Advanced Solid Tumors | Canadian Cancer Trials Group|AstraZeneca|Bristol-Myers Squibb|Hoffmann-La Roche|Pfizer | October 6 2017 | Phase 2 |
| NCT02389309 | Recruiting | Solid Tumors | M.D. Anderson Cancer Center | October 5 2015 | Phase 1 |
| NCT01687673 | Active not recruiting | Hepatocellular Carcinoma | University of California San Francisco|Robert H. Lurie Cancer Center|Pfizer | October 5 2012 | Phase 2 |
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