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Carboplatin

カタログ番号 T1058   CAS 41575-94-4
別名: NSC 241240, CBDCA, JM-8

Carboplatin (JM-8) is a cisplatin derivative, a DNA synthesis inhibitor. Carboplatin binds to DNA, inhibits replication and transcription, and induces cell death. Carboplatin has antitumor activity.

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Carboplatin, CAS 41575-94-4
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50 mg 在庫あり ¥ 8,500
100 mg 在庫あり ¥ 11,000
200 mg 在庫あり ¥ 15,500
500 mg 在庫あり ¥ 26,500
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生物学的特性に関する説明
化学的特性
保存条件 & 溶解度情報
説明 Carboplatin (JM-8) is a cisplatin derivative, a DNA synthesis inhibitor. Carboplatin binds to DNA, inhibits replication and transcription, and induces cell death. Carboplatin has antitumor activity.
In vitro METHODS: 5637 cells were treated with Carboplatin (0-10000 μM) for 4 h. Cell viability was determined by MTT.
RESULTS: Carboplatin showed a dose-dependent cell killing effect with an IC50 value of 289.3±2.90 μM. [1]
METHODS: Human RB tumor cells Y79 were treated with Carboplatin (20-80 μg/mL) for 2 days, and apoptosis was detected by Flow Cytometry.
RESULTS: Carboplatin induced an increase in the rate of early apoptosis. [2]
In vivo METHODS: To test the antitumor activity in vivo, Carboplatin (20 mg/kg) was injected intravenously into the tail of BALB/c (nu/nu) mice harboring human RB tumor Y79 every three days for one or two weeks.
RESULTS: Carboplatin successfully inhibited the growth of human RB xenografts in vivo. [2]
METHODS: To detect anti-tumor activity in vivo, Carboplatin (25-75 mg/kg) was injected intraperitoneally into immunodeficient mice bearing EOC xenograft tumors once a week for six weeks.
RESULTS: OV1946 and OV4453 were sensitive to Carboplatin, OV90 and OV4485 showed moderate response, and TOV21G and TOV112D were resistant. [3]
キナーゼ試験 Radioligand binding studies on human AT1 receptors: A radioligand binding assay is performed by using human AT1 receptor-coated microplates containing 4.4 to 6.2 fmol of receptors/well (10 μg of membrane protein/well). Membrane-coated wells are incubated with 45 μL of assay buffer (50 mM Tris-HCl, 5 mM MgCl2, 1 mM EDTA, and 0.005% CHAPS, pH 7.4) containing various concentrations of Azilsartan at room temperature. After 90 minutes, 5 μL of 125I-Sar1-Ile8-AII (final concentration 0.6 nM) dissolved in assay buffer is added to the wells, and the plate is incubated for 5 hours. In each step, the plate is briefly and gently shaken on a plate shaker. In washout experiments, the membranes are incubated with Azilsartan for 90 minutes, then immediately washed twice with 200 μL/well of assay buffer to remove unbound compounds, and further incubated for 5 hours with 125I-Sar1-Ile8-AII. Membrane-bound radioactivity is counted using a TopCount Microplate Scintillation and Luminescence Counter. In the experiments to estimate the dissociation rate of Azilsartan from AT1 receptors, membranes are incubated for 90 minutes with Azilsartan at a concentration of 30 nM for Azilsartan. Azilsartan inhibits the specific binding of 125I-Sar1-Ile8-AII to human AT1 by approximately 90%. The membranes are then immediately washed twice with 200 μL/well of assay buffer and further incubated with 125I-Sar1-Ile8-AII for 240 minutes. Membrane-bound radioactivity is counted using the TopCount Microplate Scintillation and Luminescence Counterat 30 minutes, 60 minutes, 90 minutes, 120 minutes, 150 minutes, 180 minutes, or 240 minutes. Nonspecific binding of 125I-Sar1-Ile8-AII is estimated in the presence of 10 μM unlabeled AII. Unlabeled AII is added again after washout for the washout experiment. Specific binding is defined as total binding minus nonspecific binding.
細胞研究 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide (MTT) assays: Exponentially growing A2780, SKOV3, IGROV-1 and HX62 ovarian cancer cells are plated in 96 well plates. A range of drug concentrations are added and the plates are incubated for 72 hours to allow for 3–4 doubling times. Each experiment is carried out in triplicate. Sulforhodamine B (SRB) assays: Exponentially growing A2780 cells are plated in 96 well microtitre plates. For experiments studying concomitant exposure, cells are exposed to increasing concentrations of both drugs for 96 hours. For experiments studying the effect of sequence of exposure to 17-AAG or carboplatin cells are exposed to increasing concentrations of 17-AAG or carboplatin for 24 hours. A period of 24-hour exposure to the first agent is chosen so that the A2780 cells would be exposed to the first drug for at least one doubling time (18-24 hours). The cells are then washed with sterile phosphate buffered saline and the medium is replenished. Following this, the second drug (to which the cells are not exposed to in the first 24 hours) or medium is added for 96 hours. All experiments are carried out in triplicate. The results of combination studies are analyzed using the well-established principles of median effect analysis method. The effects of the combination are calculated using an in-house spreadsheet. (Only for Reference)
別名 NSC 241240, CBDCA, JM-8
分子量 371.25
分子式 C6H12N2O4Pt
CAS No. 41575-94-4

保存条件

keep away from direct sunlight

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度情報

DMF: 1 mg/mL (2.69 mM), Sonication is recommended.

H2O: 25 mg/mL (67.34 mM), Sonication is recommended. (DMSO inactivates the activity of Carboplatin.)

参考文献

1. Wang S, et al. Analysis of the cytotoxic activity of carboplatin and gemcitabine combination. Anticancer Res. 2010 Nov;30(11):4573-8. 2. Zhou Z, et al. Comparison of the therapeutic effects of lobaplatin and carboplatin on retinoblastoma in vitro and in vivo. Int J Oncol. 2020 Sep;57(3):697-706. 3. Brodeur MN, et al. Carboplatin response in preclinical models for ovarian cancer: comparison of 2D monolayers, spheroids, ex vivo tumors and in vivo models. Sci Rep. 2021 Sep 14;11(1):18183. 4. Wang H, et al. Clin Cancer Res. 2004, 10(5), 1633-1644. 5. Liu H, et al. Anticancer Res. 2011, 31(9), 2713-2722. 6. Dela Cruz FS, et al. A case study of an integrative genomic and experimental therapeutic approach for rare tumors: identification of vulnerabilities in a pediatric poorly differentiated carcinoma. Genome Med. 2016 Oct 31;8(1):116. 7. Liu L, Liu S, Deng P, et al. Targeting the IRAK1-S100A9 Axis Overcomes Resistance to Paclitaxel in Nasopharyngeal Carcinoma[J]. Cancer Research.

引用文献

1. Liu L, Liu S, Deng P, et al. Targeting the IRAK1-S100A9 Axis Overcomes Resistance to Paclitaxel in Nasopharyngeal Carcinoma. Cancer Research. 2021 Mar 1;81(5):1413-1425. doi: 10.1158/0008-5472.CAN-20-2125. Epub 2021 Jan 5. 2. Liu L, Liu S, Deng P, et al. Targeting the IRAK1–S100A9 Axis Overcomes Resistance to Paclitaxel in Nasopharyngeal Carcinoma. Cancer Research. 2021, 81(5): 1413-1425. 3. Bi G, Liang J, Zhao M, et al. MiR-6077 promotes cisplatin/pemetrexed resistance in lung adenocarcinoma by targeting CDKN1A/cell cycle arrest and KEAP1/ferroptosis pathways. Molecular Therapy-Nucleic Acids. 2022 4. Zhu H, Rao Z, Yuan S, et al. One therapeutic approach for triple-negative breast cancer: Checkpoint kinase 1 inhibitor AZD7762 combination with neoadjuvant carboplatin. European Journal of Pharmacology. 2021: 174366. 5. Guo A, Lin J, Zhong P, et al.Phellopterin attenuates ovarian cancer proliferation and chemoresistance by inhibiting the PU. 1/CLEC5A/PI3K-AKT feedback loop.Toxicology and Applied Pharmacology.2023: 116691. 6. Lin Y, Chen X, Lin L, et al.Sesamolin serves as an MYH14 inhibitor to sensitize endometrial cancer to chemotherapy and endocrine therapy via suppressing MYH9/GSK3β/β-catenin signaling.Cellular & Molecular Biology Letters.2024, 29(1): 63.

関連化合物ライブラリー

この製品は下記化合物ライブラリに含まれています:
Anti-Cancer Drug Library Anti-Cancer Active Compound Library Anti-Cancer Approved Drug Library Inhibitor Library Drug Repurposing Compound Library Tyrosine Kinase Inhibitor Library Anti-Cancer Clinical Compound Library Anti-Lung Cancer Compound Library Clinical Compound Library NO PAINS Compound Library

関連製品

同一標的の関連化合物
Bendamustine hydrochloride PK11000 Cyclophosphamide RITA Satraplatin Streptozocin Nimustine Hydrochloride Miriplatin

投与量変換

You can also refer to dose conversion for different animals. 詳細

In vivo投与量計算 (透明溶液)

ステップ1: 以下の情報を入力してください
投与量
mg/kg
動物の平均体重
g
動物あたりの投与量
ul
動物数
溶媒の組成を入力してください
% DMSO
%
% Tween 80
% ddH2O
計算する リセット

計算器

モル濃度計算機
希釈計算機
再構成計算
分子量計算機
=
X
X

モル度計算機では以下の計算が可能です

  • 既知の体積と濃度の溶液を調製するために必要な化合物の質量
  • 質量が既知の化合物を目的の濃度まで溶解させるのに必要な溶液の量
  • 特定の体積の中に既知の質量の化合物を入れて得られる溶液の濃度
参考例

モル濃度計算機を使用したモル濃度計算の例
化合物の分子量が197.13g/molである場合、10mlの水に10mMのストック溶液を作るのに必要な化合物の質量はどれくらいですか?
[分子量(MW)]の欄に[197.13]と入力してください
[濃度]ボックスに10と入力し、正しい単位(millimolar)を選択します
[容量]ボックスに10と入力し、正しい単位(milliliter)を選択します
計算を押します
答えの19.713mgが質量欄に表示されます

X
=
X

溶液を作るのに必要な希釈率の計算

溶液の調製に必要な希釈率の算出
希釈計算機は、既知の濃度の原液をどのように希釈するかを計算することができる便利なツールです。V1を計算するためにC1、C2&V2を入力します。

参考例

Tocrisの希釈計算器を用いた希釈計算の一例
50μMの溶液を20ml作るためには、10mMの原液を何ml必要ですか?
C1V1=C2V2という式を用いて、C1=10mM、C2=50μM、V2=20ml、V1を未知数とします。
濃度(開始)ボックスに10を入力し正しい単位(millimolar)を選択してください
濃度(終了)ボックスに50を入力し正しい単位(millimolar)を選択してください
体積(終了)ボックスに20を入力し正しい単位(millimolar)を選択してください
計算を押します
100 microliter (0.1 ml) という答えが体積(開始)ボックスに表示されます。

=
/

バイアルを再構成するのに必要な溶媒の量を計算する.

再構成計算機を使えば、バイアルを再構成するための試薬の量をすぐに計算することができます.
試薬の質量と目標濃度を入力するだけで計算します。

g/mol

化合物の化学式を入力して、そのモル質量や元素組成を計算します

Tヒント:化学式は大文字と小文字を区別します。: C10H16N2O2 c10h16n2o2

化合物のモル質量(分子量)を計算する手順:
化学物質のモル質量を計算するには、その化学式を入力し、「計算」をクリックしてください。.
分子質量、分子量、モル質量、モル重量の定義:
分子質量(分子量)とは、物質の1分子の質量であり、統一された原子質量単位(u)で表されます。(1uは炭素12の1原子の質量の1/12に等しい)
モル質量(molar weight)とは、ある物質の1モルの質量のことで、単位はg/molです。

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技術サポート

Please see Inhibitor Handling Instructions for more frequently ask questions. Topics include: how to prepare stock solutions, how to store products, and cautions on cell-based assays & animal experiments, etc.

Keywords

Carboplatin 41575-94-4 Autophagy Cell Cycle/Checkpoint DNA Damage/DNA Repair DNA Alkylator/Crosslinker DNA/RNA Synthesis inhibit JM8 NSC 241240 NSC241240 JM 8 CBDCA JM-8 NSC-241240 Inhibitor inhibitor