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Oxaliplatin

カタログ番号 T0164   CAS 61825-94-3
別名: L-OHP

Oxaliplatin (L-OHP) is a DNA alkylating agent, an inhibitor of DNA synthesis. Oxaliplatin causes DNA cross-linking damage, preventing DNA replication and transcription and leading to cell death. Oxaliplatin induces autophagy.

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Oxaliplatin, CAS 61825-94-3
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50 mg 在庫あり ¥ 11,500
100 mg 在庫あり ¥ 16,000
200 mg 在庫あり ¥ 27,000
500 mg 在庫あり ¥ 32,000
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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 Oxaliplatin (L-OHP) is a DNA alkylating agent, an inhibitor of DNA synthesis. Oxaliplatin causes DNA cross-linking damage, preventing DNA replication and transcription and leading to cell death. Oxaliplatin induces autophagy.
In vitro Oxaliplatin is effective against intracerebrally implanted L1210 leukemia, MA 16-C transplantable tumors, B16 melanoma transplantable tumors, Lewis lung carcinoma transplantable tumors, and C26 colon carcinoma transplantable tumors. Intraperitoneal administration of 10 mg/kg Oxaliplatin weekly in nude mice bearing HCCLM3 hepatic tumor significantly reduces tumor volume and increases apoptotic index. In mice, Oxaliplatin induces a decrease in regressive neuroconduction.
In vivo Oxaliplatin exhibits potent inhibitory effects on various cancer cell lines, including bladder cancer (RT4 and TCCSUP), ovarian cancer (A2780), colorectal cancer (HT-29), glioblastoma (U-373 mg and U-87 mg), and melanoma (SK-MEL-2 and HT-144), with respective IC50 values of 11 μM, 15 μM, 0.17 μM, 0.97 μM, 2.95 μM, 17.6 μM, 30.9 μM, and 7.85 μM. Additionally, oxaliplatin effectively suppresses human melanoma cell lines C32 and G361, with IC50 values of 0.98 mM and 0.14 mM, respectively.
キナーゼ試験 Binding experiments of electrophysiology: CHO cells expressing the subunit of the voltage-dependent L-type Ca2+ channel are cultrured in medium without serum in the presence of different concentrations of Nisoldipine. Then Ca2+ channel current elicited from a holding potential of -100 mV or -50 mV is recorded at room temperature with the whole-cell configuration of the patch-clamp method using the List EPC-7 patch-clamp amplifer and pClamp software. The concentration of competitor inhibiting 50% of the specific binding represents IC50.
細胞研究 The cytotoxicity studies are carried out with the sulforhodamine-B microculture colorimetrie assay. Typically, cells are plated into 96-well plates on day 0 and exposed to Oxaliplatin on day 1; the sulforhodamine-B assay is carried out 48 h after Oxaliplatin exposure. The plates are incubated at 37 °C in 5% CO2 and 100% relative humidity at all times except when adding Oxaliplatin and during the final assay period. The initial number of cells plated for the assay ranged from 2-20 × 103 cells/50 /nL/well. The numbers of cells for plating and the drug exposure time are based on pilot studies using the criteria that (a) the cells in control wells are still in the log phase of growth on the day of the assay; (b) the maximum absorbance for the untreated controls on the day of the assay is in the range of 1.0 to 1.5; and (c) cells go through >2 doublings during the drug exposure. Eight wells are used per concentration. The plates are read at 570 and/or 540 nm using a Biotek Instruments model EL309 microplate reader interfaced with an IBM PC-compatible computer. The data are transferred and transformed into a LOTUS 1-2-3 format by the computer program DATALOG, and survival fractions are calculated by comparing the drug treated with control(Only for Reference)
別名 L-OHP
分子量 397.29
分子式 C8H14N2O4Pt
CAS No. 61825-94-3

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

Ethanol: < 1 mg/mL (insoluble)

DMSO: 50 mg/mL (125.85 mM), DMSO inactivates the activity of Oxaliplatin.

H2O: 3 mg/mL (7.55 mM), Sonication and heating to 60℃ are recommended.

DMF: 1.67 mg/mL (4.20 mM), Sonication is recommended.

参考文献

1. Nannizzi S, et al. Cellular and molecular mechanisms for the synergistic cytotoxicity elicited by oxaliplatin and pemetrexed in colon cancer cell lines. Cancer Chemother Pharmacol. 2010 Aug;66(3):547-58. 2. Pires IM, et al. Oxaliplatin responses in colorectal cancer cells are modulated by CHK2 kinase inhibitors. Br J Pharmacol. 2010 Mar;159(6):1326-38. 3. Li D, et al. Oxaliplatin induces the PARP1-mediated parthanatos in oral squamous cell carcinoma by increasing production of ROS. Aging (Albany NY). 2021 Jan 20;13(3):4242-4257. 4. Chen W, et al. The synergistic effects of oxaliplatin and piperlongumine on colorectal cancer are mediated by oxidative stress. Cell Death Dis. 2019 Aug 8;10(8):600. 5. Ta LE, et al. Mice with cisplatin and oxaliplatin-induced painful neuropathy develop distinct early responses to thermal stimuli. Mol Pain. 2009 Feb 26;5:9. 6. Zhou Y, Yang L, Xiong L, et al. KIF11 is upregulated in colorectal cancer and silencing of it impairs tumor growth and sensitizes colorectal cancer cells to oxaliplatin via p53/GSK3β signaling[J]. Journal of Cancer. 2021, 12(12): 3741. 7. Dong L, Shen S, Chen W, et al. Discovery of Novel Inhibitors Targeting Human O-GlcNAcase: Docking-Based Virtual Screening, Biological Evaluation, Structural Modification, and Molecular Dynamics Simulation[J]. Journal of chemical information and modeling. 2019, 59(10): 4374-4382. 8. Yang P, Liu W, Fu R, et al. Cucurbitacin E Chemosensitizes Colorectal Cancer Cells via Mitigating TFAP4/Wnt/β-Catenin Signaling[J]. Journal of Agricultural and Food Chemistry. 2020 9. Wang X, Wu F, Wang H, et al. PDCD6 cooperates with C-Raf to facilitate colorectal cancer progression via Raf/MEK/ERK activation[J]. Journal of Experimental & Clinical Cancer Research. 2020, 39(1): 1-15. 10. Huang Y, Wang H, Hao Y, et al. Myeloid PTEN promotes chemotherapy-induced NLRP3-inflammasome activation and antitumour immunity[J]. Nature Cell Biology. 2020: 1-12.(22-6 , 716–727)

引用文献

1. Chao S, Zhang F, Yan H, et al.Targeting intratumor heterogeneity suppresses colorectal cancer chemoresistance and metastasis.EMBO reports.2023: e56416. 2. Jiang Y, Feng Y, Huang J, et al.LAD1 promotes malignant progression by diminishing ubiquitin-dependent degradation of vimentin in gastric cancer.Journal of Translational Medicine.2023, 21(1): 1-15. 3. Feng Y, Cao Z, Xu A, et al.Evaluation of toxicity and mutagenicity of oxaliplatin on germ cells in an alternative in vivo model Caenorhabditis elegans.Food and Chemical Toxicology.2023: 113902. 4. Yu Y, Wu T, Zhang X, et al.Regorafenib activates oxidative stress by inhibiting SELENOS and potentiates oxaliplatin-induced cell death in colon cancer cells.European Journal of Pharmacology.2023: 175986. 5. Zhang Z, Ye J, Liu X, et al.Huangqi Guizhi Wuwu decoction alleviates oxaliplatin-induced peripheral neuropathy via the gut-peripheral nerve axis.Chinese Medicine.2023, 18(1): 1-15. 6. Feng W Q, Zhang Y C, Gao H, et al.FOXD1 promotes chemotherapy resistance by enhancing cell stemness in colorectal cancer through β‑catenin nuclear localization.Oncology Reports.2023, 50(1): 1-14. 7. Li J, Lv J, Chen Y, et al.Tumor suppressor circPDE4D inhibits the progression of colorectal cancer and regulates oxaliplatin chemoresistance.Gene.2023: 147323. 8. Zhao L, Liu S, Zhang X, et al.Satellite glial cell-secreted exosomes after in-vitro oxaliplatin treatment presents a pro-nociceptive effect for dorsal root ganglion neurons and induce mechanical hypersensitivity in naïve mice.Molecular and Cellular Neuroscience.2023: 103881. 9. Liu M, Mai J W, Luo D X, et al.NFATc2-dependent Epigenetic Downregulation of the TSC2/Beclin-1 Pathway is Involved in Neuropathic Pain Induced by Oxaliplatin.Molecular Pain.2023: 17448069231158289. 10. Glorieux C, Xia X, You X, et al. Cisplatin and gemcitabine exert opposite effects on immunotherapy with PD-1 antibody in K-ras-driven cancer. Journal of Advanced Research. 2021
11. Huang Y, Wang H, Hao Y, et al. Myeloid PTEN promotes chemotherapy-induced NLRP3-inflammasome activation and antitumour immunity. Nature Cell Biology. 2020: 1-12.(22-6 , 716–727) 12. Wang X, Wu F, Wang H, et al. PDCD6 cooperates with C-Raf to facilitate colorectal cancer progression via Raf/MEK/ERK activation. Journal of Experimental & Clinical Cancer Research. 2020, 39(1): 1-15 13. Zhou Y, Yang L, Xiong L, et al. KIF11 is upregulated in colorectal cancer and silencing of it impairs tumor growth and sensitizes colorectal cancer cells to oxaliplatin via p53/GSK3β signaling. Journal of Cancer. 2021, 12(12): 3741. 14. Lee E J, Yang J H, Choi J G, et al. Augmented Antitumor Effect of Unripe Rubus coreanus Miquel Combined with Oxaliplatin in a Humanized PD-1/PD-L1 Knock-In Colorectal Cancer Mouse Model. Cells. 2022, 11(18): 2876. 15. Lin W, Zou H, Mo J, et al. Micro1278 Leads to Tumor Growth Arrest, Enhanced Sensitivity to Oxaliplatin and Vitamin D and Inhibits Metastasis via KIF5B, CYP24A1, and BTG2, Respectively. Frontiers in Oncology. 2021 Mar 11;11:637878. doi: 10.3389/fonc.2021.637878. eCollection 2021. 16. Shen X, Zhang Y, Xu Z, et al. KLF5 inhibition overcomes oxaliplatin resistance in patient-derived colorectal cancer organoids by restoring apoptotic response. Cell Death & Disease. 2022, 13(4): 1-13 17. Dong L, Shen S, Chen W, et al. Discovery of Novel Inhibitors Targeting Human O-GlcNAcase: Docking-Based Virtual Screening, Biological Evaluation, Structural Modification, and Molecular Dynamics Simulation. Journal of chemical information and modeling. 2019, 59(10): 4374-4382. 18. Yang P, Liu W, Fu R, et al. Cucurbitacin E Chemosensitizes Colorectal Cancer Cells via Mitigating TFAP4/Wnt/β-Catenin Signaling. Journal of Agricultural and Food Chemistry. 2020 Nov 18. doi: 10.1021 19. 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 20. Qiao S, Lu W, Glorieux C, et al. Wild-type IDH2 protects nuclear DNA from oxidative damage and is a potential therapeutic target in colorectal cancer. Oncogene. 2021: 1-13. 21. Su C, Cheng C, Rong Z, et al.Repurposing fluphenazine as an autophagy modulator for treating liver cancer.Heliyon.2023 22. Lee E J, Kim Y S, Kim J H, et al.Uncovering the colorectal cancer immunotherapeutic potential: Evening primrose (Oenothera biennis) root extract and its active compound oenothein B targeting the PD-1/PD-L1 blockade.Phytomedicine.2024: 155370.
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この製品は下記化合物ライブラリに含まれています:
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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

Oxaliplatin 61825-94-3 Autophagy Cell Cycle/Checkpoint DNA Damage/DNA Repair DNA/RNA Synthesis DNA Alkylator/Crosslinker L-OHP DNA cross-links anticancer Inhibitor apoptosis inhibit inhibitor