Oxaliplatin
Catalog No.S1224 Synonyms: L-OHP
Molecular Weight(MW): 397.29
Oxaliplatin inhibits DNA synthesis by conforming DNA adducts in RT4, TCCSUP, A2780, HT-29, U-373MG, U-87MG, SK-MEL-2, and HT-144 cells.
5 Customer Reviews
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Cleaved caspases and p-H2AX expression were detected by western blot in HCT116 cells (E) and HT29 cells (F). The cells were co-cultured with F. nucleatum or treated with CQ, and different concentrations of Oxaliplatin and 5-FU.
Cell, 2017, 170(3):548-563.e16. Oxaliplatin purchased from Selleck.
Intracellular ratio between reduced and oxidized glutathione of the indicated cells treated with oxaliplatin or irinotecan for 6h was measured with spectrophotometric analysis.
Theranostics, 2018, 8(5): 1312–1326. Oxaliplatin purchased from Selleck.
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Immunocytochemical staining of SW620 (metastatic) cells after treatment with 10 uM oxaliplatin (F) or 10 uM ginsenosides 20(S)-Rg 3 (G) and negative staining (H). Cells demonstrated differential expression of histone H4.
J Proteomics 2014 10.1016/j.jprot.2014.10.009. Oxaliplatin purchased from Selleck.
PDT and oxaliplatin combination treatment. A) Bar graph showing response (total volume of residual viale nodules normalized to no treatment control) to PDT treatmen (2.5 J/cm2), oxaliplatin treatment (10 μM), and PDT followed by oxaliplatin at the same doses. The dramatic enhancement, beyond the additive effect of the two modalities independently suggests there may be a synergistic interaction. B) A representative region from a culture stained with calcein AM and ethidium bromide following treatment with the PDT + oxaliplatin combination shows relatively small pockets of viable disease and many dead relative to untreated cultures.
Optical Methods for Tumor Treatment and Detection 2013 10.1117/12.2010730. Oxaliplatin purchased from Selleck.
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Growth inhibitory effects of Oxaliplatin in human pancreatic cancer cells. MiaPaCa-2 cells were plated in triplicates into 48-well plates at a density of 10,000 cells/ml. After 24 hours, complete culture medium was changed into fresh low-serum-containing medium (1% FBS) containing DMSO (control) or indicated doses of Oxaliplatin (Selleckchem). Cell viability 72 hours after treatment was determined by AlamarBlue assay (Invitrogen) according to manufacturer's instructions. Results are expressed as percentages of control, which was arbitrarily assigned 100% viability, and represented as the mean ± standard deviation (SD) of the tripicate wells.
2013 Dr. Edita Aksamitiene from Thomas Jefferson University. Oxaliplatin purchased from Selleck.
Purity & Quality Control
Choose Selective DNA/RNA Synthesis Inhibitors
Biological Activity
| Description | Oxaliplatin inhibits DNA synthesis by conforming DNA adducts in RT4, TCCSUP, A2780, HT-29, U-373MG, U-87MG, SK-MEL-2, and HT-144 cells. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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| In vitro |
The main mechanism of action of Oxaliplatin is mediated through the formation of DNA–adducts. Oxaliplatin induces primary and secondary DNA lesions that lead to cell apoptosis. [1] Oxaliplatin is active against human melanoma cell lines C32 and G361 with IC50 of 0.98 mM and 0.14 mM, respectively. [2] Oxaliplatin effectively inhibits bladder carcinoma cell lines RT4 and TCCSUP, ovarian carcinoma cell line A2780, colon carcinoma cell line HT-29, glioblastoma cell lines U-373MG and U-87MG, and melanoma cell lines SK-MEL-2 and HT-144 with IC50 of 11 μM, 15 μM, 0.17 μM, 0.97 μM, 2.95 μM, 17.6 μM, 30.9 μM and 7.85 μM, respectively. [4] |
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| Cell Data |
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| In vivo | A weekly i.p. injection of Oxaliplatin at 10 mg/kg to nude mice bearing hepatocellular HCCLM3 tumors significantly reduces tumor volume and apoptotic index. [6] Oxaliplatin (5mg/kg, i.v. on days 1, 5 and 9) is active on T-leukemia-lymphoma L40 AKR with T/C of 1.77. Oxaliplatin is also efficient on intracerebrally grafted L1210 leukemia, MA 16-C xenografts, B16 melanoma xenografts, Lewis lung xenografts and C26 colon carcinoma xenografts. [7] Oxaliplatin induces impairment of retrograde neuronal transport in mice. [8] |
Protocol
| Cell Research:[4] |
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| Animal Research:[6] |
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References
- [1] Raymond E et al, Ann Oncol, 1998, 9(10), 1053-1071.
- [2] Mohammed MQ, et al. Anticancer Drugs, 2000, 11(10), 859-863.
- [3] Kirstein MN, et al. Anticancer Drugs, 2008, 19(1), 37-44.
- [4] Pendyala L, et al. Cancer Res, 1993, 53(24), 5970-5976.
- [5] Espinosa M, et al. Cancer Chemother Pharmacol, 2005, 55(3), 301-305.
- [6] Wang Z, et al. Expert Opin Investig Drugs, 2009, 18(11), 1595-1604.
- [7] Math?G, et al. Biomed Pharmacother, 1989, 43(4), 237-250.
- [8] Schellingerhout D, et al. PLoS One, 2012, 7(9), e45776.
Solubility (25°C)
| In vitro | Water | 3 mg/mL warmed (7.55 mM) |
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| Ethanol | 0.01 mg/mL (0.02 mM) | |
| DMF | Insoluble | |
| In vivo | Add solvents to the product individually and in order(Data is from Selleck tests instead of citations): 5% glucose (with warming) For best results, use promptly after mixing. |
3mg/mL |
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
Chemical Information
| Molecular Weight | 397.29 |
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| Formula | C8H14N2O4Pt |
| CAS No. | 61825-94-3 |
| Storage | powder |
| in solvent | |
| Synonyms | L-OHP |
Bio Calculators
Molarity Calculator
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Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).
Dilution Calculator
Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )
* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
Molecular Weight Calculator
Enter the chemical formula of a compound to calculate its molar mass and elemental composition:
Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2
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Definitions of molecular mass, molecular weight, molar mass and molar weight:
Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.
Molarity Calculator
Clinical Trial Information
| NCT Number | Recruitment | Conditions | Sponsor/Collaborators | Start Date | Phases |
|---|---|---|---|---|---|
| NCT03784326 | Not yet recruiting | Clinical Stage II Esophageal Adenocarcinoma AJCC v8|Clinical Stage II Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IIA Esophageal Adenocarcinoma AJCC v8|Clinical Stage IIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IIB Esophageal Adenocarcinoma AJCC v8|Clinical Stage IIB Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage III Esophageal Adenocarcinoma AJCC v8|Clinical Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IB Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IB Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IC Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IC Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage II Esophageal Adenocarcinoma AJCC v8|Pathologic Stage II Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIA Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIB Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IIB Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage III Esophageal Adenocarcinoma AJCC v8|Pathologic Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIA Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IIIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIB Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IIIB Gastroesophageal Junction Adenocarcinoma AJCC v8 | M.D. Anderson Cancer Center|National Cancer Institute (NCI) | May 31 2019 | Early Phase 1 |
| NCT03784326 | Not yet recruiting | Clinical Stage II Esophageal Adenocarcinoma AJCC v8|Clinical Stage II Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IIA Esophageal Adenocarcinoma AJCC v8|Clinical Stage IIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IIB Esophageal Adenocarcinoma AJCC v8|Clinical Stage IIB Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage III Esophageal Adenocarcinoma AJCC v8|Clinical Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IB Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IB Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IC Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IC Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage II Esophageal Adenocarcinoma AJCC v8|Pathologic Stage II Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIA Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIB Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IIB Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage III Esophageal Adenocarcinoma AJCC v8|Pathologic Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIA Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IIIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIB Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IIIB Gastroesophageal Junction Adenocarcinoma AJCC v8 | M.D. Anderson Cancer Center|National Cancer Institute (NCI) | May 31 2019 | Early Phase 1 |
| NCT03626922 | Not yet recruiting | Metastatic Colorectal Cancer | NSABP Foundation Inc|Merck Sharp & Dohme Corp.|Eli Lilly and Company | April 2019 | Phase 1 |
| NCT03626922 | Not yet recruiting | Metastatic Colorectal Cancer | NSABP Foundation Inc|Merck Sharp & Dohme Corp.|Eli Lilly and Company | April 2019 | Phase 1 |
| NCT03366155 | Recruiting | Colorectal Cancer|Liver Metastases|Colorectal Adenocarcinoma|Colorectal Cancer With Hepatic Metastases|Colorectal Carcinoma | National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) | March 1 2019 | Phase 2 |
| NCT03813784 | Not yet recruiting | Gastric Cancer|GastroEsophageal Cancer | Jiangsu HengRui Medicine Co. Ltd. | March 2019 | Phase 3 |
Tech Support
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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Frequently Asked Questions
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Question 1:
Is it ok to dissolve Oxaliplatin in DMSO?
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Answer:
Even though cis-platin is soluble in DMSO, the use of DMSO to dissolve cis– or trans-diamminedichloroplatinum (DDP) in biological studies is strongly discouraged. The DMSO inserts itself into the ligand and inactivates platin-containing compounds. DMF is a much better choice than DMSO.
