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.
Cited by 7 Publications
4 Customer Reviews
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.
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.
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
|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.|
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.  Oxaliplatin is active against human melanoma cell lines C32 and G361 with IC50 of 0.98 mM and 0.14 mM, respectively.  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. 
|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.  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.  Oxaliplatin induces impairment of retrograde neuronal transport in mice. |
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|In vitro||Water||3 mg/mL warmed (7.55 mM)|
|Ethanol||0.01 mg/mL (0.02 mM)|
|In vivo||Add solvents individually and in order:
5% glucose (with warming)
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT01928290||Recruiting||Stomach Neoplasms|Esophageal Neoplasms||Washington University School of Medicine||November 8, 2013||Phase 2|
|NCT03050814||Not yet recruiting||Colorectal Cancer||National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)||February 3, 2017||Phase 2|
|NCT02997228||Not yet recruiting||Colorectal Adenocarcinoma|High-Frequency Microsatellite Instability|Stage IV Colorectal Cancer|Stage IVA Colorectal Cancer|Stage IVB Colorectal Cancer||National Cancer Institute (NCI)||November 2017||Phase 3|
|NCT02912559||Not yet recruiting||Colon Adenocarcinoma|DNA Repair Disorder|Lynch Syndrome|Microsatellite Instability|Stage IIIA Colon Cancer|Stage IIIB Colon Cancer|Stage IIIC Colon Cancer||National Cancer Institute (NCI)||September 2017||Phase 3|
|NCT03043729||Not yet recruiting||Rectal Cancer|Rectosigmoid Cancer||AIO-Studien-gGmbH|Institut für Klinisch-Onkologische Forschung (IKF) Frankfurt|Sanofi||February 2017||Phase 2|
|NCT03000374||Not yet recruiting||Rectal Cancer||Grupo Espanol Multidisciplinario del Cancer Digestivo|Pivotal S.L.|Amgen||February 2017||Phase 2|
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Frequently Asked Questions
Is it ok to dissolve Oxaliplatin in DMSO?
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.