Oxaliplatin is a DNA synthesis inhibitor. Oxaliplatin causes DNA crosslinking damage, prevents DNA replication and transcription and induces apoptosis. Oxaliplatin can be used for cancer research^[1][2][3].

IC50: DNA synthesis^[1]

Oxaliplatin (24-72 hours; 2-128 μM; HCC, HCCLM3 and Hep3B cells) inhibits cell growth and induces apoptosis^[1].
Oxaliplatin (10 μM; 15-240 mins; CEM cells ) induces primary and secondary DNA lesions, including DNA cross-links (ISC) and DNA-protein cross-links (DPC)^[2].
Oxaliplatin (0.01 to 100 μM; 24 hours) potently 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^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Oxaliplatin (5-10 mg/kg; i.p.; for 32 days; nude mice) inhibits tumor growth^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

397.29

C₈H₁₄N₂O₄Pt

61825-94-3

Solid

White to off-white

O=C(O1)C(O[Pt]21[NH2][C@@H]3CCCC[C@H]3[NH2]2)=O

Room temperature in continental US; may vary elsewhere.

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

• [1]. Raymond E, et al. Oxaliplatin: a review of preclinical and clinical studies. Ann Oncol. 1998 Oct;9(10):1053-71.  [Content Brief]

  [2]. Mohammed MQ, et al. Oxaliplatin is active in vitro against human melanoma cell lines: comparison with NSC 119875 and NSC 241240. Anticancer Drugs. 2000 Nov;11(10):859-63.  [Content Brief]

  [3]. Pendyala L, et al. In vitro cytotoxicity, protein binding, red blood cell partitioning, and biotransformation of oxaliplatin. Cancer Res. 1993 Dec 15;53(24):5970-6.  [Content Brief]

  [4]. Wang Z, et al. Oxaliplatin induces apoptosis in hepatocellular carcinoma cells and inhibits tumor growth. Expert Opin Investig Drugs. 2009 Nov;18(11):1595-604  [Content Brief]

  [5]. Mathé G, et al. Oxalato-platinum or 1-OHP, a third-generation platinum complex: an experimental and clinical appraisal and preliminary comparison with cis-platinum. Biomed Pharmacother. 1989;43(4):237-50.  [Content Brief]

  [6]. Schellingerhout D, et al. Impairment of retrograde neuronal transport in oxaliplatin-induced neuropathy demonstrated by molecular imaging. PLoS One. 2012;7(9):e45776. doi: 10.1371/journal.pone.0045776. Epub 2012 Sep 20.  [Content Brief]

  [7]. Park GY, et al. Phenanthriplatin, a monofunctional DNA-binding platinum anticancer drug candidate with unusual potency and cellular activity profile. Proc Natl Acad Sci U S A. 2012 Jul 24;109(30):11987-92.  [Content Brief]

  [8]. Yi Yao, et al. Comparative proteomic analysis of colon cancer cells in response to oxaliplatin treatment. Biochim Biophys Acta. 2009 Oct;1794(10):1433-40.  [Content Brief]

  [9]. Garrett MJ, et, al. Capecitabine, Oxaliplatin, and Bevacizumab (BCapOx) Regimen for Metastatic Colorectal Cancer. Hosp Pharm. 2017 May;52(5):341-347.  [Content Brief]