1. Cell Cycle/DNA Damage
    Autophagy
  2. DNA Alkylator/Crosslinker
    DNA/RNA Synthesis
    Autophagy
  3. Oxaliplatin

Oxaliplatin 

Cat. No.: HY-17371 Purity: 99.86%
Handling Instructions

Oxaliplatine est un inhibiteur de la synthèse d'ADN. Oxaliplatine provoque des dommages de réticulation de l'ADN, empêche la réplication et la transcription de l'ADN et provoque la mort cellulaire. Oxaliplatine inhibe les lignées cellulaires de mélanome humain C32 et G361 en fonction du temps avec des valeurs IC50 de 0,98 μM et 0,14 μM, respectivement. Oxaliplatine induit l'autophagie cellulaire.

Oxaliplatin ist ein Inhibitor der DNA synthesis. Oxaliplatin verursacht Schäden an der DNA-Vernetzung, verhindert die DNA-Replikation und -Transkription und verursacht den Zelltod. Oxaliplatin hemmt zeitabhängig die menschlichen Melanomzelllinien C32 und G361 mit IC50-Werten von 0,98 μM bzw. 0,14 μM. Oxaliplatin induziert die autophagy.

Oxaliplatin is a DNA synthesis inhibitor. Oxaliplatin causes DNA crosslinking damage, prevents DNA replication and transcription and causes cell death. Oxaliplatin time-dependently inhibits human melanoma cell lines C32 and G361 with IC50 values of 0.98 μM and 0.14 μM, respectively. Oxaliplatin induces cell autophagy.

For research use only. We do not sell to patients.

Oxaliplatin Chemical Structure

Oxaliplatin Chemical Structure

CAS No. : 61825-94-3

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Customer Review

Based on 31 publication(s) in Google Scholar

Top Publications Citing Use of Products

    Oxaliplatin purchased from MCE. Usage Cited in: Nat Med. 2019 Sep;25(9):1428-1441.

    Quantification of CD3+IFN-γ+ T cells in lung lobes taken from urethane-induced primary lung cancer models (n = 5 mice for SD group, n = 6 mice for all the other groups). Three coronal sections containing five pulmonary lobes from each mouse near the maximal diameters are quantified. Each dot represents one view field. A representative result from two independent experiments is shown.
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    Description

    Oxaliplatin is a DNA synthesis inhibitor. Oxaliplatin causes DNA crosslinking damage, prevents DNA replication and transcription and causes cell death. Oxaliplatin time-dependently inhibits human melanoma cell lines C32 and G361 with IC50 values of 0.98 μM and 0.14 μM, respectively. Oxaliplatin induces cell autophagy[1][2].

    IC50 & Target

    IC50: DNA synthesis[1]

    In Vitro

    Oxaliplatin acts through the formation of DNA-adducts. Oxaliplatin induces primary and secondary DNA lesions leading to cell apoptosis[1]. Oxaliplatin inhibits human melanoma cell lines C32 and G361 with IC50 values of 0.98 μM and 0.14 μM, respectively[2]. Oxaliplatin 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].

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

    In Vivo

    Oxaliplatin (10 mg/kg, i.p.) significantly reduces tumor volume and apoptotic index in the nude mice bearing hepatocellular HCCLM3 tumors[4]. Oxaliplatin (5 mg/kg, i.v.) is effective on T-leukemia-lymphoma L40 AKR with T/C of 1.77. Oxaliplatin is efficient on intracerebrally grafted L1210 leukemia, MA 16-C xenografts, B16 melanoma xenografts, Lewis lung xenografts and C26 colon carcinoma xenografts[5]. Oxaliplatin induces impairment of retrograde neuronal transport in mice[6].

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

    Clinical Trial
    Molecular Weight

    397.29

    Formula

    C₈H₁₄N₂O₄Pt

    CAS No.

    61825-94-3

    SMILES

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

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage

    4°C, protect from light, stored under nitrogen

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

    Solvent & Solubility
    In Vitro: 

    H2O : 3.33 mg/mL (8.38 mM; ultrasonic and adjust pH to 3 with HCl; DMSO can inactivate Oxaliplatin's activity)

    DMF : 1.67 mg/mL (4.20 mM; Need ultrasonic; DMSO can inactivate Oxaliplatin's activity)

    Ethanol : < 1 mg/mL (insoluble; DMSO can inactivate Oxaliplatin's activity)

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 2.5171 mL 12.5853 mL 25.1705 mL
    5 mM 0.5034 mL 2.5171 mL 5.0341 mL
    10 mM --- --- ---
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  5% w/v Glucose Solution

      Solubility: 5 mg/mL (12.59 mM); Clear solution; Need ultrasonic and warming and heat to 50°C

    *All of the co-solvents are provided by MCE.
    References
    Cell Assay
    [3]

    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.

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

    Animal Administration
    [4]

    HCC tumor models produced by HCCLM3 are established in nude mice by subcutaneous injection of 5×105 HCCLM3 cells in 0.2 mL of serum-free culture medium into the left upper flank region. Three days later, the mice are randomLy assigned to receive one of the following three treatments: i) a weekly intraperitoneal (i.p.) injection of distilled water (control group, n=8); ii) a weekly i.p. injection of oxaliplatin at 5 mg/kg (low dose group, n=7); or iii) a weekly i.p. injection of oxaliplatin at 10 mg/kg (high dose group, n=7). Tumor growth is monitored by measuring two bisecting diameters of each tumor with a caliper every 5 days. The tumor volume is calculated using the formula (V=a×b2/2), with a as the larger diameter and b as the smaller diameter. Mice are euthanized by day 32 after oxaliplatin administration. Tumors of each group are completely removed, weighed, photographed, and fixed in 10% formalin/PBS or stored in liquid nitrogen for histological examination.

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

    References

    Purity: 99.86%

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    Keywords:

    OxaliplatinDNA Alkylator/CrosslinkerDNA/RNA SynthesisAutophagyInhibitorinhibitorinhibit

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    Cat. No.:
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