1. Apoptosis
  2. Apoptosis

Cisplatin (Synonyms: CDDP; cis-Diaminodichloroplatinum)

Cat. No.: HY-17394 Purity: >99.0%
Handling Instructions

Cisplatin is a potent inducer of growth arrest and/or apoptosis in most cell types.

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

Cisplatin Chemical Structure

Cisplatin Chemical Structure

CAS No. : 15663-27-1

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Estimated Time of Arrival: December 31
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Customer Review

    Cisplatin purchased from MCE. Usage Cited in: Oncol Lett. 2018 Feb;15(2):2583-2589.

    MLN4924 increases CDDP induced apoptosis of esophageal cancer cells. EC1 and Kyse450 cells are treated with 1.6 μg/mL CDDP alone or in combina¬tion with 0.3 μM MLN for 72 h. Cleaved PARP are detected by western blotting.

    Cisplatin purchased from MCE. Usage Cited in: Cell Signal. 2017 May 1;36:108-116.

    PAQR3 affects DNA damage repair. AGS cells are treated with different doses of Etoposide (for 24 h), Cisplatin (for 24 h) and Doxorubicin (for 10 h) as indicated, followed by immunoblotting with the antibodies.

    Cisplatin purchased from MCE. Usage Cited in: Oncotarget. 2017 Apr 25;8(17):29125-29137.

    Knockdown of ROC1 significantly enhances CDDP-induced apoptosis. TE1 and Kyse450 cells are transfected with siROC1 for 48 h and then treated with 1 μg/mL CDDP for 48 h. Knockdown efficiency and cleaved PARP are assessed by western blotting analysis. Protein expression is quantified and statically analyzed.

    Cisplatin purchased from MCE. Usage Cited in: Neurosci Lett. 2018 Jun 18;682:112-117.

    After treatment of CDDP with or without the autophagy inhibitor CQ, the expression of LC3-II in the CQ+CDDP group is less than that in the CQ group but is higher than that in the CDDP group at 24 h and 96 h.
    • Biological Activity

    • Protocol

    • Technical Information

    • Purity & Documentation

    • References


    Cisplatin is a potent inducer of growth arrest and/or apoptosis in most cell types.

    IC50 & Target

    Apoptosis inducer[1]

    In Vitro

    Cisplatin (CDDP) causes apoptosis of HeLa cells in a dose-dependent manner, with a concentration of 30 μM Cisplatin resulting in death of greater than 90% of the cell population by 24 h of treatment. The kinetics of Cisplatin-induced apoptosis are examined using a 30 μM concentration. Cisplatin Activates the MEK/ERK Signaling Pathway, 20 and 30 μM Cisplatin, both of which results in significant apoptosis, leads to strong activation of ERK[1]. Cisplatin (50 μM) produces time-dependent apoptosis in renal proximal tubular cell (RPTCs), causing cell shrinkage, a 50-fold increase in caspase 3 activity, a 4-fold increase in phosphatidylserine externalization, and 5- and 15-fold increases in chromatin condensation and DNA hypoploidy, respectively[2].

    In Vivo

    In melanoma-bearing mice, Cisplatin (4 mg/kg B.W.) reduces the size and weight of the solid tumors, and HemoHIM supplementation with Cisplatin enhances the decrease of both the tumor size and weight[3]. Cisplatin administration results in significant increases in the kidney weight as a percentage of the total body weight, urine volume, serum creatinine, and blood urea nitrogen by about 132, 315, 797, and 556% in comparison with the control rats, respectively[4].

    Clinical Trial
    Preparing Stock Solutions
    Concentration Volume Mass 1 mg 5 mg 10 mg
    1 mM 3.3328 mL 16.6639 mL 33.3278 mL
    5 mM 0.6666 mL 3.3328 mL 6.6656 mL
    10 mM 0.3333 mL 1.6664 mL 3.3328 mL
    Please refer to the solubility information to select the appropriate solvent.
    Cell Assay

    HeLa and A549 cells are maintained in Dulbecco's modified Eagle's medium supplemented with 10% fetal bovine serum, 100 units of Penicillin, and 100 μg of Streptomycin/mL. They are cultured at 37°C in a humidified chamber containing 5% CO2. For the induction of apoptosis, cells are plated in 60-mm dishes 1 day prior to Cisplatin (0-30 μM) treatment[1]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration

    Cisplatin is prepared in water (Mice)[3].
    Cisplatin is prepared in physiological saline solution (Rats)[4].

    Mice are divided randomly into three groups (Control, Cisplatin and Cisplatin+HemoHIM), and each group consists of twenty mice. B16F0 melanoma (5×105 cells/mouse) is inoculated into subcutaneous femoral left region of mice at 3 days before an initial injection of Cisplatin. Cisplatin is injected intraperitoneally at 4 mg/kg body weight (B.W.) on day 0, 7 and 14 (total three injections). Experimental group is intubated with HemoHIM at a final concentration of 100 mg/kgB.W. by everyday from day -1 to day 16, while the control group received only water. On day 17 after initial injection of Cisplatin, all mice of each group are experimented, respectively, to evaluate tumor weight or tumor size. The tumor size is calculated as follows: tumor size=ab2/2, where a and b are the larger and smaller diameters, respectively.
    Male Sprague-Dawley rats weighing 200 to 250 g are divided at random into 4 groups of 4 or 5 animals each. The first group (control) received a vehicle (5% carboxymethyl cellulose sodium solution (CMC-Na), 5 mL/kg body wt., p.o.) used for Capsaicin (Cap). The second group received Cap (10 mg/kg/d, p.o.) in 5% CMC-Na (5 mL/kg), and the third received 5% CMC-Na for 6 consecutive days injected with Cisplatin (5 mg/kg in physiological saline solution, i.p.). The fourth group received Cap (10 mg/kg/d, p.o.) in 5% CMC-Na for 6 consecutive days after Cisplatin injection (5 mg/kg, i.p.). For all groups, Cap or vehicle is given twice daily. The selected Cap concentration and the dose administration schedule without inducing any rat intestinal damage are chosen using data from our preliminary experiments. MCE has not independently confirmed the accuracy of these methods. They are for reference only.


    Purity: >99.0%

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