Cisplatin (CDDP) is an antineoplastic chemotherapy agent by cross-linking with DNA and causing DNA damage in cancer cells. Cisplatin activates ferroptosis and induces autophagy^[1][2][3].

DNA Alkylator/Crosslinker^[1]

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].

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

In melanoma-bearing mice, Cisplatin (CDDP; 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].

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

300.05

Pt(NH₃)₂Cl₂

15663-27-1

Solid

Light yellow to yellow

Cl[Pt](Cl)([NH3])[NH3]

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]. Wang X, et al. Requirement for ERK activation in cisplatin-induced apoptosis. J Biol Chem. 2000 Dec 15;275(50):39435-43.  [Content Brief]

  [2]. Cummings BS, et al. Cisplatin-induced renal cell apoptosis: caspase 3-dependent and -independent pathways. J Pharmacol Exp Ther. 2002 Jul;302(1):8-17.  [Content Brief]

  [3]. Park HR, et al. Enhanced antitumor efficacy of cisplatin in combination with HemoHIM in tumor-bearing mice. BMC Cancer. 2009 Mar 17;9:85.  [Content Brief]

  [4]. Shimeda Y, et al. Protective effects of capsaicin against cisplatin-induced nephrotoxicity in rats. Biol Pharm Bull. 2005 Sep;28(9):1635-8.  [Content Brief]

  [5]. Hall MD, et al. Say no to DMSO: dimethylsulfoxide inactivates cisplatin, NSC 241240, and other platinum complexes. Cancer Res. 2014 Jul 15;74(14):3913-22.  [Content Brief]

  [6]. Wu K, et al. Cisplatin inhibits the progression of bladder cancer by selectively depleting G-MDSCs: A novel chemoimmunomodulating strategy. Clin Immunol. 2018 Aug;193:60-69.  [Content Brief]

  [7]. Noha Alassaf, et al. Autophagy and necroptosis in cisplatin-induced acute kidney injury: Recent advances regarding their role and therapeutic potential. Front Pharmacol. 2023 Jan 30:14:1103062.  [Content Brief]

  [8]. Ryan M Williams, et al. Kidney-Targeted Redox Scavenger Therapy Prevents Cisplatin-Induced Acute Kidney Injury. Front Pharmacol. 2022 Jan 3:12:790913.  [Content Brief]