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Cisplatin

CAS: 15663-27-1 F: Cl2H6N2Pt W: 300.05

Cisplatin (CDDP) is an antineoplastic chemotherapy agent by cross-linking with DNA and causing DNA damage in cancer cell
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Bioactivity 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].
Target DNA Alkylator/Crosslinker
Invitro 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 (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 nitrogenby about 132, 315, 797, and 556% in comparison with the control rats, respectively[4].
Name Cisplatin
CAS 15663-27-1
Formula Cl2H6N2Pt
Molar Mass 300.05
Appearance Solid
Transport Room temperature in continental US; may vary elsewhere.
Storage

4°C, protect from light

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

Reference [1]. Wang X, et al. Requirement for ERK activation in cisplatin-induced apoptosis. J Biol Chem. 2000 Dec 15;275(50):39435-43. [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. [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. [4]. Shimeda Y, et al. Protective effects of capsaicin against cisplatin-induced nephrotoxicity in rats. Biol Pharm Bull. 2005 Sep;28(9):1635-8. [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. [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.