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Cisplatin

MCE China：Cisplatin

Brand：MedChemExpress (MCE)

Cat. No.HY-17394

CAS：15663-27-1

Synonyms：cis-Platinum; CDDP; cis-Diaminodichloroplatinum

Purity：99.84%

Storage：4°C, protect from light *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Shipping：Room temperature in continental US; may vary elsewhere.

Description：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.

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：Cisplatin can be used to induce acute kidney injury models[7][8]. .f12{ font-size: 12px; } .fwb{ font-weight: bold; } .lh22{ line-height: 22px;; } .lh23 { line-height: 23px; } .pl13{ padding-left: 13px;; } .part { margin-top: 18px; } .mold-first-tit { width: 100%; height: 44px; line-height: 44px; background: #F9F7FB; border-bottom: 1px solid #EBE4F6; padding-left: 16px; box-sizing: border-box; margin-bottom: 17px; } .mold-second-tit:before { content:""; width: 6px; height: 6px; display: inline-block; border-radius: 50%; background: rgba(255,102,0,0.4); margin-right: 12px; position: relative; top: -3px; } .lft-border { border-left: 1px dotted #EBE4F6; padding-right: 12px; margin-left: 3px; box-sizing: border-box; padding-bottom: 12px; } /* .part .dec:last-child { border-bottom: 0; } */ .dec { margin: 10px 15px 0; padding-bottom: 10px; border-bottom: 1px dashed #EBE4F6; } .btm-border { border-left: 1px dashed #EBE4F6; } .text-bg { margin-top: 10px; background: #FFFBF1; padding: 14px; border-bottom: 0; position: relative; } .text-note-bg { margin-top: 10px; background: #FFFDF7; padding: 12px; border-bottom: 0; position: relative; } .text-note { width: 51px; height: 20px; line-height: 20px; background: #FFE2AA; text-align: center; border-radius: 0 0 8px 0; position: absolute; top: 0; left: 0; } .text-note-dec { margin-top: 15px;; } Induction of Acute Kidney Injury (AKI)[7][8] Background The pathogenesis of Cisplatin-induced acute kidney injury (AKI) is complex and Oxidative stress, mitochondrial dysfunction, inflammation, and apoptosis are all participating in the progression of Cisplatin-induced AKI.Oxidative stress is a predominant mechanism of injury in cisplatin-induced AKI. Specific Mmodeling Methods Mice: C57BL/6 • male • 6-week-old (period: 2 weeks)Administration: 5 mg/kg • ip • once daily for 2 weeks Note (1) Suggest using male mice as female mice are more resistant to renal injury.(2) Mice can be deprived of food and water for 18 h prior to induction, and food and water are returned after administration.(3) Cisplatin can be dissolved in sterile saline solution to prepare injection working solution while protecting from light. Modeling Indicators Molecular changes: Increased indicators: Serum creatinine (SCr) levels, blood urea nitrogen (BUN) levels, neutrophil gelatinase-associated lipocalin (NGAL), 3-nitrotyrosine. Correlated Product(s): 84-B10 (HY-44307) Opposite Product(s): /

Animal Administration：Mice[3] 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. Rats[4] 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.

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].

IC50 & Target：DNA Alkylator/Crosslinker[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]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> Cisplatin Related Antibodies

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References：

[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]