Network Version
Cisplatin Data Sheet
| Product Name: | Cisplatin |
 |
|---|---|---|
| CAS No.: | 15663-27-1 | |
| Cat. No.: | HY-17394 | |
| MWt: | 300.05 | |
| Formula: | Pt(NH₃)₂Cl₂ | |
| Purity : | >98% | |
| Solubility: | DMSO : ≥ 300 mg/mL;H<sub>2</sub>O : 1 mg/mL (ultrasonic;warming;heat to 60°C);DMF : 10 mg/mL (ultrasonic;warming;heat to 60°C) | |
| Mechanisms: | Target: Cancer | |
| Biological Activity: | ||
|
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].
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]. 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 nitrogen by about 132, 315, 797, and 556% in comparison with the control rats, respectively[4]. Note:
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 Modeling 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)
|
||
1 Deer Park Dr, Suite F, Monmouth Junction, NJ 08852, USA
Tel: 609-228-6898 Fax: 609-228-5909 Email: [email protected] Web:www.medchemexpress.com