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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Cisplatin is a highly effective and broad-spectrum chemotherapeutic agent [1].
Cisplatin is an anticancer agent with some side effects. It is believed to induce apoptosis through several mechanisms. The traditional mechanism is that cisplatin enters the cell, interacts with the DNA guanine bases and forms the inter- or intra-strand chain cross-linking, then prevents the replication of DNA. This formation can also induce apoptosis by activating p53. Cisplatin was also found to cause ROS generation and increase lipid peroxidation, which leads cells to the apoptotic pathway. In addition, cisplatin induces apoptosis with the caspase-dependent pathway. In cochlear cells, cisplatin treatment results in the increase of caspases-3 and -9 and causes the cochlear damage side effect [1].
References:[1] Casares C, Ramírez-Camacho R, Trinidad A, et al. Reactive oxygen species in apoptosis induced by cisplatin: review of physiopathological mechanisms in animal models. European Archives of Oto-Rhino-Laryngology, 2012, 269(12): 2455-2459.
Cell lines
L1210/0 cells
Preparation method
The solubility of this compound in DMF is >12.5 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.
Reaction Conditions
0, 0.5, 1, 2, 4 and 8 μg/mL; 2 hrs
Applications
At low concentrations, Cisplatin induced minimal cell death. At higher concentrations, cell death was obvious with only 4% viability. By 10 days after incubation, these few survivors begun to grow and became the predominant cells in the population.
Animal models
Nude mice bearing human ovarian cancer OVCAR-3 cell xenografts
Dosage form
5 mg/kg, i.v.; at day 0 and day 7
Cisplatin (5 mg/kg) given at the day 0 and 7 induced a tumor growth inhibition (GI) (85.1%) of the OVCAR-3 cell xenografts.
Other notes
Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.
References:
[1]. Sorenson CM, Eastman A. Mechanism of cis-diamminedichloroplatinum(II)-induced cytotoxicity: role of G2 arrest and DNA double-strand breaks. Cancer Res. 1988 Aug 15;48(16):4484-8.
[2]. Molthoff CF, Pinedo HM, Schlüper HM, Rutgers DH, Boven E. Comparison of 131I-labelled anti-episialin 139H2 with cisplatin, cyclophosphamide or external-beam radiation for anti-tumor efficacy in human ovarian cancer xenografts. Int J Cancer. 1992 Apr 22;51(1):108-15.
