Nedaplatin - CAS 95734-82-0
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Not Intended for Therapeutic Use. For research use only.
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Nedaplatin is a derivative of cisplatin and DNA damage agent for tumor colony forming units with IC50 of 94 μM.
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1.Phase I trial of nedaplatin chemotherapy concurrent with radiotherapy for untreated locoregionally advanced nasopharyngeal carcinoma.
Liang Z1,2, Wang S2, Lin Z3, Feng S4, Cheng Z2, Yang Y1, Kuang Y1, Fidelis C1, Ullah S1, Li F5,6. Cancer Chemother Pharmacol. 2016 Mar;77(3):643-51. doi: 10.1007/s00280-016-2971-4. Epub 2016 Jan 30.
PURPOSE: In this phase I study, single-agent chemotherapy was conducted in patients with locoregionally advanced nasopharyngeal carcinoma (NPC) using nedaplatin (NDP) and concomitant radiotherapy. The study sought to determine the maximum tolerated dose (MTD), recommended dose (RD) and the clinical efficacy of this treatment in locoregionally advanced NPC patients.
2.The role of the equatorial ligands for the redox behavior, mode of cellular accumulation and cytotoxicity of platinum(IV) prodrugs.
Göschl S1, Varbanov HP2, Theiner S3, Jakupec MA4, Galanski M1, Keppler BK3. J Inorg Biochem. 2016 Mar 17. pii: S0162-0134(16)30069-1. doi: 10.1016/j.jinorgbio.2016.03.005. [Epub ahead of print]
The current study aims to elucidate the possible reasons for the significantly different pharmacological behavior of platinum(IV) complexes with cisplatin-, carboplatin- or nedaplatin-like cores and how this difference can be related to their main physicochemical properties. Chlorido-containing complexes are reduced fast (within hours) by ascorbate and are able to unwind plasmid DNA in the presence of ascorbate, while their tri- and tetracarboxylato analogs are generally inert under the same conditions. Comparison of the lipophilicity, cellular accumulation and cytotoxicity of the investigated platinum compounds revealed the necessity to define new structure-property/activity relationships (SPRs and SARs). The higher activity and improved accumulation of platinum(IV) complexes bearing Cl- in equatorial position cannot only be attributed to passive diffusion facilitated by their lipophilicity. Therefore, further platinum accumulation experiments under conditions where active/facilitated transport mechanisms are suppressed were performed.
3.Phase II trial of neoadjuvant chemotherapy with docetaxel, nedaplatin, and S1 for advanced esophageal squamous cell carcinoma.
Tanaka Y1, Yoshida K1, Tanahashi T1, Okumura N1, Matsuhashi N1, Yamaguchi K1. Cancer Sci. 2016 Apr 7. doi: 10.1111/cas.12943. [Epub ahead of print]
Although standard chemotherapy for esophageal cancer patients is fluorouracil and cisplatin (FP), the prognosis is still unsatisfactory. A new therapeutic regimen combining docetaxel, cisplatin, and 5-Fu (DCF) was recently developed to improve both local and distant tumor control. We developed a new regimen of docetaxel, nedaplatin, and S1 (DGS) and previously reported the recommended dose in a Phase I dose-escalation study. We then performed a phase II study of DGS for advanced esophageal squamous cell carcinoma (SCC). Patients with clinical stage II/III were eligible. Patients received two courses of chemotherapy: docetaxel 35 mg/m2 with nedaplatin 40 mg/m2 on day 8, 80 mg/m2 S1 on days 1-14, and 2 weeks off. After completion of chemotherapy, patients underwent esophagectomy. The primary endpoint was the completion rate of protocol treatment (completion of two courses of preoperative chemotherapy and R0 surgery). We enrolled 32 patients.
4.Nedaplatin sensitization of cisplatin-resistant human non-small cell lung cancer cells.
Wang H1, Zhu X1, Huang J1, Chen P2, Han S1, Yan X1. Oncol Lett. 2016 Apr;11(4):2566-2572. Epub 2016 Feb 24.
Cisplatin (DDP) has been one of the most widely used chemotherapy drugs for advanced non-small cell lung cancer. However, the increase in the number of DDP-resistant cancer cells has become a major impediment in the clinical management of cancer. In the present study, for the first time, the 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide assay was used to demonstrate that nedaplatin (NDP) could have a stronger inhibitory effect than DDP alone in DDP-resistant A549 (A549DDP) cells and that it could attenuate the resistance of these cells. Additionally, flow cytometry analysis showed that the apoptosis rate of these resistant cells when exposed to NDP was markedly increased and the number of cells in the G2 stage of the cell cycle was significantly increased. Furthermore, western blot analysis indicated that NDP decreased the protein expression of P-glycoprotein, tumor protein p53 and B-cell lymphoma 2, and increased the expression of Bcl-2-associated X protein, all of which could possibly improve the NDP intracellular drug concentration and promote cell apoptosis.
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CAS 95734-82-0 Nedaplatin

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