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Journal articles on the topic 'Satraplatin'

Author: Grafiati

Published: 19 October 2022

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1

Lamphere, L., F. Obermayr, M. Caligiuri, G. Unteregger, M. S. Rudoltz, K. Wosikowksi, and A. M. Casazza. "Satraplatin, an oral platinum analog, is active and synergistic with paclitaxel and docetaxel in prostate carcinoma models." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 14620. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.14620.

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14620 Background: Satraplatin is a novel oral platinum analog with potent cytotoxic and antitumor activity in preclinical models. Satraplatin showed activity in hormone refractory prostate cancer (HRPC) and other tumor types in Phase II trials. A pivotal Phase III trial evaluating satraplatin as 2nd-line therapy for HRPC completed accrual of > 900 patients in 2005. Satraplatin’s activity, safety profile and ease of administration make it attractive for combination regimens. Methods: Satraplatin and its active metabolite JM-118 were tested in vitro as single agents in the androgen-sensitive LNCaP and the androgen-insensitive PC-3 and DU-145 human prostate carcinoma (ca.) cell lines. For in vitro combination studies, PC-3 cells were treated with satraplatin or JM-118 either prior to, after, or concomitantly with paclitaxel or docetaxel. The PC-3 cell line was used for in vivo xenograft experiments in nude mice. Paclitaxel was given intravenously on Day 1, satraplatin orally on Days 2 to 6, and paclitaxel again on Day 8. Results: Satraplatin and JM-118 as single agents inhibited the growth of all three prostate ca. cell lines in vitro in a dose dependent fashion. IC50 values for JM-118 were < 1μM. Strong synergism was noted when PC-3 tumor cells were treated in vitro with paclitaxel or docetaxel followed by satraplatin or JM-118. Satraplatin administered orally inhibited the growth of PC-3 xenografts in nude mice. Treatment of advanced PC-3 tumors with paclitaxel (40 mg/kg) and satraplatin (35 mg/kg) was well tolerated and resulted in a Tumor Growth Delay equivalent to 3 Log Cell Kill, an effect superior to that of the single agents. Conclusions: In vitro, satraplatin and its metabolite JM-118 are active as single agents against human prostate ca. cells, and are synergistic with taxanes. In vivo, treatment with paclitaxel followed by satraplatin showed synergism without increased toxicity. These preclinical data support ongoing Phase I and II clinical trials that are evaluating combinations of satraplatin with paclitaxel or docetaxel. [Table: see text]

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2

&NA;. "Satraplatin." Drugs in R & D 8, no. 2 (2007): 125–32. http://dx.doi.org/10.2165/00126839-200708020-00008.

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&NA;. "Satraplatin." Drugs in R & D 3, no. 1 (2002): 67–71. http://dx.doi.org/10.2165/00126839-200203010-00017.

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4

Sonpavde, G., and C. N. Sternberg. "Satraplatin." Drugs of the Future 34, no. 12 (2009): 962. http://dx.doi.org/10.1358/dof.2009.034.12.1414781.

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5

Sternberg, Cora N., Daniel P. Petrylak, Oliver Sartor, J. Alfred Witjes, Tomasz Demkow, Jean-Marc Ferrero, Jean-Christophe Eymard, et al. "Multinational, Double-Blind, Phase III Study of Prednisone and Either Satraplatin or Placebo in Patients With Castrate-Refractory Prostate Cancer Progressing After Prior Chemotherapy: The SPARC Trial." Journal of Clinical Oncology 27, no. 32 (November 10, 2009): 5431–38. http://dx.doi.org/10.1200/jco.2008.20.1228.

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Purpose This multinational, double-blind, randomized, placebo-controlled, phase III trial assessed the efficacy and tolerability of the oral platinum analog satraplatin in patients with metastatic castrate-refractory prostate cancer (CRPC) experiencing progression after one prior chemotherapy regimen. Patients and Methods Nine hundred fifty patients were randomly assigned (2:1) to receive oral satraplatin (n = 635) 80 mg/m2 on days 1 to 5 of a 35-day cycle and prednisone 5 mg twice daily or placebo (n = 315) and prednisone 5 mg twice daily. Primary end points were progression-free survival and overall survival (OS). The secondary end point was time to pain progression (TPP). Results A 33% reduction (hazard ratio [HR] = 0.67; 95% CI, 0.57 to 0.77; P < .001) was observed in the risk of progression or death with satraplatin versus placebo. This effect was maintained irrespective of prior docetaxel treatment. No difference in OS was seen between the satraplatin and placebo arms (HR = 0.98; 95% CI, 0.84 to 1.15; P = .80). Compared with placebo, satraplatin significantly reduced TPP (HR = 0.64; 95% CI, 0.51 to 0.79; P < .001). Satraplatin was generally well tolerated, although myelosuppression and GI disorders occurred more frequently with satraplatin. Conclusion Oral satraplatin delayed progression of disease and pain in patients with metastatic CRPC experiencing progression after initial chemotherapy but did not provide a significant OS benefit. Satraplatin was generally well tolerated. These results suggest activity for satraplatin in patients with CRPC who experience progression after initial chemotherapy.

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Ivanova, Stefka. "Comparative assessment of clinical trials, indications, pharmacokinetic parameters and side effects of approved platinum drugs." Pharmacia 69, no. 1 (January 5, 2022): 1–7. http://dx.doi.org/10.3897/pharmacia.69.e78813.

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Platinum complexes are among the most commonly applied anticancer agents. The aim of current work is collection, analysing and comparative estimation of clinical trials and pharmacological indications of currently approved for application platinum detivatives: Cisplatin, Carboplatin, Oxaliplatin, Nedaplatin (Japan), Lobaplatin (China), Heptaplatin (North Korea), and Satraplatin. The other aim of the study includes the summarizing of the hystoric data for the stages of the developlement of these drugs, and the comparison of pharmacokimetic parameters, side effecs and the dose-liniting factors of the drugs. The observational study on pharmacokinetic parameters shows that protein binding decreases in order: 95% (Cisplatn); 90% (Oxaliplatin); 50% (Nedaplatin); low (Carboplatin). For every of Cisplatin, Carboplatin, Oxaliplatin have been reported more than 1000 clinical trials; for Lobaplatin, Nedaplatin, Satraplatin - about 10 trials. The differenses in dose-limiting effects are: neuro-, nephro-, ototoxicity (Cisplatin); neurotoxicity (Oxaliplatin); nephrotoxicity (Heptaplatin); myelosuppression: thrombocytopenia, neutropenia, leukopenia (Carboplatin, Nedaplatin, Satraplatin).

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Olszewski-Hamilton, U., M. Svoboda, T. Thalhammer, V. Buxhofer-Ausch, K. Geissler, and G. Hamilton. "Organic Anion Transporting Polypeptide 5A1 (OATP5A1) in Small Cell Lung Cancer (SCLC) Cells: Possible Involvement in Chemoresistance to Satraplatin." Biomarkers in Cancer 3 (January 2011): BIC.S7151. http://dx.doi.org/10.4137/bic.s7151.

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Background The role of organic anion transporting polypeptide 5A1 (OATP5A1) a member of a family of drug transporters that mediate cellular uptake of drugs has not been characterized so far. Methods Gene expression levels of OATP5A1 in small cell lung cancer (SCLC) cell lines were determined by real-time qPCR and chemosensitivity of HEK-293- SLCO5A1-transfected cells to satraplatin in MTT assays. Results Significant expression of this transporter was found at the mRNA level, primarily in drug-resistant SCLC cells, and SLCO5A1-transfected HEK-293 cells showed higher resistance to satraplatin. OATP5A1 is found preferentially in cytoplasmic membranes of tumor cells, including SCLC. Conclusions OATP5A1 seems to effect intracellular transport of drugs and may participate in chemoresistance of SCLC by sequestration, rather than mediating cellular uptake. Since satraplatin failed to improve survival in SCLC patients, the relation of OATP5A1 expression to clinical drug resistance and its use as marker of chemoresistance should be further investigated.

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Obreshkova, Danka, Stefka Ivanova, and Pavlina Yordanova-Laleva. "Influence of chemical structure and mechanism of hydrolysis on pharmacological activity and toxicological profile of approved platinum drugs." Pharmacia 69, no. 3 (July 19, 2022): 645–53. http://dx.doi.org/10.3897/pharmacia.69.e87494.

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The problems with platinum complexes are resistance and toxicity of anticancer therapy. The aim of current study is the comparison of the influence of chemical structure and mechanism of hydrolysis on pharmacological activity and toxicological profile of approved in platinum drugs: Cisplatin, Carboplatin, Oxaliplatin, Nedaplatin, Lobaplatin, Heptaplatin, Satraplatin. Hydrolysis of Carboplatin and Nedaplatin occurs by double step hydration, to obtain the same active products as with Cisplatin: diaqudiamine-platinum. The similarity in mechanisms of hydrolysis of Oxaliplatin, Lobaplatin Heptaplatin, and Satraplatin is that the first part of the hydrolysis corresponds to the ring-opening and addition of the first water molecule, and in the second step of reaction occur the loss of the ligand and the formation of the di-aquated product by the addition of a second water molecule. Cisplatin, Carboplatin, and Oxaliplatin are nephrotoxic. Cisplatin and Heptaplatin are nephrotoxic. The similar dose-limiting effects of Carboplatin, Oxaliplatin, Nedaplatin, Lobaplatin, and Satraplatin is myelosuppression.

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Akshintala, Srivandana, Leigh Marcus, Katherine E. Warren, Robert F. Murphy, Wendy J. Goodspeed, Anne Goodwin, Carmen C. Brewer, et al. "Phase I trial and pharmacokinetic (PK) study of satraplatin in children and young adults with refractory solid tumors including brain tumors." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 2554. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.2554.

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2554 Background: Satraplatin is an orally bioavailable platinum analog. Based on pre-clinical activity (IC500.02-8 µg/ml) including activity in cisplatin resistant cell lines, and clinical activity without neuro-, nephro-, or ototoxicity in adults with refractory tumors, we developed a phase 1 trial to determine the toxicities, maximum tolerated dose (MTD), and PKs of satraplatin in children with refractory solid tumors. Methods: Satraplatin (10 and 50 mg capsules) was administered orally once daily on days 1 - 5 of a 28 day cycle to cohorts of 3-6 patients (pts) at 60 mg/m2/dose (DL 1) and 80 mg/m2/dose (DL 2). Plasma ultrafiltrate (PUF) platinum was measured using atomic absorption spectroscopy during cycle 1 for PK analysis. Results: 9 pts [5 male, 4 female, median age 17 years (range 8-19)] with malignant glioma (n=4), ependymoma (n=2), medulloblastoma (n=1), osteosarcoma (n=1), or hepatoblastoma (n=1) received 1-10+ cycles (median 2). The MTD was exceeded at DL 2 as 2/4 pts had dose limiting toxicities (DLT) of delayed and prolonged myelosuppression (grade 3 thrombocytopenia, n=1; grade 3-4 neutropenia, n=2). 0/5 pts at DL 1 had DLTs. Grade 1 ototoxicity was seen in 1 pt at cycle 10. Non-DLTs included myelosuppression, gastrointestinal toxicities, fatigue, headache, liver enzyme elevation, and electrolyte abnormalities. No objective responses were observed, but 1 pt with gliomatosis cerebri has had radiographic stable disease through cycle 10+. Satraplatin mean exposure (AUC) and peak concentration (Cmax) were similar at both dose levels [day 1 PUF AUC0-24h 1.22 ± 0.55 µg/ml*h at DL1 (n=3), 1.02 ± 0.45 µg/ml*h at DL2 (n=3); Cmax0.17 ± 0.08 µg/ml at DL 1 (n=3), 0.16 ± 0.05 µg/ml at DL 2 (n=3)]. Terminal half-life was 14 ± 6 h and apparent clearance was 76 ± 29 L/h (n=6). Conclusions: The MTD of oral satraplatin in children with solid tumors is 60 mg/m2/dose daily x 5 q28 days. The toxicity profile was similar to adults, and delayed myelosuppression was DLT. Satraplatin exposure appears higher in pediatric pts compared to adults (PUF AUC0-24h 0.25-0.47 µg/ml*h at 60-80 mg/m2/dose). DL 1 will be expanded to gain additional experience regarding toxicities and PKs in a broader age range. Clinical trial information: NCT01259479.

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Liaw, Bobby Chi-Hung, Sonia Maria Seng, Matt D. Galsky, Che-Kai Tsao, Phillip G. Febbo, and William K. Oh. "Biomarker development trial of satraplatin in patients with metastatic castrate-resistant prostate cancer." Journal of Clinical Oncology 32, no. 4_suppl (February 1, 2014): 170. http://dx.doi.org/10.1200/jco.2014.32.4_suppl.170.

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170 Background: While satraplatin, a fourth generation oral platinum analogue, failed to improve overall survival (OS) in an unselected metastatic castrate-resistant prostate cancer (mCRPC) population (Sternberg, JCO 2009), anti-tumor activity was demonstrated, suggesting a “platinum-sensitive” subset of patients. Predictive biomarkers may not only select patients most likely to benefit from novel “targeted” therapies but also from standard (even discarded) cytotoxic agents. Development of predictive biomarkers in mCRPC is hampered by the fact that PC is associated with a long natural history and evolving genetic changes, highlighting the need for immediate pre-treatment metastatic tissue samples for biomarker development. In this trial, we sought to determine the feasibility of obtaining metastatic biopsies in patients with mCRPC treated with satraplatin. Methods: Docetaxel-refractory mCRPC patients underwent image-guided biopsy of metastatic lesions prior to treatment with satraplatin 80 mg/m2 PO on days 1 to 5 of a 35-day cycle and prednisone 5 mg PO twice daily. Biopsy samples are analyzed by whole exome and RNA sequencing, and peripheral blood samples are undergoing transcriptional profiling, to facilitate biomarker development. Results: Thirteen patients were enrolled with a median age of 71 (range: 55 to 80), prostate-specific antigen (PSA) of 82 ng/ml (0.04-3057), and Gleason score 8 (7 to 9). All patients received prior docetaxel, four (31%) had more than or eqaul to two prior chemotherapies, and two (15%) received abiraterone. Drug-related grade 3/4 toxicities included leukopenia (23%), neutropenia (8%), thrombocytopenia (8%), fatigue (8%), renal failure (8%), dysphagia (17%), and diarrhea (8%). A median of four cycles of satraplatin were completed, with declines of serum PSA of greater than or equal to 30% achieved in 4 of 13 patients (31%; 95% CI, 57.3 to 85.4%). Median time to PSA progression was 12.4 weeks (95% CI, 7.2 to 29.7+ weeks). Metastatic pre-treatment biopsies were collected in all study patients; genomic analysis is ongoing. Conclusions: This study confirms that satraplatin has anti-cancer activity in a subset of patients with mCRPC. Trials that require pre-treatment metastatic tumor biopsies are feasible. Analysis of the correlation between molecular signatures and treatment response will be presented at the meeting. Clinical trial information: NCT01289067.

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Kerr, Cathel. "Satraplatin for hormone-refractory prostate cancer." Lancet Oncology 8, no. 4 (April 2007): 290. http://dx.doi.org/10.1016/s1470-2045(07)70096-7.

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12

Hutchinson, Lisa. "Satraplatin delays progression in prostate cancer." Nature Reviews Clinical Oncology 7, no. 2 (February 2010): 69. http://dx.doi.org/10.1038/nrclinonc.2009.230.

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Hutchinson, Lisa. "Satraplatin delays progression in prostate cancer." Nature Reviews Urology 7, no. 2 (February 2010): 59. http://dx.doi.org/10.1038/nrclinonc.2009.230x.

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Doshi, Gury, Guru Sonpavde, and Cora N. Sternberg. "Clinical and pharmacokinetic evaluation of satraplatin." Expert Opinion on Drug Metabolism & Toxicology 8, no. 1 (November 19, 2011): 103–11. http://dx.doi.org/10.1517/17425255.2012.636352.

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Zhang, Jian-Qiang, Ke Li, Kun-Ming Jiang, Yan-Wei Cong, Shao-Ping Pu, Xiao-Guang Xie, Yi Jin, and Jun Lin. "Development of an oral satraplatin pharmaceutical formulation by encapsulation with cyclodextrin." RSC Advances 6, no. 21 (2016): 17074–82. http://dx.doi.org/10.1039/c5ra27182g.

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A novel water-soluble oral satraplatin/β-cyclodextrin inclusion complex was prepared and characterized with a variety of techniques. The inclusion complex showed much higher antitumor activity in vitro cytotoxicity test and in vivo antitumor test.

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&NA;. "Satraplatin shows benefit in refractory prostate cancer." Inpharma Weekly &NA;, no. 1641 (June 2008): 4. http://dx.doi.org/10.2165/00128413-200816410-00008.

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Heidenreich, A. "Satraplatin in der Sekundärtherapie des kastrationsresistenten Prostatakarzinoms." Der Onkologe 16, no. 3 (February 7, 2010): 314–15. http://dx.doi.org/10.1007/s00761-010-1784-z.

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&NA;. "Satraplatin EU marketing authorisation application to be withdrawn." Inpharma Weekly &NA;, no. 1649 (August 2008): 22. http://dx.doi.org/10.2165/00128413-200816490-00074.

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&NA;. "Satraplatin increases progression-free survival in prostate cancer." Inpharma Weekly &NA;, no. 1557 (September 2006): 7. http://dx.doi.org/10.2165/00128413-200615570-00020.

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Karmakar, Subhendu, Isabella Poetsch, Christian R. Kowol, Petra Heffeter, and Dan Gibson. "Synthesis and Cytotoxicity of Water-Soluble Dual- and Triple-Action Satraplatin Derivatives: Replacement of Equatorial Chlorides of Satraplatin by Acetates." Inorganic Chemistry 58, no. 24 (December 2, 2019): 16676–88. http://dx.doi.org/10.1021/acs.inorgchem.9b02796.

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Sonpavde, Guru, and Cora N. Sternberg. "Satraplatin for the therapy of castration-resistant prostate cancer." Future Oncology 5, no. 7 (September 2009): 931–40. http://dx.doi.org/10.2217/fon.09.84.

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Pu, Shao Ping, Yan Wei Cong, Wen Gui Gao, Jin Hu, Qing Kun Wang, and Jia Lin Sun. "Preparation and Characterization of Satraplatin - A New Bioactivity Material." Advanced Materials Research 233-235 (May 2011): 1192–97. http://dx.doi.org/10.4028/www.scientific.net/amr.233-235.1192.

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Satraplatin is a platinum coordination with antitumour activity, which is the first platinum-based antitumour drug administrated by oral route. The phase III clinical trial used in the treatment of patients with hormone-refractory prostate cancer of Ssatraplatin has been finished. Its prepararation method was introduced in this paper, and its chemical structure was identified by using the modern apparatus analysis means such as elemental analyses, mass spectrum, infrared spectrum and nuclear magnetic resonance spectrum. The results showed that its composition and structure were consistent with the theoretical one

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McKeage, M., J. Carr, and M. Tingle. "555 Metabolic activation of satraplatin by haemoglobin in vitro." European Journal of Cancer Supplements 2, no. 8 (September 2004): 169. http://dx.doi.org/10.1016/s1359-6349(04)80563-9.

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24

Sternberg, Cora N. "Satraplatin in the treatment of hormone-refractory prostate cancer." BJU International 96, no. 7 (November 2005): 990–94. http://dx.doi.org/10.1111/j.1464-410x.2005.05799.x.

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25

Wu, Yao, and Rebecca Y. Lai. "Electrochemical Detection of Platinum(IV) Prodrug Satraplatin in Serum." Analytical Chemistry 87, no. 21 (October 26, 2015): 11092–97. http://dx.doi.org/10.1021/acs.analchem.5b03215.

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Bhargava, Ashish, and Ulka N. Vaishampayan. "Satraplatin: leading the new generation of oral platinum agents." Expert Opinion on Investigational Drugs 18, no. 11 (November 2009): 1787–97. http://dx.doi.org/10.1517/13543780903362437.

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27

Wosikowski, Katja, Lou Lamphere, Gerhard Unteregger, Volker Jung, Faith Kaplan, Jimmy P. Xu, Benno Rattel, and Maureen Caligiuri. "Preclinical antitumor activity of the oral platinum analog satraplatin." Cancer Chemotherapy and Pharmacology 60, no. 4 (May 31, 2007): 589–600. http://dx.doi.org/10.1007/s00280-007-0502-z.

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McKeage, Mark J. "Satraplatin in Hormone-Refractory Prostate Cancer and Other Tumour Types." Drugs 67, no. 6 (2007): 859–69. http://dx.doi.org/10.2165/00003495-200767060-00003.

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Selting, K. A., X. Wang, D. L. Gustafson, C. J. Henry, J. A. Villamil, D. L. McCaw, D. Tate, M. Beittenmiller, C. Garnett, and J. D. Robertson. "Evaluation of Satraplatin in Dogs with Spontaneously Occurring Malignant Tumors." Journal of Veterinary Internal Medicine 25, no. 4 (May 12, 2011): 909–15. http://dx.doi.org/10.1111/j.1939-1676.2011.0727.x.

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30

Laino, Charlene. "Oral Platinum Drug Satraplatin Shows Promise for Refractory Prostate Cancer." Oncology Times 29, no. 8 (April 2007): 33. http://dx.doi.org/10.1097/01.cot.0000269633.04157.5f.

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Leal, T. B., G. Wilding, J. Eickhoff, D. McNeel, D. Alberti, and G. Liu. "Phase I study of satraplatin and docetaxel in solid malignancies." Journal of Clinical Oncology 26, no. 15_suppl (May 20, 2008): 2570. http://dx.doi.org/10.1200/jco.2008.26.15_suppl.2570.

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ZANDER, THILO, JIA XUE, GABRIEL MARKSON, FELIX DAHM, and CHRISTOPH RENNER. "Satraplatin Demonstrates High Cytotoxic Activity Against Genetically Defined Lymphoid Malignancies." Anticancer Research 42, no. 4 (March 28, 2022): 1821–32. http://dx.doi.org/10.21873/anticanres.15658.

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Choy, Hak. "Satraplatin: an orally available platinum analog for the treatment of cancer." Expert Review of Anticancer Therapy 6, no. 7 (July 2006): 973–82. http://dx.doi.org/10.1586/14737140.6.7.973.

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Fuerst, Mark L. "Satraplatin on Fast Track for Approval for Hormone-Refractory Prostate Cancer." Oncology Times 29, no. 2 (January 2007): 39. http://dx.doi.org/10.1097/01.cot.0000265647.12509.ad.

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Kelland, Lloyd R. "An update on satraplatin: the first orally available platinum anticancer drug." Expert Opinion on Investigational Drugs 9, no. 6 (June 2000): 1373–82. http://dx.doi.org/10.1517/13543784.9.6.1373.

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Choy, H., C. Park, and M. Yao. "Current Status and Future Prospects for Satraplatin, an Oral Platinum Analogue." Clinical Cancer Research 14, no. 6 (March 15, 2008): 1633–38. http://dx.doi.org/10.1158/1078-0432.ccr-07-2176.

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Carr, Jocelyn, Malcolm Tingle, and Mark McKeage. "Rapid biotransformation of satraplatin by human red blood cells in vitro." Cancer Chemotherapy and Pharmacology 50, no. 1 (July 1, 2002): 9–15. http://dx.doi.org/10.1007/s00280-002-0462-2.

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Carr, Jocelyn L., Malcolm D. Tingle, and Mark J. McKeage. "Satraplatin activation by haemoglobin, cytochrome C and liver microsomes in vitro." Cancer Chemotherapy and Pharmacology 57, no. 4 (September 20, 2005): 483–90. http://dx.doi.org/10.1007/s00280-005-0069-5.

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Sartor, A. O., D. P. Petrylak, J. A. Witjes, W. R. Berry, G. S. Chatta, D. J. Vaughn, J. Ferrero, T. Demkow, J. C. Eymard, and C. N. Sternberg. "Satraplatin in patients with advanced hormone-refractory prostate cancer (HRPC): Overall survival (OS) results from the phase III satraplatin and prednisone against refractory cancer (SPARC) trial." Journal of Clinical Oncology 26, no. 15_suppl (May 20, 2008): 5003. http://dx.doi.org/10.1200/jco.2008.26.15_suppl.5003.

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40

Hamilton, G., R. Zeillinger, E. Ulsperger, K. Geissler, and U. Olszewski. "1083 In vitro comparison of the platinum (IV) drugs oxoplatin and satraplatin." European Journal of Cancer Supplements 7, no. 2 (September 2009): 110. http://dx.doi.org/10.1016/s1359-6349(09)70376-3.

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Nathan, F. E., C. Sternberg, O. Sartor, D. Petrylak, F. Witjes, K. Wosikowski, M. E. Petrone, and M. Rozencweig. "Satraplatin: A new treatment option for patients with hormone refractory prostate cancer." Journal of Clinical Oncology 23, no. 16_suppl (June 2005): 4802. http://dx.doi.org/10.1200/jco.2005.23.16_suppl.4802.

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Swancutt, Katy L., Stephen P. Mezyk, and James J. Kiddle. "Free Radical-Induced Redox Chemistry of Nedaplatin and Satraplatin under Physiological Conditions." Radiation Research 173, no. 6 (June 2010): 843–48. http://dx.doi.org/10.1667/rr2081.1.

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Hong, D. S., M. Galsky, E. Chiorean, D. Mulkerian, D. Greene, F. E. Nathan, M. Petrone, and L. H. Camacho. "Phase I study of the effects of renal impairment on the pharmacokinetic (PK) and safety of satraplatin in patients (Pts) with refractory non-hematologic cancer." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 2044. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.2044.

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2044 Background: Satraplatin (S) is a novel oral platinum analog with demonstrated activity in the treatment of pts with platinum-sensitive malignancies. A worldwide, double-blind, placebo-controlled randomized trial evaluating S as 2nd line therapy for hormone refractory prostate cancer (HRPC) has recently completed enrollment. The current study wasis designed to understand the effect of varying degrees of renal impairiment on the safety and PK of satraplatin. Methods: The study includes 4 levels of renal dysfunction, and 8 pts/cohort: Group 1 (G1) = Normal Renal Controls; G2 = Mild renal impairment (CrCl 50–80 mL/min); G3 = Mod. impairment (CrCl 30-<50 ml/min); G4 = Severe impairment (CrCl <30 mL/min). S was administered orally at 80mg/m2/d on d1–5 every 35 days. Results: 21 pts (of a planned total of 32) have been enrolled (13M/8F), median age 63 (range 45–72). Tumor types: Bladder (6), Renal (3), Breast (2), Prostate (2), Colon (2), Other (6). Among 15 evaluable pts, the cohort distribution is G1: 6 pts, G2: 4, G3: 4, and G4: 1. Twenty-six cycles of S have been delivered, and 11 pts have completed at least 2 cycles of therapy. Hematologic toxicities during the first 2 cycles include grade (G) 3/4 neutropenia (0 pts), G 3/4 thrombocytopenia (1), and G 3/4 anemia (1). No significant cardiac, renal, hepatic, or neurologic toxicity has been observed. Nausea, vomiting, and diarrhea were mild to moderate, and controlled with oral therapy. Of 4 pts with evaluable disease, 1 has stable disease, and 3 have progressed. Conclusions: S is well tolerated in pts with varying degrees of renal dysfunction. Updated safety and PK data will be presented at the meeting. [Table: see text]

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44

Avan, Abolfazl, Auke Adema, Eveline Hoebe, Charlotte Huijts, Amir Avan, Gareth Veal, Rob Ruijtenbeek, Katja Wosikowski, and Godefridus Peters. "Modulation of Signaling Enhances the Efficacy of the Combination of Satraplatin and Erlotinib." Current Drug Targets 15, no. 14 (December 16, 2014): 1312–21. http://dx.doi.org/10.2174/1389450115666141107110321.

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Šebesta, Filip, Katarína Baxová, and Jaroslav V. Burda. "Redox Potentials for Tetraplatin, Satraplatin, Its Derivatives, and Ascorbic Acid: A Computational Study." Inorganic Chemistry 57, no. 3 (January 24, 2018): 951–62. http://dx.doi.org/10.1021/acs.inorgchem.7b01894.

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Fromer, Margot J. "ODAC Recommends Deferral of Decision on Satraplatin Until All Survival Data Are Available." Oncology Times 29, no. 16 (August 2007): 10. http://dx.doi.org/10.1097/01.cot.0000288875.02501.8c.

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Bradáč, Ondřej, Tomáš Zimmermann, and Jaroslav V. Burda. "Can Satraplatin be hydrated before the reduction process occurs? The DFT computational study." Journal of Molecular Modeling 19, no. 11 (May 30, 2012): 4669–80. http://dx.doi.org/10.1007/s00894-012-1442-z.

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Berthold, Dominik R., Cora N. Sternberg, and Ian F. Tannock. "Management of Advanced Prostate Cancer After First-Line Chemotherapy." Journal of Clinical Oncology 23, no. 32 (November 10, 2005): 8247–52. http://dx.doi.org/10.1200/jco.2005.03.1435.

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Hormone refractory prostate cancer (HRPC) causes substantial morbidity and mortality. There are increasing options for both first- and second-line therapy in the palliative treatment of patients with HRPC. Medications to control symptoms should first be optimized in patients with late-stage disease, and radiotherapy applied to dominant painful bone lesions. Docetaxel, mitoxantrone, satraplatin, and ixabepilone are active chemotherapeutic agents in the first- and/or second-line setting for patients with HRPC, and this may be true also of older drugs such as oral cyclophosphamide and vinorelbine. Radioisotopes such as strontium and samarium are useful for treatment of more generalized bone pain. Third-line hormonal maneuvers including glucocorticoids, ketoconazole, and estrogens can lead to further palliation in some patients, and there are provocative data that chemotherapy might restore hormonal sensitivity in a subset of patients.

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Ritacco, Ida, Merriam Al Assy, Mohamed K. Abd El-Rahman, Sherif Ashraf Fahmy, Nino Russo, Tamer Shoeib, and Emilia Sicilia. "Hydrolysis in Acidic Environment and Degradation of Satraplatin: A Joint Experimental and Theoretical Investigation." Inorganic Chemistry 56, no. 10 (April 28, 2017): 6013–26. http://dx.doi.org/10.1021/acs.inorgchem.7b00945.

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Peters, G. J., E. K. Hoebe, C. M. Huijts, A. D. Adema, and K. Wosikowski. "614 POSTER Synergistic interaction between erlotinib and JM-118, the active metabolite of satraplatin." European Journal of Cancer Supplements 4, no. 12 (November 2006): 185. http://dx.doi.org/10.1016/s1359-6349(06)70619-x.

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