Phase II multicenter trial of voreloxin as second-line therapy in chemotherapy-sensitive or refractory small cell lung cancer.

Published

Journal Article

INTRODUCTION: Voreloxin is an anticancer quinolone derivative that intercalates DNA and inhibits topoisomerase II, causing double-strand breaks in DNA, irreversible G2 arrest, and rapid onset of apoptosis. Based on preclinical activity of voreloxin in chemoresistant tumors, early phase I clinical activity, and a mechanism of action similar to other topoisomerase II inhibitors such as the anthracyclines and etoposide, this phase II trial was undertaken as second-line treatment of small cell lung cancer (SCLC). METHODS: Patients with extensive stage SCLC previously treated with one prior chemotherapy regimen were eligible. Patients with chemotherapy-sensitive or chemotherapy-refractory disease were considered as separate cohorts. Voreloxin (48 mg/m) was administered on the first day of each 21-day cycle for up to six cycles. The primary end point was objective response rate. RESULTS: Fifty-five patients were enrolled including 28 with refractory SCLC and 27 with sensitive SCLC; 47 were evaluable for response. Three patients with sensitive SCLC had an objective response, including one complete response and two partial responses (11% response rate based on intent to treat). No patients in the refractory cohort had a response. The primary grade 3 toxicity was neutropenia. CONCLUSION: Voreloxin has minimal activity in relapsed SCLC when administered at 48 mg/m in a 3-week schedule.

Full Text

Duke Authors

Cited Authors

  • Krug, LM; Crawford, J; Ettinger, DS; Shapiro, GI; Spigel, D; Reiman, T; Temel, JS; Michelson, GC; Young, DY; Hoch, U; Adelman, DC

Published Date

  • February 2011

Published In

Volume / Issue

  • 6 / 2

Start / End Page

  • 384 - 386

PubMed ID

  • 21252718

Pubmed Central ID

  • 21252718

Electronic International Standard Serial Number (EISSN)

  • 1556-1380

International Standard Serial Number (ISSN)

  • 1556-0864

Digital Object Identifier (DOI)

  • 10.1097/jto.0b013e318200e509

Language

  • eng