Vosaroxin (SNS-595)
in clinical trials
General information
Class/mechanism: Anticancer quinolone derivative (AQD). Vosaroxin intercalates DNA and inhibits topoisomerase II activity, which results in site-specific double-strand DNA breaks, G2 arrest in the cell cycle, and apoptosis. It is hypothesized that it may not be vulnerable to certain mechanisms of resistance since it is not a P-glycoprotein (P-gp) substrate. The vosaroxin naphthyridine core is believed to be less chemically promiscuous and to generate fewer reactive oxygen species (ROS), which could decrease the risk of cardiotoxicity. Its activity is independent of the p53 family.[1][2][3]
Route: IV
Extravasation: no information
For conciseness and simplicity, HemOnc.org currently will focus on treatment regimens and not list information such as: renal/hepatic dose adjustments, metabolism (including CYP450), excretion, monitoring parameters (although this will be considered for checklists), or manufacturer. Instead, for the most current information, please refer to your preferred pharmacopeias such as Micromedex, Lexicomp, UpToDate (courtesy of Lexicomp), or the package insert.
Clinical trials
- Study of Vosaroxin and Decitabine in Older Patients With Acute Myeloid Leukemia and High-risk Myelodysplastic Syndrome
- Vosaroxin and Azacitidine in Treating Patients With Myelodysplastic Syndromes
- Vosaroxin for Intermediate 2 or High-risk MDS After Failure With Hypomethylating Agent-based Therapy
- Study of Vosaroxin or Placebo in Combination With Cytarabine in Patients With First Relapsed or Refractory Acute Myeloid Leukemia (AML)
Patient drug information
No information available.
Also known as
SNS-595, Voreloxin.