What is VALSTAR (Valrubicin)?
VALSTAR is an anthracycline topoisomerase inhibitor indicated for intravesical therapy of BCG-refractory carcinoma in situ (CIS) of the urinary bladder in patients for whom immediate cystectomy would be associated with unacceptable morbidity or mortality.
What is the most important information about VALSTAR?
- Risk of Metastatic Bladder Cancer with Delayed Cystectomy - Inform patients that VALSTAR has been shown to induce complete responses in only about 1 in 5 patients, and that delaying cystectomy could lead to development of metastatic bladder cancer, which is lethal. Discuss the relative risk of cystectomy versus the risk of metastatic bladder cancer [see Clinical Trials (14)] and that the risk increases the longer cystectomy is delayed in the presence of persisting CIS
- The major acute toxicities from VALSTAR are related to irritable bladder symptoms that may occur during instillation and retention of VALSTAR and for a limited period following voiding.
- For the first 24 hours following administration, red-tinged urine is typical.
- Report prolonged irritable bladder symptoms or prolonged passage of red-colored urine immediately to their physician.
- Patients to maintain adequate hydration following VALSTAR treatment.
- Females of reproductive potential of the potential risk to a fetus and to use effective contraception during treatment with VALSTAR and for 6 months after the last dose. Advise females to inform their healthcare provider of a known or suspected pregnancy.
- Male patients with female partners of reproductive potential to use effective contraception during treatment with VALSTAR and for 3 months after the last dose.
- Females not to breastfeed during treatment with VALSTAR and for 2 weeks after the last dose.
How does VALSTAR work?
VALSTAR (Valrubicin) is an anthracycline that affects a variety of interrelated biological functions, most of which involve nucleic acid metabolism. In cells, it inhibits the incorporation of nucleosides into nucleic acids, causes chromosomal damage, and arrests the cell cycle in G2. Although valrubicin does not bind strongly to DNA, valrubicin metabolites interfere with the normal DNA breaking-resealing action of DNA topoisomerase II
