FAQ

Cabazitaxel is classified as a microtubule inhibitor and belongs to the taxane class of chemotherapy agents.

Mechanism of Action:
Cabazitaxel disrupts cell division by binding to tubulin, the protein subunit of microtubules. This binding stabilizes microtubules, preventing their depolymerization (breakdown) during mitosis. As a result, cancer cells are unable to complete cell division, leading to cell cycle arrest and apoptosis (programmed cell death). Unlike some other taxanes, cabazitaxel is less susceptible to multidrug resistance proteins (e.g., P-glycoprotein), making it effective against tumors that have developed resistance to other taxanes like docetaxel.

Clinical Use:
Cabazitaxel is specifically indicated for the treatment of metastatic castration-resistant prostate cancer (mCRPC), particularly in patients who have previously received docetaxel-based chemotherapy. It is typically administered in combination with prednisone or prednisolone to enhance efficacy and manage side effects.

Administration:
Administered intravenously, cabazitaxel requires careful preparation and dilution before infusion. It is dosed at 20–25 mg/m² every three weeks, with dosing adjustments based on patient tolerance and hematologic parameters (e.g., neutrophil counts).

Key Characteristics:

• Second-Line Therapy: Approved for use after disease progression on docetaxel.
• Microtubule Stabilization: Acts by inhibiting microtubule dynamics, distinct from other microtubule-targeting agents that may promote depolymerization.
• Cross-Resistance Profile: Demonstrates activity in taxane-resistant tumors due to its unique binding affinity and reduced susceptibility to efflux pumps.

Comparison with Other Taxanes:
While cabazitaxel shares structural similarities with docetaxel and paclitaxel, its pharmacokinetic and pharmacodynamic properties differ. For instance, cabazitaxel has a longer half-life and higher plasma protein binding, contributing to its sustained antitumor effects.