What is the mechanism of action of Enzalutamide (generic name) in treating castration-resistant prostate cancer?

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Enzalutamide Mechanism of Action

Enzalutamide is a potent androgen receptor inhibitor that blocks multiple critical steps in the androgen receptor signaling pathway, including competitive inhibition of androgen binding (with 5- to 8-fold higher affinity than bicalutamide), prevention of nuclear translocation, inhibition of DNA binding, and blockade of coactivator recruitment. 1

Multi-Step Androgen Receptor Blockade

Enzalutamide acts at four distinct points in the androgen receptor (AR) signaling cascade, making it substantially more effective than first-generation antiandrogens:

  • Competitive androgen binding inhibition: Enzalutamide competitively blocks testosterone and dihydrotestosterone from binding to the androgen receptor with 5- to 8-fold greater affinity compared to bicalutamide, preventing initial receptor activation. 1

  • Nuclear translocation blockade: After androgen binding occurs, enzalutamide prevents the androgen receptor from translocating from the cytoplasm into the cell nucleus, which is essential for the receptor to exert its transcriptional effects. 1, 2

  • DNA binding inhibition: Even if the receptor reaches the nucleus, enzalutamide inhibits the androgen receptor's ability to bind to androgen response elements on DNA, preventing gene transcription initiation. 1, 2

  • Coactivator recruitment blockade: Enzalutamide blocks the recruitment of coactivator proteins that are necessary for androgen receptor-mediated gene transcription, representing a final checkpoint in the signaling pathway. 1

Reduced Agonist Activity Profile

  • Enzalutamide demonstrates reduced agonist activity compared to other nonsteroidal androgen receptor antagonists, meaning it is significantly less likely to paradoxically activate the androgen receptor under certain conditions (such as AR overexpression or mutation). 1

  • This reduced agonist activity distinguishes enzalutamide from first-generation antiandrogens like bicalutamide, which can exhibit agonist properties in castration-resistant settings. 3

Active Metabolite Contribution

  • The major metabolite N-desmethyl enzalutamide exhibits similar in vitro activity to the parent compound, contributing to the overall therapeutic effect. 2

  • Both enzalutamide and N-desmethyl enzalutamide achieve clinically relevant steady-state concentrations, with mean minimum concentrations of 11.4 µg/mL and 13.0 µg/mL respectively. 2

Critical Distinction from Abiraterone

  • Enzalutamide should not be confused with abiraterone: Enzalutamide directly blocks the androgen receptor at multiple steps in the signaling pathway, while abiraterone inhibits androgen synthesis by blocking the CYP17A1 enzyme upstream in the steroidogenesis pathway. 1

  • These represent complementary but mechanistically distinct approaches to targeting the androgen signaling axis in castration-resistant prostate cancer. 1

Clinical Pharmacology Impact

  • Enzalutamide's multi-step mechanism results in decreased proliferation and induced cell death of prostate cancer cells in vitro, with demonstrated tumor volume reduction in mouse xenograft models. 2

  • The drug requires therapeutic trough levels greater than 10 µg/mL to achieve effective androgen receptor blockade, reflecting its strong but not absolute receptor affinity. 3

  • Once-daily dosing of 160 mg enzalutamide reduces PSA levels to undetectable levels (<0.2 ng/mL) in 68% of patients with metastatic castration-sensitive prostate cancer. 2

References

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This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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