What is the mechanism of action of Darolutamide (generic name: darolutamide) in treating non-metastatic castration-resistant prostate cancer?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: February 1, 2026View editorial policy

Personalize

Help us tailor your experience

Which best describes you? Your choice helps us use language that's most understandable for you.

Darolutamide Mechanism of Action

Darolutamide is an androgen receptor (AR) antagonist that competitively inhibits androgen binding to the AR, blocks AR nuclear translocation, and prevents AR-mediated transcription. 1, 2

Molecular Mechanism

Darolutamide works through three distinct steps in blocking androgen receptor signaling 2:

  • Competitive inhibition of androgen binding: Darolutamide competes with testosterone and dihydrotestosterone for binding sites on the androgen receptor, preventing these hormones from activating the receptor 2

  • Blockade of AR nuclear translocation: Even if the androgen receptor is activated, darolutamide prevents it from moving into the cell nucleus where it would normally activate gene transcription 2

  • Prevention of AR-mediated transcription: Darolutamide stops the androgen receptor from turning on genes that promote prostate cancer cell growth and survival 2

Active Metabolite

  • Darolutamide has a major active metabolite called ketodarolutamide that exhibits similar in vitro activity to the parent compound 2

  • Ketodarolutamide achieves total plasma exposure that is 1.7-fold higher compared to darolutamide itself, contributing significantly to the overall therapeutic effect 2

Additional Receptor Activity

  • Darolutamide also functions as a progesterone receptor (PR) antagonist in vitro, though this activity is approximately 1% compared to its AR activity 2

Functional Outcomes

The molecular mechanism translates to measurable anti-tumor effects 2:

  • Decreased prostate cancer cell proliferation in vitro studies 2

  • Reduced tumor volume in mouse xenograft models of prostate cancer 2

  • PSA suppression: In clinical trials, 24.2% of nmCRPC patients achieved undetectable PSA levels at 12 months (versus 0.4% with placebo), and 60.2% of mHSPC patients achieved undetectable PSA levels at 12 months when combined with docetaxel (versus 26.1% with placebo plus docetaxel) 2

Structural Uniqueness

  • Darolutamide is described as a structurally unique androgen receptor antagonist, distinguishing it from other second-generation AR inhibitors like enzalutamide and apalutamide 3, 4

Important Clinical Distinction

  • Darolutamide does not suppress testosterone production itself and must be continued with concurrent androgen deprivation therapy (ADT) to maintain castrate testosterone levels 5

  • However, when used as monotherapy in hormone-sensitive disease, darolutamide causes serum testosterone levels to increase (median increase of 44.3 ng/dL at week 24) while still achieving profound PSA suppression through potent AR blockade 6

Related Questions

What are the findings of the EMERALD-1 (Emerald One) study?
Can darolutamide be used after Zytiga (abiraterone) in patients with castration-resistant prostate cancer?
What are the outcomes of 6-month vs 18-month hormone therapy with Darolutamide (generic name: Darolutamide) or Abiraterone (generic name: Abiraterone) plus Relugolix (generic name: Relugolix) in combination with radiation therapy for an elderly male patient with a history of prostate cancer, who has undergone a radical prostatectomy and now has a recurrence with cancer in the prostate bed and a pelvic lymph node?
What is the recommended use of Darolutamide (generic name: darolutamide) in patients with metastatic castration-resistant prostate cancer (mCRPC)?
Is Darolutamide (generic name: Darolutamide) effective for treating metastatic castration-resistant prostate cancer (mCRPC)?
How does hypoalbuminemia affect drug distribution in a patient?
What is the anatomy and physiology, definition, risk factors, causes, signs and symptoms, priority assessments, diagnostic testing, treatment, and nursing considerations for Congestive Heart Failure (CHF)?
When do drugs typically reach steady state in the body?
Does susceptibility to cefuroxime (Cefuroxime) sodium indicate susceptibility to cefuroxime (Cefuroxime) axetil in a patient?
What is the role of nonsteroidal antiandrogens (NSAAs), such as bicalutamide (Casodex), in the treatment of a patient with advanced or metastatic prostate cancer?
What is a key factor in drug absorption?

Professional Medical Disclaimer

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.

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.