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Updated: Jun 19, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
An overview on 5alpha-reductase inhibitors.
Saurabh Aggarwal1, Suresh Thareja, Abhilasha Verma
1University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160014, India. aggarwalsau@gmail.com
Benign prostatic hyperplasia (BPH) treatments include 5alpha-reductase inhibitors that block testosterone conversion. These drugs, like Finasteride and Dutasteride, effectively reduce prostate size and dihydrotestosterone levels.
Area of Science:
- Urology
- Pharmacology
- Androgen Biology
Background:
- Benign prostatic hyperplasia (BPH) is a common condition causing lower urinary tract symptoms (LUTS) due to prostate gland enlargement.
- Prevalence increases with age, affecting approximately 70% of men by 70 years old.
- Elevated dihydrotestosterone (DHT) levels, driven by 5alpha-reductase activity, are central to BPH pathogenesis.
Purpose of the Study:
- To review all categories of 5alpha-reductase inhibitors for BPH treatment.
- To discuss steroidal and non-steroidal inhibitors targeting testosterone to DHT conversion.
Main Methods:
- Review of existing literature on 5alpha-reductase inhibitors.
- Analysis of steroidal inhibitors (Finasteride, Dutasteride) and non-steroidal compounds.
- Examination of their mechanisms of action and efficacy in reducing DHT and prostate size.
Main Results:
- Finasteride, a steroidal inhibitor, reduces prostatic DHT by 70-90% and prostate size.
- Dutasteride, a dual inhibitor of 5alpha-reductase isozymes, reduces DHT levels by over 90%.
- Development of various non-steroidal 5alpha-reductase inhibitors has also been explored.
Conclusions:
- 5alpha-reductase inhibitors are a logical therapeutic strategy for BPH.
- Both steroidal and non-steroidal inhibitors offer effective means to suppress androgen action in the prostate.
- Continued research into novel inhibitors aims to improve BPH management.
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