Something I missed - apologies if it has been discussed.
Dutasteride "was approved by the FDA for the treatment of BPH in November 2001 and was introduced into the United States market the following year under the brand name Avodart." ... "The patent protection of dutasteride expired in November 2015" [1]
"Dutasteride is a 5α-reductase inhibitor ...{&}... works by decreasing the production of dihydrotestosterone (DHT) ..." (from testosterone). [1]
It is not approved for treating PCa. When I initially asked for a prescription, my doctor warned me that I might have a problem getting insurance to pay for it, but that was not the case.
There has been some skepticism here as to its value as an ADT add-on. After all, ADT all but eliminates testoterone [T] - the source of DHT. Dr. Myers has pointed out that the real purpose of ADT is to inhibit DHT production - not T. We have targets for T, but DHT is rarely measured. Some patients produce DHT even when T is at castrate levels, but Avodart can inhibit this.
My concern has not been so much with measurable DHT, but with DHT produced within PCa cells. This can happen as the cells become resistant to ADT. There are potential pathways to DHT that do not require T. Avodart might therefore block one route to CRPC.
& now there is another reason for Avodart use:
From a 2016 paper (Cleveland Clinic) [2]:
"Abiraterone {Abi} blocks androgen synthesis and prolongs survival in castration-resistant prostate cancer, which is otherwise driven by intratumoral androgen synthesis."
{i.e. while it is often noted that Abi shuts down adrenal production of hormones that might be converted to androgens, Abi also does the same thing within PCa cells.}
"Abiraterone is metabolized in patients to D4A, which has even greater anti-tumor activity and structural similarities to endogenous steroidal 5α-reductase substrates, such as testosterone."
"Here, we show that D4A is converted to at least 3 5α-reduced ... metabolites. The initial 5α-reduced metabolite, 3-keto-5α-abi, is more abundant than D4A in patients with prostate cancer taking abiraterone, and is an androgen receptor (AR) agonist, which promotes prostate cancer progression."
"In a clinical trial of abiraterone alone, followed by abiraterone plus dutasteride (a 5α-reductase inhibitor), 3-keto-5α-abi and downstream metabolites are depleted, while D4A concentrations rise, effectively blocking production of a tumor-promoting metabolite and permitting D4A accumulation."
A co-author of that paper was Mary-Ellen Taplin [Dana-Farber]. From a 2018 paper from Taplin & team [3]:
"Interestingly, the addition of dutasteride resulted in a 2-fold increase in serum abiraterone, which may reflect decreased abiraterone metabolism by 5α-reductases. This would be consistent with recent data indicating that an abiraterone metabolite, Δ4-abiraterone (D4A), is metabolized by 5α-reductases."
"We also observed a trend towards lower serum androgen levels (and higher progestin levels) in patients with higher serum abiraterone, and found that a subset of patients had lower abiraterone levels at progression with reciprocal changes in upstream and downstream hormone levels."
...
Is it common for doctors to add Avodart to Zytiga?
-Patrick
[1] en.wikipedia.org/wiki/Dutas...
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