Watching the results of the EMBARK trial with great interest as they had a ‘Lutamide monotheraoy’ arm that has performed very well and now questions are being asked about needing ADT for high risk of BCR in the hormone sensitive.
Not matching my position of course ( there is no population that does) buy it is hormone sensitive -and high risk of progression which is me Difference is they are not advanced whereas I am advanced but treated back to stable and NED.
Maybe moving to a lutamide mono is worth considering for me,
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Brysonal
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interesting. I would love to just be on just darolutamide. Im curious if allowing testosterone to come back into circulation will solve some side effects even though the AReceptors are inhibiting the T from being taken up. I also wonder if these lutamide inhibitors is enough to keep the cancer happy, fed and caged.
You can ask your MO, but the problem is all these drugs are paired with lupron, eligard, etc in trials, and consequently, it is gonna take an MO that can think out of the box to look objectively at the situation. Most will say it is given together in the trials, so follow the SOC.. end of subject..
That is why I am interested in EMBARK as 10 years ago they had the foresight to put a ‘lutamide’ monotherapy arm in and it has performed really well from what I can see and the onco twitterarti are talking about it being practice changing. I asked ages ago on the other forum why do we need to block testosterone if the ARSI inhibits the signal and was told it was like adding a few drops of water when we needed a litre ( paraphrasing’!) but these 10 year results fo look gamechanging in a potential unbundling of ADT from the ARSI mindset.
Will be having this on the agenda for my May meeting!
I agree... always put it on the meeting.... you never get anything without asking... I won't say my MO is like a genie in a bottle, but he does take time to explain why he chooses not to do something... ( I have had a few wishes...)
QOL should be a factor.... Is QOL better on strictly enza/apa/daro and what are the risks--dna mutation status, severity of disease- adenocarcinoma, ductal, intraductal... bone lesions--lytic vs blastic...
Things for each patient to weigh out...
Is vacationing a possibility for you, or is the MO against it...
When I was diagnosed (a quarter of my lifetime ago), I was aware of Casodex (Bicalutamide) as an add-on to Lupron. Since my aim was to avoid castration until it was needed, I wasn't interested in Casodex.
So, some years later, I was surprised to read of it being used as monotherapy in Germany. I discovered that this was not uncommon.
But in the U.S. (Wikipedia):
"Bicalutamide is approved for and mainly used in the following indications:
... "Metastatic prostate cancer (mPC) in men in combination with a gonadotropin-releasing hormone (GnRH) analogue or surgical castration at 50 mg/day
... "Locally advanced prostate cancer (LAPC) in men as a monotherapy at 150 mg/day (not approved for this use in the United States)"
"The drug is registered for use as a 150 mg/day monotherapy for the treatment of LAPC in at least 55 countries, with the U.S. being a notable exception"
Brysonal - Adding to Patrick's comments, I started using bicalutamide after having a second BCR in mid-2020. My first "test" of it was a ten-day trial of 50mg daily which cut my PSA in half. A short time later I did a 30-day "trial" of 50 mg bical daily, which reduced my PSA from 0.132 to 0.039.
That short trial proved to not be durable and I let PSA "run" for a PSMA scan in early 2021. Since that time I have done two months of lupron mono (to knock PSA back down to sub 0.1) and various combos and dosages of bicalutamide + dutasteride + tamxoifen (recently scripted for gynecomastia caused primarily by bical.) During this time PSA has ranged from a high of 2.6 (after I delayed additional treatment due to second opinion of PSMA results, etc.) to a low of <0.04. Of note during the above period (outside of the 2 months on lupron), my T has averaged around 600. (450-773) That is about 30-50% above the T range prior to bical use. I am due for gyno RT this week and will restart daily 50 mg bicalutamide for 30 days and test for PSA response. Based on those results, I will then consider modifying that to add dutasteride (5ARi) and/or tamoxifen (pharma SERM) and possibly reduce bical dosage. (Justfor_ is the resident expert in bical mono dosage adjustment for stable-state disease. See link below: )
Since bicalutamide is known to boost T by as much as 50% (and cause gynecomastia in +/- 70% of users), it has taken me a while to understand its companion use with lupron (for the intial T flush*); i.e., how could a med that raises total T be of use to stop the initial rise when starting lupron? The attached illustration from Patrick Walsh's book helped decipher that. AR inhibitors, like bicalutamide, block the uptake of T at the cellular level regardless of serum T levels - so even with it possibly boosting T as lupron depresses it, the action at the cellular level negates the action of rising T long enough for lupron's initial flush to dissipate.
*As has been posted and commented on here and elsewhere, the ADT flush has been shown to be beneficial when timed to peak during RT. If you are not familiar with that concept, here is a link to one of the posts:
Having had even the two short ADT treatments (3 mos and 2 mos), I can vouch for the fact that in my case, bicalutamide has had zero discernible impact on my QOL. In fact, since my free-T seems to historically range in the 1% range of total T (vs the 2% considered ideal), I have obviously benefited from the T boost, since the free (available) T is what contributes to one's energy level, ability to build/retain muscle mass, libido, etc.
The largest concerns with long-term bical use seem to be (#1) gynecomastia, (#2) eventual switch from PCa antagonist to agonist, and (#3) possible boost to E2alpha (and thus BCL2) as a result of the T rise. (It seems to me that Tamoxifen might be useful for #3.) I am trying to do interval treatments with mixed combos to keep the diverse cellular populations in competition - so that treatment-resistant types do not come to predominate. All being done seat-of-the-pants, but so far with the co-op of my MO.
I hope this gives you some better perspective on bicalutamide specifically and the "lutamides" in general. Bical is considered the weakest of the group and the one that most promotes man-boobs. If cost is not an issue, the newer drugs may be better alternatives. Others who are using them can comment on that.
Most important, the above is all just form my n=1 experience. So far, I have made QOL my priority. That is easier to justify at my advanced age of 75 than it might be for someone considerably younger. We all make our deals with the devil when it comes to metastatic cancer of any type.
Best of luck to you with charting your course through the often treacherous water of PCa treatment. If we can survive the stormy seas, we soon find ourselves in calm waters. Sail on, Brother. Sail on!
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Prostate cancer - repurposed drugs?
