Hi friends, When the Embark study came out, and the FDA approved Xtandi for its use, my MO was enthusiastic that I add Xtandi to my intermittent ADT treatment. What I'm wondering is, I can certainly understand that adding Xtandi to the intermittent ADT treatment delays average time to metastasis, but in doing so, am I just borrowing from what would otherwise by my standard post-intermittent-ADT treatment, and making that post treatment less potent, so that the net result is the same? Robbing Peter to pay Paul, sort of? Thanks!
Embark study: Hi friends, When the... - Advanced Prostate...
Embark study
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I'm doing the mono enzalutimide per the EMBARK trial. I would say not to think that way. In ten years there will be additional treatments some of which will resensitize you to Xtandi.
Here's an article on EMBARK:
prostatecancer.news/2023/05...
" ...am I just borrowing from what would otherwise by my standard post-intermittent-ADT treatment, and making that post treatment less potent, so that the net result is the same?"
Why would the post-iADT-treatment be less potent? Everything we know is that the net oncologic benefit is greater when advanced hormone therapy is used earlier. While the survival data are not yet mature, so far mortality has been reduced by 41% in men using the EMBARK protocol.
THANKS TA, THAT's exactly what I want to know. If my post-ADT treatment were an AR inhibitor like Nubeqa, I'd think that using an AR inhibitor like Xtandi early might diminish it later on, but weighing it all out, the tentative evidence is that the net results are NOT the same in terms of mortality.
Why would you follow Enzalutamide with Darolutamide? Isn't the latter similar, but primarily for metastatic patients?
Thanks friend, The Nubeqa was part of my original treatment plan, following Lupron, when the Lupron stopped working. We replaced that plan with EMBARK.
Yes, but I was unclear on what you were saying about "diminish it" related to Enza and Daro. Sorry; I guess I'm a little foggy this AM. Last question, I promise (and maybe I'm not asking it clearly
If you already used Daro, and then you use Enza, what would be diminished later on?
PLEASE ask me all the questions you like! I'm no TA, but I'd love to try to be helpful. So for me, I've never taken anything but Lupron, until last month. After my radiation & recurrence, without mets, my plan became intermittent Lupron, and whenever in the future that stopped working, the plan called for Nubeqa. After EMBARK was announced, my MO switched me to Lupron+Xtandi. Xtandi and Nubeqa are similar (AR inhibitors), and I was wondering if I was "using up" my AR-inhibitor defense unnecessarily, since the Lupron alone was still working fine for me, and might have continued to work fine alone for years.
OK thanks very much. I have it now. Yes, I've been on nothing but Lupron for metastatic PCa, so all developments about the next level (AA, Enza, Daro, etc.) are much more relevant today then a year ago.
As I say, I'm no TA, but I'm surprised you've been on Lupron alone for metastatic PCa. I thought its standard of care has, for years, been to combine Lupron with, say, Zytiga. And lately, have I been reading? that triplet therapy is now the ideal? with a chemo?drug added?
Yes, you are correct. Back in 2018, the doubling therapy hadn't reached every corner, although within a year it had. However, being stable on Lupron a couple of years in, my MO left it to me after we discussed, pointing out the research was done on newly diagnosed patients. We discuss it each time (and chemo as well), but we decided (subject to change) to add treatment when PSA rises 2 points above nadir (0.5), or scans show progression. Last Axumin PET on 1/3 shows no progression, though PSA has crossed 1 (it has done that before before falling back, but may be more persistent this time).
I may go with chemo first, but not sure just yet.
We may run PSMA if we can get Medicare to cover it. Of course, we have no earlier PSMA for baseline, but might be good to get my footing the PSMA door.
EMBARK is for recurrent men after initial treatment. Are you recurrent? Or did your MO just swap Darolutamide to Enzalutimide based on the EMBARK trial? I'm not sure if you can extrapolate results but I'm guessing the results would be similar.Have you ever been diagnosed with metastasis beyond the pelvic area?
Well, where mortality has been reduced by 41%, that seems to be a comparison with men on Lupron only. But your statement that "net oncologic benefit is greater when advanced hormone therapy is used earlier" speaks directly to my question.
Good report. Do you have something similar for patients on ADT (Lupron) only who have become castrate resistant? I'm not there yet but could happen at any time.
Thanks for the article TA. Just learned today that the curative attempt did not work. Even though my psa is only 1.07,the bone scan revealed a single metastatic lesion on my right shoulder blade. Looks like I will be starting the EMBARK protocol in the next week. Just need to wait until my MO speaks to my RO to see if the hospital will approve a pet psma first, in which case I have to postpone the ADT until after the pet psma scan. Your article mentions 36 weeks of ADT which confirms the 9 months of ADT my MO just talked to me about.
EMBARK is for non-metastatic hormone sensitive recurrent prostate cancer. And the 9 months is for men whose PSA is <0.2 after 36 months. The primary end point was metastasis free survival.
I have hormone sensitive recurrent prostate cancer. Maybe the doctor believes that a single legion which they will likely zap with radiation was not enough to exclude me from EMBARK.
I hate to quibble over METs... maybe but he could have given you Xtandi regardless.I hope you do well regardless. I recall reading you struggled with casodex so hopefully this will be different.
It's not the EMBARK protocol per se, which you would not qualify for. But there was another trial, the ENZAMET trial, that looked at men like yourself who originally had no distant metastases but after treatment, but later had bone scan-detected metastases. The benefited from ADT+ enzalutamide. However, hormone therapy was not stopped after 9 months.
sciencedirect.com/science/a...
Thanks for the info. Unless I react better to orzigovix and xtandi than I did on Lupron and abiraterone, I can't see being on adt permanently. The only reason I took them for the miserable two years and a half was for the curative intent, with the hope that I could get back to a semi normal life afterwards.
Sadly, your only choices are to be miserable with hormone therapy or to be miserable with painful and crippling bone metastases.
I too find it sad but when the pain will become too much, I can get the MAID program where I live. My main goal is to try to stay alive and keep on working for the next 10 years so that my wife ends up with a fully paid house and if I die before then while employed, at least the work insurance will be more than enough to reimburse the mortgage.
While I was on my previous ADT, I was often difficult for me to read or incredibly difficult and slow to do write programs. If it is as bad with the new set of ADT, I don't think I will be able to keep my job. My boss has been very tolerant during those 2.5 years but keeping me employed for the rest of my days when I can't pull my weight would not be a sound business decision for him.
Best scenario was if I would be able to reach the age of retirement doing intermittent ADT and zapping the metastisis whenever they appear. If I no longer worked, then long term ADT from that point onward would not cripple me as much.
At least this time, there is no prednisone in the protocol. That wrecked my metabolism greatly. My treatments was over in May 2023 and it is only since late March 2024 that I managed to rid myself of the insulin resistance and feet that were all red, puffy and excruciatingly painful in the evening. If 2.5 years of this stuff damaged my body so much, I don't want to consider how much more damage (feet amputation?) would happen with a lifetime on it.
I'm in the similar situation except that I don't have visible Mets. I started mono - Eligard initially July 2022 after recurrence, then at my July 2023 appt my MO discussed the EMBARK trial. I finally added the Xtandi in November (half dose) while still on Eligard. January 2024, my MO wanted me to stop the Eligard and continue with a full dose of Xtandi. Overall I feel really good. Better than when I was on ADT + Abiraterone Acetate for my initial treatment.
Good question. I've been on its first cousin, Nubeqa, for four months as mono therapy and my PSA still rose. Will start Orgavyx this week in advance of a spot radiation treatment on a chest node and a surgical removal of a pelvic node . Certainly a small percentage chance of cure, my team is contending that this cutting edge, but certainly inconvenient treatment plan will " re-set the clock" insofar as my PSA/ Metastasis goes.
I just tabulated in my spreadsheet my PSA results from 2 days ago and it is regrettable that I need to start treatments next weeks because of the shoulder blade met that they found in my bone scan results because my latest PSA result looked promising.
Here are all of my PSA test results since my initial curative intent treatment ended a year ago.
PSA 2023-08-18 : 0.09
PSA 2023-10-06 : 0.14 (55.56% increase from previous result)
PSA 2023-12-05 : 0.22 (57.14% increase from previous result)
PSA 2024-02-06 : 0.39 (77.27% increase from previous result)
Then on Feb 16, I began taking Ivermectin 12mg once a day, 4 days on, 3 days off.
PSA 2024-04-16 : 0.9 (130.77% increase from previous result)
Then on April 24, I began taking HydroxyChloroquine 200mg 2 times a day.
PSA 2024-05-15 : 1.07 (18.89% * from previous result).
Note that this latest test was only 30 days later, not 60. Still, even if I double it to 37% to mimic the regular span between my test, the growth has been slowed dramatically where it had been in a ever increasing upward trend before that.
With not even a full month of trying having passed since I began testing HydroxyChloriquine, the drastic reduction in growth looked good to me. I only wish I would have had 2 or 3 more months ahead of me before starting ADT treatments again as it would have enabled me to see if it was possible to actually decrease not just the psa progression but potentially lower my psa.
That shoulder blade metastasis surprise has derailed what would have been an interesting experiment of one.
☹️ Would you consider taking them together now?
I am not sure it would be worth it to take them during the 9 months I'll be on ADT as it would confound which drug is doing what. But if after the treatment is over the PSA starts going up rapidly once more, then yes I will resume my experimentation to see how it does over a longer period than just 3 weeks.
I've found this study classic.clinicaltrials.gov/... which says results posted on June 16, 2022 but I can't seem to actually find what the outcome was on that page.
I've been googling and I can't find it either. But yes indeed, resume the experimentation as you say, and good luck.
You may find this of interest.cinj.org/process-cancer-cel....
Love it. Investigators "pairing HCQ with other chemo regimens in order to increase the effectiveness of treatment." Hmm! I'll mention it to my MO next month. He'll dismiss it, but I'd still like to gauge his reaction. Too bad it got caught up in politics.