I just discovered that Eligard is superior to Lupron in one respect.
It is injected into fatty tissue as opposed to muscle and as a result maintains more stable levels of leuprolide acetate than do Lupron injections.
The one disadvantage is that it appears almost no insurance covers Eligard.
My question is of Lupron 1 month, 3 month, or 6 month injections how does the relative stability of their Leuprolide levels compare? And how do they compare with that of Eligard?
Does anyone have any knowledge, ideas or even inklings?
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Also:
What about Firmagon (degarelix). I understand that it is an antagonist whereas Eligard and Lupron are agonists? Is that so? That doesn't sound so right to me?
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Lupron is $564.78 (1 kit (2.8ml vial) of leuprolide 1mg/0.2ml)
In researching my Medicare Part D, it seems like none of the options I am looking include it in their formularies. And I am attempting to stick with the better plans, not the cheap ones.
I get an injection every six months at the Hosiptal infusion center. It is covered under part b, 100 percent covered by medicare care and supplemental part F. Part D drugs are under the doughnut hole rule, that an added 5k expense.
This study I think shows that the initial drug surge is lower for Eligard that Lupron and Eligard delivers a more even dose. Please let me know if I’m not understanding it correctly
"Histrelin is also available in a 12-month subcutaneous implant (Vantas) for the palliative treatment of advanced prostate cancer, since 2005 in the US, and since Jan 2010 in the UK."
It has been around a while. Other than convenience, what are the pros and cons of Vanta vis a vis Lupron?
I take monthly injections instead of the 3 or 6 months or 1 year. I did this based upon some research we did when we could find NO research and findings were released by the drug maker, nor would they respond when we contacted them in order to obtain this information.
Further, depending upon body size and other factors, I would suggest that the longer the drug is in your body, the more likely that it will released faster or slower than designed, thus leading to a greater chance of inconsistency in results.
So, a greater cost for the 1 month, yet more needles but I taken this approach.
I also only stay on the combo IHT I undertake for three or max four months, which in most instances, had my Nadir reached.
1. "Further, depending upon body size and other factors, I would suggest that the longer the drug is in your body, the more likely that it will released faster or slower than designed, thus leading to a greater chance of inconsistency in results."
Seems logical
2. "NO research and findings were released by the drug maker, nor would they respond when we contacted them in order to obtain this information."
Hmmm so they don't want the Docs or patients to know about this. They are defensive about stability. That would indicate there is some kind of problem with stability that they are hiding.
3. So the question is what incorrect assumption will make them more money? Hard to speculate on that one.
Nal, could you post more about killing gently vs killing aggressively? Or direct me to literature/research?
If PSA is still low but increasing quickly would is restarting ADT with Vantas implant reasonable or would an initial shot of degarilex then switching to Vantas be a good plan? (We are of course discussing this with his MO but I appreciate opinions from people on this board who I know give these issues lots of thought and study and also bring their own experience) Husband’s been on a break from ADT at MO’s suggestion since April and PSA stayed “undetectable” (nadir 0.01) for 7 months until his T reached 610 (T low was ~10) and is now 0.52 increasing quickly (from 0.41 to 0.52 in 17 days.) MO wants to do Axumin scan when PSA gets a little higher and possibly spot treat any mets (none previously identified) but I’m afraid to wait to restart ADT with that velocity. So far ADT following RP is his only treatment. His T went from <10 to 476 in 5 months. When T was 476 PSA was 0.071 from 0.014 in June.
(And is Axumin the best scan to do ??)
I am only looking for perspectives, learned opinions, experiences and we will discuss with his MO.
His PSA was very high (17 and rising) after RP (34 at surgery) and I wish we would have demanded scans before ADT was started last year at that time, and it’s disappointing to me the doctor didn’t order them, but he was anxious to start ADT because the PSA was rising quickly. After everything I’ve learned since then I would have demanded it.
That’s why I appreciate hearing alternate opinions from people on this board.
Was on lupron for a year then doctor switched me over to Eligard. They both worked lupron shot in my butt hurt for a week or more. Eligard shot in my belly hurts like all get out for a while . Can’t tell the difference in what they do. Have Medicare and a part D. Since I get the shot as a in house procedure it’s covered by insurance.
My doc switched me from Lupron to Eligard last year. Result on T-level seems to be the same (<10). My Eligard shot is given every 3 months in the butt. Try relaxing the muscle before the shot by standing on a stool and letting that (soon-to-be-shot) side leg hang free.
Nal, you mean that it kills the cancer cells continuously instead releasing large Lupron bombs once a week or so? I tried voice dictation earlier while in the sun and couldn't see the words that ended up on the page.
I feel like an orphan. My MO has me on the 4-mo Lupron shot. I've heard rumors that it's not "as effective" as the 3 mo, but I can find no proof. I've asked on this site, but no one has answered. Any body have any info on the 4 mo shot?
cesces: I wouldn't worry, except my psa is no longer going down to ND; it's hung up at about 0.4 (21 yrs after diagnosis with GS6, T2b, so, again, not really too worried). I did get one Psa after 3 months and it was lower (0.3, vs 0.4).
Thank you for your response, Nal. My husband’s PSA right now is 0.52 and his MO suggests waiting till his PSA is a little higher to do scans before restarting ADT. I think we will test PSA again in two weeks to see how fast it’s moving. He had a great response with Firmagon last year.
I am currently on 3 month shots, always have been.
Insurance paid for both.
My PSA was stable with both.
My only issue, and it may be just me, but the injection of Eligard hurt like a MF'r.
To me it was worse than a wasp sting plus the pain lasted full strength for about 10 minutes. And then it took up to an hour for all the pain to dissipate.
After the second injection of Eligard I demanded to go back to Lupron.
The doctors office said the only reason they went to Eligard was due to Lupron being more expensive. But they happily put me back on Lupron.
I've been on one or the other for 6 1/2 years and except for the occasional ADT vacation, my PSA has stayed under 1.0.
I'm not sure if this was answered.
Firmagon is a GnRH antagonist. Lupron is an agonist.
They kind of achieve the same end result but in different ways. A GnRH antagonist reduces GnRH to zero. That takes LH to zero. With LH zero, T goes to zero and stays there.
A GnRH agonist takes GnRH high. So T goes high but then when your body figures out that GnRH isn't fluctuating very much, LH goes low and so does T and stays there.
The takeaway is that GnRH fluctuations are responsible for T production. No fluctuations, regardless of the level, = no LH = no T.
I ran this by my urologist and MO and they both said "yeah, probably" - I think I wrote it correctly here: LH can be thought of as being a clamped smoothed (constant times the first derivative of GnRH). Step up GnRH but hold it constant, the derivative goes high as an impulse function and then to zero as time goes on (so it is smoothed). Step down GnRH and LH goes to the low clamp (zero). Stays there. So T goes to zero and stays there. In practice there is a little lag.
Interesting stuff. I had the same question as you did so I started researching what the heck was going on. And then tried to get to make some sense in a mathematical world.
For some guys they have to worry about a T-flare. I think it's mostly guys with bone mets. They can either use casodex for a month to get past the T-flare of Lupron or just use an antagonist. My experience is that Firmagon is a pain - itching and lumpy belly for days or even weeks. Lupron is a simple intramuscular injection. I had no pain (get a nurse to do it or get an MO who will allow you to be trained to do it yourself). My insurance turned me down for Orgovyx or I would have gone that route. No T-flare, oral, I think it has better T control. But, I don't have the 4k+ a month for Orgovyx out of pocket.
"And then tried to get to make some sense in a mathematical world."
There are severe limits to this approach with complex biological systems.
It's useful for developing conjectures, but biological systems have their own logic that they do not easily share with us.
That's why we need to rely on clinical trials.
For instance you mentioned agonists and antagonists. Logically you would think they should act the same, but they don't. There are way way way too many moving parts for that to be so.
And many, if not most, of the moving parts, we are blissfully unaware of.
In the end we need to rely on statistically validated trial and error.
Yes. And that is why I posted the charts. They represent data taken from hundreds of men. If that is what you want to see, the charts should tell all. You can go to clinicaltrials.gov to get some clarification. Pubmed also has some studies. I picked up research from both sites.
Agonists and antagonists are not the same. They are opposites.
They do not act the same and the intermediate step is not the same but the eventual final result is the same.
In general, we can look at trial data but that shouldn't prevent us from figuring out why we see what we see. In this case, it was known well before the trial data. There were no surprises that I am aware of. My MO and urologist were in complete agreement when I ran this by them (it was originally my urologist who got me thinking about how an agonist and an antagonist could arrive at the same result).
I like to understand what I see. If theory and reality match it is much better than "it works, but we don't know why so let's not change anything, and doing a new trial is a shotgun approach because we don't know what we can expect". I look at some trials and studies and I occasionally think of this shotgun approach. A good way to waste time and money. Others are simply brilliant and I wish the brilliant researchers would mentor the shotgunners.
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