It is a rainy stormy day in Perth, Western Australia, called the "most remote city in the world". I arrived here yesterday with more than 30 hours of travel from Oregon USA. Tomorrow I will get my first infusion of Lutetium 177-PSMA (mAb)-J591. An experimental and unproven new form of radioactive ligand therapy for advanced prostate cancer. The question is: "Why?"
Why am I doing this? It is not SOC. There is not even a proof of concept for it. It is an outgrowth or extension just hoping to build upon the limited success of Lu-PSMA-617 used in the VISION trial and recently approved for mCRPC under the branded name Pluvicto.
There is a Randomized Phase III Clinical Trial (RCT) for this new drug and treatment approach for metastatic CRPC that is now recruiting. But I do not qualify for that trial called the PROSTACT trial. I am "not advanced enough: That trial uses this same drug, variously called 177Lu-DOTA-rosopatamab, AKA Lu-DOTA-TLX591 (by Telix Pharmaceuticals), or as I know it Lu-PSMA-J591. It uses a humanized monoclonal antibody to very strongly bind to the PSMA protein on the PC cancer calls' surface. Much more strongly held than the PSMA-617 small molecule "ligand" used in the VISION trial (now Pluvicto) and has been in extensive use in other countries for several years.
The PROSTACT Trial is being led by chief investigator, Dr. Nat Lenzo, who is also the one advising, treating and monitoring me in my experimental treatment. The trial, which is now enrolling patients, is for those with mCRPC who are progressing, with a PSA >2.0 after previous ADT plus at least 12 weeks of an Advanced Androgen Receptor drug, and at least one series of a taxane chemotherapy. And also must have at least one metastatic site with strong PSMA avidity (SUVmax) on a PSMA PET scan. In other words for highly advanced, highly pre-treated stage 4 prostate cancer. Then they will be randomized 2:1 to receive 2 doses of the treatment drug (45 mCi equal to 2.8 GBq of radiation dosage) given two weeks apart. Vs. Placebo in an open-label protocol.
177Lu-DOTA-rosopatamab With Best Standard of Care (SoC) for
the Second Line of Treatment for Metastatic Castrate-resistant
I do not meet the entry requirements for this study in that I am metastatic hormone-sensitive PC; Have not been on an AAR drug; And I have no PSMA avid sites left after SBRT of the only 2 visible nodes a month ago. And my PSA remains < 0.20. The risks of this treatment are substantial, with no proven benefits. Because theTLX591 (rosopatamab) monoclonal antibody binds so strongly to the PSMA protein it is not eliminated from the circulation nearly as fast. It goes everywhere and for much longer than Pluvicto. This causes much more bone marrow toxicity, certainly in the short term and possibly for the long term. Anemia is expected, sometimes severe, with 25% of patients requiring transfusions. Thrombocytopenia can also be severe with 10% requiring platelet transfusions. Fortunately, renal toxicity is absent since it is not excreted by the kidneys but rather the liver. But that is why it stays in the system so much longer and releases more radiation in the body rather than being rapidly excreted.
So the question I want to address now is: "Why?" Why am I doing this tomorrow morning at 9 AM? In order to answer that I must look at who I am as a person, and who I have always been. How do I live and have I lived my whole life? I embrace life and have always embraced challenges and sought out adventures that stretch me to my limits. Because I love life. Because I want to know and to live the fullness of my life- Of all that is possible. Of myriad dimensions and arenas of action, of knowledge, of being, and of love. I want to seek and to know THAT love that holds us all and sustains life. A life of fullness and celebration in every stage of life.
So that includes now. Even as an "old man" in body with cancer that cannot be cured that has diminished my capacities along with the changes of aging. But I will not be stopped from living as strongly and robustly and intensely as I am able. I fight against frailty and infirmity. And I fight against my cancer (that has also been my teacher).
So this experimental, a non SOC, non tested treatment, which is a new and different application of targeted radio-isotope treatment to earlier stage cancer, as I am now. Hormone-sensitive. oligometastatic, low tumor burden, no remaining PSMA avidity, with low PSA < 0.20. Yet still with metastatic prostate cancer). And I'm not on long-term ADT, but rather using high-dose cyclic testosterone treatment, which is also unproven and not SOC.
This is part of a two component treatment plan: First, treat the PSMA avid metastatic sites with SBRT. This was done last month.Then one month later do the two radio-ligand treatments with Lu-PSMA-TLX591.
This is what adventurers do. This is what explorers do, climbers do, astronauts do. This is what I choose to do because that is who I am. And how I (still) want to live for all of my days, be they few or many. So tomorrow May 13, 2022 here in Perth West Australia we proceed. The Great Adventure continues! - MateoBeach -Paul
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So well explained. Thank you. I will save your explanation with others you have written since I discovered your postings a couple of years ago. I hope this adventure goes well and you’re on your favorite beach in Mexico again soon. Take care.
Hi Paul, Thanks so much for sharing your thought process. I really hope it goes well -- we're pulling for you!
I also identify with the need to take difficult decisions. After tons of consideration I will start with something not yet SoC -- triplet ADT (ADT + Darolutamide + Docetaxel) + SBRT for metachronous mCSPC (that is low volume but rapidly advancing).
I've done a lot of research and gained invaluable input from this group and many qualified specialists. One of the best known oncologists here in California said it well and gave me some peace of mind by noting "there is no right answer" at this juncture. The data just isn't there yet.
In the end these are intensely personal decisions, essentially calculated high-stake gambles, but ones we are required to take at certain points. All the best! Keep us posted.
Hi, I've been battling PCa diagnosis for some time now, controversial with my past treatments. Fortunately, have great relationship with my Dana-Farber team, so SoC was a basis, which we ventured forward from.
"I've done a lot of research and gained invaluable input this group and from many trained specialists."
Great, I've given this advise to many with our plight, don't follow a generic checklist, instead push forward and understand (accept) the risks and aggressively attack the PCa . For instance, after my initial Lupron injection, my PSA 1000+ went to undetectable in just a few months!
At this point, no time to celebrate, we added Docetaxel!
And then while PSA was hovering a bit over "undetectable" we moved forward with SBRT to the hot spots.
In a nutshell, we didn't wait around for PSA tests to act...
Absolutely, forgot to mention the step of going on ADT vacation (about 10 months) with frequent PSA tests. So, a rise to PSA 2.17, (from PSA <0.02) we did a PSMA PET/CT scan, which clearly marked the 2 targets for SBRT.
So if you have had SBRT to all of the hotspots visible on a PSMA scan, then you are essentially in the same situation as me. If you would consider it you could arrange a virtual consult with Nat Lenzo of GenesisCare Australia to discuss posible treatment with the Lu-J591 monoclonal antibody ligand. Very much an experimental unproven approach with risks as well as out of pocket costs. It is available now though the clinical trial will be years down the road. The patients they are treating (less advanced the currently enrolling trial) will comprise a series of individual experiences that could lead to a future trial for oligometastatic, SBRT treated, low burden disease. A very personal choice.
And same back at you, PGDuan. Your planned multi-pronged approach sounds well thought out. Best of luck and see you on the other side of the SBRT and chemo. Paul
I am not cured but I went to India to have autologous dendritic cell vaccines. I had mets all over and the vaccines took it out of my bones etc. I hear you and I hope the best for you!
The treatment is at APACBiotech.com. They do it different from the vaccines here for advanced prostate cancer. They use your tumor to activate the vaccines. I was lucky it really helped me. Almost at 8 years with PSA at 212 at the beginning. I am not cured, just kicking the can down the road. So far so good. I am still very low on the PSA so far. It was .02. It seems it always comes back. So far the tumors are not great. Just one of those things. There was someone from Perth and it was interested in the treatment. He wasn’t able to do it back then. His name was Paul.
Bravo! I am early in my journey but have already hypothesized (and so have Doctors) that Radioligand treatment given at much earlier stages could be curative or in the least provide a dramatic increase in time to further distant metastases. That is great they are letting you in! I will be very interested to follow your journey on this!
Yes, it is the next step forward. Recognizing that cancer cells don’t need to be seen on the PSMA PET scan in order for the radio ligands to find them, bind to them and kill them. Earlier is very likely to be better.
I read your initial post and it resonated so well with my thinking. I am castrate sensitive (maybe depending on what the next PSA is, but think earlier treatment makes a lot of sense.
I have an appointment with a specialist in this area on May 24(Dr. Aggarwal UCSF) and look forward to what he has to say. I did not qualify for the one castrate sensitiveLu 177 trial for some reason which I forget now.
I look forward to hearing of your progress as I hope to do the same soon. Tired of being half the person I was two years ago. Half the energy, no good sleep and of course no sex life at all. I can still ride my bike in the mountains (where I live) but had to switch to e-assist. If I can't enjoy where I live I see no point in continuing.
I agree with you in principle that earlier is better.
However, I wonder if you can clarify something for me: if there are no cancer cells that can be seen in a scan, and if the subsequent radioligands use the same PSMA “affinity” to bind and kill, how can the PSMA-based radioligands succeed where the PSMA-based imaging did not?
Perhaps my assumption about the “same PSMA affinity” is misguided? Or perhaps it’s that there isbinding during the scan, but it’s not enough to be seen visually in the subsequent radiologist image analysis…?
IOW this is a hypothesis about micro-mets: yes, there is PSMA binding, and while it’s not enough to show up in imaging, it is enough to allow radioligand therapy to be effective.
Thanks for helping me out on this one, and apologies if this is a “duh” question.
It is a good question. The other binding molecules (ligands) have rather low binding affinities. Loosely held so to speak. So much of it washes out through the kidneys in just a few hours. This goes for the imaging agents like Pylarify PET, and the approved treatment agents like Pluvicto (Lu-PSMA-617). In order to be seen on the scans you need a very large cluster of PSMA positive cells. About 4mm at the very least. And for treatment with Pluvicto it is also helpful to have clustered groups of the cells so that the Lu isotope also has a chance of killing nearby neighbors.With monoclonal antibody ligands such as the J591, it binds very specifically and very strongly. I it finds a PSMA molecule on a cell it will attach and hold on and likely kill it. E cause of this it does not depend on having a larger lesion of grouped cells. It can be below the threshold for being visible on the scans. That is the principle and the hope in why you can attempt to eliminate or reduce micromets that cannot be seen.
Paul, Thanks for this clear explanation. This tread is assembling the information that you have worked very hard to organize and understand for your own care. Your work and thought processes are much appreciated. Thank you.
I wonder if you believe that the ligand will find and destroy micro metastases and if you are worried about having significant side effects since most the radioactivity will go to kidneys, gut and salivary glands since the cancer load is very small after the SBRT treatment of the mets.
That is a key difference with this J591 monoclonal antibody ligand. Low affinity in salivary glands and not excreted in urine (too big) so no kidney toxicity. It is metabolized then mostly hepatic excretion. But it does circulate in the body considerably longer, so more total radiation exposure. Hence the marrow toxicity. So, yes, dosing is very important yet hard to estimate. Enough to saturate cancer binding and not too much left over to circulate freely. Pharmacodynamics were explored in Phase I, but I haven’t seen the data. Will have that discussion this morning of course on dosage selection. There be dragons . . .
Can you wait for more Data? If the cancer is not PSMA avid, how will the radiation find the target? If i would you I would delay this experiment until the scientist have more Data.
Thanks for your questions Seasid. No I cannot wait for more data. There is none coming until future clinical trials hat are not even planned yet for this isotope on hormone sensitive. The only one recruiting is for mCRPC and that one will not have data until after 2024. I am in the exploratory proof of concept phase. If similar show good results it may lead to a clinical trial down the road for Lu-J591 in HS PC
The major new consideration is that you do not actually need to have PSMA avid visible mets on scan. I know my cancer makes PSMA even though my sites were already treated with SBRT. This is to go after unseen cancer cells and sites yet too small to be visible on the scans. The Lu-J591 isotope goes after the individual cancer cells wherever in the body they may be hiding. Anywhere and everywhere they seek out the PSMA protein on the cells, bind strongly to them, then kill them with radiation from the Lu177.
It is a next level treatment using monoclonal antibody radioligands. I had my first of two doses this morning and I feel so fortunate.
Actually they started with a single higher dose. But the bone marrow suppression (anemia and thrombocytopenia) appeared to correlate with peak levels rather than total dose. So they switched to dividing the dose into two portions two weeks apart to limit the peak level of radiation.
Ok, but do you really need 2 doses now? I am just wondering. Can you see the effects of the first dose and then to make a decision about the second dose? If you are targeting micromets maybe one dose is enough so you would have less toxicity and save some money. Beside this radioactive isotope treatment what is actually your present therapy? Are taking ADT? Are you taking ensalutamide or any similar drugs? I am now only on Degarelix and my PSA is slowly rising. Now it is 0.52. i am relactan to add anything as it could maybe just accelerate the cancer. The cancer goes around every treatment. Nubequa looks good but I can't get it here. What do you think about the CAR-T trial at Dana Farber? Why don't you join?
He must surely be aware of Drs Lenzo and McFarlane at Genesis Care in Perth and Sydney. The theranostics / Lutetium radio-ligand groups in Australia seem well connected. Peter Mac is extraordinary.
Ask Professor Hofman about his opinion regarding your personal cancer situation (therapy). I know that they are connected. Maybe he can give you a good advice. You can only benefit.
Asked Nat Lenzo about that very question this morning. He is on the review committee for the Phase I study on the pharmacodynamics, absorption, distribution, binding, metabolism and elimination dynamics of the J591 ligand. He says they are meeting next week to review those findings and implications. So he will give me the update when I return in two weeks for the second dose. Currently plans for the same 2.0 GBq dose as today if my blood counts are okay.
Pretty pleased with my post treatment scans. I have had them read twice and put through the London Multi- Disciplinary Team. Getting same view from both- phew.
Signed up for 20 lots of pelvic radiation plus 3x SBRT to Th9 which still has a small SUV. Risks of adding ‘whack a mole ‘ in understood but happening. In a flat in Helsinki for the month of May both working from here , joined a gym with Tallinn visit planned this weekend and grown up kids coming out for long weekend in Finnish lakes at start of June.
J591 is new to me! Hats off to Australia and to you! Rooting for you.
Best of luck with this approach. You being a physician yourself can fully understand risk benefits of non SOC treatments. Its only brave who dare to deviate from the path the herd is supposed to walk.
Best of luck! I admire your spirit. Besides the Lutetium 177-PSMA (mAb)-J591 information and your personal perspective explanation, the thing that sticks in my mind is the 30 hours of travel. I probably would have required hospitalization to recover from that.
Wow! Mateo!!! Can't tell you how amazingly humbled I am at reading your journey. Much admiration and appreciation for your deep dive into understanding and wanting to formulate an individualized treatment plan. Of course, as a spectator, wishing you all the success you have envisioned and plan for. The power of attraction cannot be easily dismissed, just as an athlete can foresee their success prior to an event, I'm wishing and sincerely hoping you have done the same!
That all said, there's a dozen questions that immediately pop into my brain when I see these type of posts. Mainly because I too have considered a few alternate paths, but have submitted to the SOC for now. I don't wish to eliminate them from possible future exploration.
First question is, how did you locate AUS as being friendly to accepting a patient who wanted to do what they wanted to do? Accept a mHSPC patient too? I'll assume already that this is outside any insurance coverage of course, but am interested in those discussions and how cost and payment is arranged for. Of course these are all aside from the treatment itself and how you come to chose this as the best for you? Was your tissue tested for certain markers? Especially the metastatic tissue lesions? What preliminary steps were taken to illustrate your staging and your plan of attack? How did you focus on the team you found and what was their initial response? I'm an inquiring mind obviously...
I'm sorry if these are intrusive, and welcome the PM path if you feel it is more appropriate.
Reasons being I had a few conversations with my care team and MO in regard to going off script. Largely due to how my PCa presented itself in an extremely rare manifestation. We talked about treatments used in other cancers which my PCa's characteristics mimic, but the tissue is most certainly PCa. I too am still hormone sensitive. I also discussed not waiting until "failure" to journey into another line of therapy. I believe that HAMMER is appropriate in dealing with cancer and don't feel that today's Oncologist are with that program. Susceptible to all the complexity of the regulation and control of the SOC, it works for many, but for those who fall outside that box, we are all standing alone as individualize treatment plans really just don't exist yet. We are nearly placed into these risk stratification boxes and then given a checklist to see what matches best. But we all know that doesn't work for all.
Again, much kudos and accolades for your choices you've made. Best wishes and hope that this is all going to do exactly what you want it to do for you and you'll enjoy success cutting a new path for others who might follow!
East Coast US, I've had a long held desire to travel to Perth myself. Its held my intrest for years, as it's so far from anything, but a modern metropolis with the ocean on one side the desert on the other. Thousands of miles to any civilization.
Twenty years ago I applied to see if I'd qualify to emigrate to Australia, but didn't have the right mix of occupation, age, and the big one that would have qualified me kids. Never had any.
So these days I'm going through my bucket list of places to see. Last summer completed 48 states in my RV. This past winter added Hawaii. You've probably guesses Alaska is coming up as well.
Still have Africa, to see animals in the wild. Some places in Europe I haven't been to as well. But Perth is on my list, I thought I might travel for medical reasons like yourself.
See Australia and New Zealand at the same time.
Enjoy your adventure, despite the risks this can still be the time of your life.
Paul, your words, so powerful. I feel I have just attended a Rock Concert. Every inch of my soul points to “Early is often Better”. You are clearly early here. When. I first read about LU-177, I thought…..game changer. Liquid radiation. This will take care of the circulating Cancer activity. BUT, we have learned it is far from perfect with 1/3 doing well, 1/3 Neutral, and 1/3 having a terrible time with it. This LU-J591, with a ligand having better attachment, and only 2 treatments, done early could give you a serious shot at remission.
“Life is either an adventure….or nothing at all”.
Thank you for making this solo ascent up a yet un-named mountain. We appreciate your well thought out unchartered journey. Please keep us posted as you are able.
Wow, thank you for your courage and walking a path ahead of us. I hope that all goes well for you and if there are any downsides that they are minor and quickly resolved. Thanks,
Is selection for non-PSMA avid PCa any cause for concern?
Whatever the answer to that, I find it extremely stimulating to digest your well researched and courageous pioneering path. Needless to say, please keep us posted.
It is a possible concern and is unknown if tiny micromets may harbor PSMA- sub population. Only time will tell. FDG PET not sensitive enough with no visible sites and PSA <0.20
Paul, I wish you the very best of luck in this great adventure.
Mateo, from from guinea pig (2004) to another (2022), I wish you the best. I read your post with interest as my ROs who in 2003 provided adjunctive primary treatment before referring to me a MO in 2004. All three at the time were Professors and Researchers at Baylor College of Medicine. After the divorce from Baylor, Methodist Research Hospital associated themselves with Weill-Cornel Medical School. The ROs made that conversion, my MO did not and moved on to Memorial Hermann and the McGovern School of Medicine.
Interesting that all three Professors research told them that attacking micro-metastasis was the key to cure of Metastatic Prostate Cancer. This is were I first heard the term and have spent hours seeking to understand.
Both ROs told me in 2005, that if my current clinical trial did not resolve my cancer, then come back as both Drs Brian Butler and Bin Teh we’re embarking in research on radioimmunotherapy vaccines. I never had to resort to their trials as Dr Robert Amato protocols yielded success for me. For me, early systemic treatment when the body was strong and the corresponding tumor burden minimal was key; essentially using combinations to killed micro-metastatic cells before they became invasive.
Your post caused me to review what is going on at Weill-Cornell with regard to radioimmunotherapy vaccines. Here is what I found:
I recently found out that Baylor College of Medicine is using the same protocols that Dr Amato, etal research at Baylor for Metastatic Breast Cancer; attacking micro-metastasis. Kind tells you that research dollars is critical in finding a cure.
I truly believe that APACBiotech is on the right path in their attack on unseen micro-metastatic cells. Where their research goes, I do not know; however, the research is 17 years in the making. Best wishes in killing your cancer cells.
Okay GourdDancer, you have blown my mind! Amazing they had a Phase II RCT with Lu-J591 that long back for BCR. Whatever happened with it? Did they publish? That article and the link to the study are not dated. I had no idea about this prior history. Must have been sometime back if they were using Ketoconazole for hormonal therapy. Thanks for the information and congratulations on your great results. Paul
Hi Paul, I’m just wondering how you’re going with the J591, have you been back here for the 2nd dose, is there improvement in PSA and cancer progression. Side effects? Probably too early to tell. Have you any knowledge of how the trial is going.
Im hopeful of going on the trial, I’m mCRPC and meet the conditions except for prior chemo. Dr Lenzo told me I still qualified because I’d refused chemo. He referred me to the PA hospital in Brisbane, close to where we live, which is also running the trial. They said no, that, according to their notes I had to previously had chemo. There’s been a bit of tooing and froing which is taking a lot of time meanwhile no treatment yet and my PSA is climbing, probably 50 now. If I am accepted the treatment probably won’t for at least another 6 weeks. Is it worth the wait or should I be doing something much sooner, Chemo, LUT 617, Radium 223. or Abi though I have done Enzalutamide.
Hi Ausi Ian. Doing well here. All mild side effects cleared within two weeks. Will get first meaningful PSA test in about 3 weeks. Would be concerned about delaying active treatment for you with PSA up around 50. Maybe more tumor burden.
Why not email Nat Lenzo and ask him to call the doc at PA hospital in Brisbane to see if they can reconsider?
Otherwise I would probably go for the chemotherapy first, if you can handle that. Or PSMA-617. What does your PSMA PET scan show?
My last PET scan in April when I started the process showed that there is a PSMA avid recurrent bony metastasis superiorly in the rightinnominate bone, and a new PSMA avid bony metastatic lesion more anteriorly in the right iliac bone.
I’ve phoned the PA and spoke The trial coordinator who had passed my details onto an Onc. I meet with my Onc tomorrow. I think you’re right and I may go for chemo.
Hi Paul, following my appointment today my Onc got onto the PA and he’s told me I am accepted into the trial. I’ll be interested in following your progress as it is a new drug hence the trial. During my consult with the Trials Onc he said that the SUV is a good indication of success. He said mine was moderately good. I suppose yours would be low because of your low PSA and consequently low cancer burden.
That is wonderful news, Ian. Promising a better way of targeting PSMA expressing cancer cells wherever they may hide. And with much stronger binding from the monoclonal antibody. I wish you well of course. And will also keep you updated as my results unfold. PSA in early July will be the first indicator. With a month off of the high testosterone cycle for me.
Congratulations on your courage and wish the best of luck with your adventure.I too have been out of soc, but to a lesser degree than you, as I have continued my ancestral type eating, which is centered around red meat and wild caught fatty fish, and avoids processed foods, seed oils, sugar and carbs in general.
Hi Jalbom. That is excellent. Have to go back to very remote ancestors for me, hunter gatherers of the Steppes probably. But I thrive on ketogenic regimen of mostly animal proteins in large amounts with above ground veggies. So very similar. And indeed feel like a hunter on it. Able to hike mountains and deserts every day without hunger. What is your heritage if I may ask?
Askenasi Jewish from Poland and Russia but I have reddish hair probably from some Viking ancestor somewhere. I took up the diet to save myself from a lifetime of obesity, diabetes and sleep apnea. All gone now for nine years. Feel much better at 73. Than at 43.
Am in remission with undetectable psa after oligometastatic pc.
Paul, what was your platelet count before the lu-177 procedure? Did it change much? I read that it was 89 afterwards. I just got a blood test today and my platelets have dropped to 90 even though I have not done any new treatment. The only change is that I have become Castration resistant. Maybe the resistance is causing a reduction in platelets? I had two other vials taken an hour before this blood draw. That doesn't seem like it would be enough to drop me from 150 where it was a few months ago.
It's encouraging and good news to see your numbers following the procedures of LU-177. Have you had other radiation or chemo in the past, which may have affected your blood counts.
Thanks for being courageous. Another great guy on this site, went to India last year for LU177 and had good results from it.
My platelets dropped from 151 to 89 at 6 weeks after the last Lu-J591. That is expected to be the nadir so is not dangerous. Told to expect it to be recovered by next test in September.
Not sure why CR would necessarily cause platelet drop unless also accelerating bone mets? Of course all radiation and chemo have some cumulative effect on marrow over the long haul. Some cancer-triggered idiopathic or immune thrombocytopenia? Keep a close eye on it amigo.
Pluvicto is Lu177-PSMA-617. It is the brand name by Novartis FDA Approved in the USA. But only for castrate resistant metastatic and failed both taxane and an AR drug. Also specific requirements for scan PSMA avidity. I meet almost none of those criteria and am HSPC. Lu treatment appears to work better in early disease stages. So that is why I went abroad for Lu treatments now.
Pluvicto is fine for those who are more advanced already and qualify. Someday I expect it to be approved for HSPC.
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