How long on a CDK 4/6 inhibitor (Ibrance/verzenio/Kisqali)?
I’m sure this info is buried deep in the various stage iv threads, but I’m hoping people will post their experiences and success stories here. I think the median from the initial studies was about 2 years, but obviously there is more real world experience as time passes. Thank you!
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Verzenio/Anastrozole
- dose reduction to 100mg for SEs after about 8 mos (NED in 7½)
36 mos and counting
- currentlywaiting/watching for possible recurrence/progression
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I've been on Ibrance for almost 7 years. I've been stable-next scans are in October so we'll see.
Never been NED but I'll take stable.
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Ditto exactly Chicagoan - nearly 7 years stable on Femara & Ibrance and next scan in October.
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this is great - thanks so much!
Let’s keep it going!
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Verzenios + femara since September 2022. Dose reduction to 100 mg October 2022. NED shortly afterwards but increased activity July 2023.
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I have been on a Ribociclb since March 2021. I am stable, I am not sure but with bone mets, I dont think you can be NED?
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Ibrance/letrozole - December 2019-September 2021 but I didn't fully come off it until February 2022 for reasons. Like everything else it was a long, slow decline on this drug. Started at 150, down to 100 after first cycle, and stayed there until my very last cycle in Jan 2022 at 75. It didn't do a whole lot for me other than shrink my primary a little bit and otherwise hold the bones stable. For some de novo women it seems to completely resolve the breast and axillary tumors!
Mel is also in the 7 Year Club. I think if you respond really well to this combo you can go a long time but I dont think they've figured out yet the super responders secret sauce yet. I hope they do!
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Ooh, Chicagoan & Chico, you guys are like the exceptional responders from the first trials of Ibrance!!
I happily made it to the 8 year mark this summer- 5 of those were on Femara-Ibrance and then another 3 on Faslodex-Ibrance (switched to Verzenio in Jan this year due to neuropathy)
Have slight progression on bone scan and figuring out what's next, expect to change after upcoming scans in Oct…
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Hello to everyone,
wishing all the best to everyone of you. I would like to ask you if the long term (7 years and more) responders ( Chicagoan, curious, Mel… ) are all of you de novo. My mother was diagnosed as metastatic after 26 years of initial diagnosis and has been on verzenio for 1 year. She is doing well and I hope she will continue for a long time.0 -
margarita12 I am pleased to hear that you mother is doing well. I was Dx mbc 12 years after Dx bc so I was not de novo. I have extensive bone mets and I have noted that Ibrance appears to work well for some of us who are bone only.
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Margarita12,
My story is a bit complicated. I likely had breast cancer since 2004 but did not pursue conventional treatment until 2016. So I was technically de novo but very sick by the time I sought conventional treatment. I had extensive bone mets and pleural effusion. I am glad your mom is doing well and wish her all the best.
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Chico, Chicagoan,
Thank you for your answers. Your stories are encouraging. Good luck and all the best are my wishes for you.
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I was de novo bone only but BRCA1+ and I guess I got this crappy p53 gene too. I guess I would just caution about extrapolation - its great to hope you will be one with the lucky number to come up, but if you get the median thats still worth celebrating.
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I agree, I was kind of hesitant to answer the original question, CD/46 inhibitors are not a cure and they dont seem to know why some do well on them and some dont do as well.
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My first diagnosis was Oct 2003, then extensive bone mets in summer of 2015, almost to the point of needing a rod in my femur, but instead I got a kidney stone(s) from all the calcium in the bloodstream and the mets could be seen in the Xray.
And, like Chico, I got a good response to Ibrance, despite the cancer being ER+ PR- (Her2-)
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Cure, has there been any research on why some people do well on CDK4/6 inhibitors and some don't do as well?
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I think there was some sort of analysis of super-responders in general being spun up at UW-Madison but the last I heard about that was a year or two ago. I suspect with more time and more ladies on these drugs (including those coming on from earlier stages as a prophylactic) more information will come to light. I mean, even in the last two years Kisqali was shown to have better effect than Ibrance and there was all of a sudden shift to Kisqali prescribing.
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Sunnidays, I like this 2020 paper by Richard Finn at UCLA (link below). They were involved in some of the earliest studies on Ibrance, and he noted an interesting finding that although most people respond at some level to CDK4,6i, those who don't often have high PD1/PDL1 or in some way are more likely to be more responsive to immunotherapy. So he suggests a sort of possible mutual exclusion between CDK4,6i and immunotherapy. They also noted cancers with growth factor signaling also get extra benefit from CDK4,6i. Most cancers respond, so at the start they were just noting which cancer types get the most help from having Ibrance included, and those were the cancers that were less responsive to anti-estrogens alone. Its worth a new search to see if more is understood now about biomarkers for a long response.
There was a lot of excitement at the beginning in lab studies indicating that CDK4,6i would make cancer more responsive to immunotherapy, however combination trials doing that in firstline did not pan out. However, we now have the PACE trial which suggests that immunotherapy might be more effective after treatment with CDK4,6i. They are now trying to identify biomarkers that could be used to determine who might be a good candidate for immunotherapy combination trials. Recent studies have also suggested that CDK4,6i can drive a forward loop that extends the amount of time that the cancer is endocrine-dependent, but I haven't seen a mechanism explaining that
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Oh, I see more genes have been identified as a source of resistance to CDK4,6i, including high tumor mutation burden, p53 mutation, loss or mutation of Rb or the PTEN tumor suppressor, AURKA or cMyc mutation, there are multiple routes…
https://www.sciencedirect.com/science/article/pii/S0960977622000145
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Bumping
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