Topic: Abemaciclib Verzenio for Stage IV

Forum: Stage IV/Metastatic Breast Cancer ONLY — Please respect that this forum is for members with stage IV/metastatic breast cancer ONLY. There is a separate forum for caregivers and friends: Caring for Someone with Stage IV or Mets.

Posted on: Jan 1, 2018 02:03AM - edited Jun 17, 2018 09:19PM by zarovka

Posted on: Jan 1, 2018 02:03AM - edited Jun 17, 2018 09:19PM by zarovka

zarovka wrote:

Luckylegs and friends on Abemaciclib - I am bumping the Verzenio discussion in the hopes that more people have started abemaciclib. We need to get a community going. I have not started abemaciclib but it is on my short list. Like many I am very interested in how people do on this treatment do, both as a monotherapy and in combination with hormone suppression and other treatment. I am hoping that this thread can capture the experience of everyone on Abemaciclib in whatever combination. This is a very important treatment option that we all need to be evaluating.

I would expect more people on the drug given the significant advantages of abemaciclib over the first generation CDK 4/6 inhibitors. However, the FDA has approved abemaciclib for only limited indications. We have not established its use as a first line treatment nor as something to switch to from Ibrance. At the same time, they haven't made it clear that the drug can and should be used after Ibrance. As a result, the setting for using abemaciclib is supremely unclear.

I believe abemaciclib can be used either instead of or after palbo/ribo depending on whether you view abemiciclib as another class of drug or the same class of drug with significant improvement. One can make arguments for either strategy. If you've already done palbo/ribo, it is certainly worth trying abemaciclib. If you haven't done palbo/ribo, the current guideline that you start with the first generation CDK 4/6 is reasonable, but not necessary IMO. A lot depends on the side effect profile you can tolerate the best as the drugs have significant differences in side effects and also whether you are at risk of brain mets. Abemaciclib is better at crossing the blood brain barrier.

The following summary of abemaciclib data taken from a thread started by Constantine on Inspire. I moved his entire discussion from three posts because it's that good. Thank you Constantine.

ABEMACICLIB (VERZENIO)
Preliminary data from a phase I study of abemaciclib [SABCS 2014] in patients with five different tumor types including HR-positive metastatic breast cancer, with I note a median of seven prior systemic therapies (outliers out to 11 lines) found an objective response rate of 19% and a disease control rate (including stable disease (SD) under RECIST definition of >24 weeks of ) of 81% for HR-positive MBC patients. This Phase I study was expanded to evaluate abemaciclib plus fulvestrant in HR-positive MBC [ASCO 2014.] with patients having a median of four prior systemic therapies (and outliers out to the eight line), finding an objective response rate of 62% confirmed PRs.

A subsequent Phase I study [Tolaney et al, J Clin Oncol 2015;33(Suppl 1).] of abemaciclib in combination with different endocrine therapies for HR-positive MBC (median lines of treatment = 3, with outliers out to 8) demonstrated a disease control rate (CR + PR + SD) was 67% for those on abemaciclib + AI therapy, and 75% for those on abemaciclib + tamoxifen.

The phase II MONARCH-1 trial evaluated abemaciclib MONOTHERAPY in HR-positive, HER2-negative MBC patients with a median of 3 lines of prior therapy for advanced disease, including a median of 2 lines of chemotherapy (as opposed to endocrine or biological therapy) for advanced disease, yielding an objective response rate (ORR) of 17.4% and a clinical benefit rate (CBR) of 42.4%.

What's important to remember about MONARCH-1 is that many women in the study had already received multiple lines of endocrine treatment (median 3 - 5 previous lines in the metastatic setting, with outliers beyond that), developed resistance and were refractory to all of these treatments, AND progressed, many of whom also received chemotherapy, and these results were for MONOTHERAPY in a heavily pretreated population, which as I determined through examination of historical controls with any other agent achieves at best only 10 to 20% clinical benefit rates - half of that achieved by single-agent abemaciclib, and with responses of short duration.

Hence, the collective results of these trial, including MONARCH 1 (MONARCH-2 (with letrozole) and MONARCH-3 (with fulvestrant) are exceptionally exciting breakthrough in breast cancer therapeutics.

BREAKTHROUGH SURVIVAL
In addition, for me, the overall survival (OS) of these heavily pretreated MBC patients was 17 months, and that compares to historical control I review from all clinical trials to date, as significantly better than other survival results, which are usually are at best 13 months. Thus, consider that for the current champ, eribulin chemotherapy in this setting, the EMBRACE trial achieved a median overall survival (OS) was 13 months, we clearly have here a major advance and improvement in overall survival in the highly challenging later-line settings (past at least 3 lines of therapy).

HIGH TOLERABILITY
The major limiting constraint with all CDK4/6 inhibitors to date, like palbociclib (Ibrance), is their most common adverse effect, that of myelotoxicity via neutropenia (low WBC neutrophils), with palbociclib (Ibrance inducing some degree of neutropenia in over half of women on it, with associated dose interruptions and sometimes dose reductions, a toxicity that so fat from the available data seems to also afflict ribociclib.
But abemaciclib (Verzenio) evades a good deal of this because although strictly a CDK4/6 inhibitor, it is more specific in inhibiting CDK4, that is it is CDK4-selective, and myelotoxicity including neutropenia is primarily associated with CDK6, making the incidence of neutropenia on abemaciclib significantly lower and more manageable.

CLINICAL LESSONS ON ABEMACICLIB (VERZENIO)
And unlike palbociclib (Ibrance):

1. abemaciclib has strong single-agent activity in HR–positive MBC,
2. has durable response in later line settings,
3. a good tolerability profile with reduced neutropenia, and
4. to date the highest OS in these challenging heavily pretreated settings of any oncotherapeutic agent, whether endocrine therapy, chemotherapy, or biological therapy.

SOME NUANCES
1. The ESMO-reported MONARCH 3 Trial found an response rate of 48.2% for all patients, BUT for the subgroup of patients with measurable disease, a response rate (ORR) of 59.2%, these being the highest ever response rates achieved to date for ANY endocrine therapy in breast cancer.
2. And although data needs to mature further for survival outcomes, it is anticipated based on exploratory analyses that PFS will weigh in at an improvement of close to 12 months, again an extraordinary gain.
3. In addition, Verzenio was most effective in challenging populations like those with visceral metastases (especially liver) and those with rapidly recurrent (short disease-free-interval (DFS)) patients.
4. Finally, 16 patients across two of the three MONARCH trials were NED (complete response (CR)), likely to increase once the MONARCH-3 data matures, more still I anticipate when results are reported from the MONARCH PLUS and other trials.

DIARRHEA AND ITS MANAGEMENT
To put the adverse events into a bit of perspective, although it is true that with Verzenio, all-grade diarrhea was between 86 - 90%, yet serious (Grade 3+) incidence was 13 - 20% but this is aggregated across the trials, and note further that diarrhea incidence is concentrated during the first month, and more narrowly the MTO (median time to onset) of the first diarrhea event was 6 days, lasting a median duration of just 6 days for Grade 3. Furthermore, for the most recent MONARCH-3 RCT, grade 4 diarrhea was zero, and grade 3 diarrhea was just 9.5%.

An aggressive proactive regimen of:

- high-dose loperamide/Imodium (4 mg but NOT ever de-escalated down to 2mg (and up to 16 -32 mg daily);
- "Big Pink" (Petpto Bismol Extra Strength) used in "priming" mode (started on day 4 and also used for immediate relief during loperamide dosing;
- budesonide (Symbicort) for recalcitrant cases;
PLUS "adjunct interventions:
- high-dose probiotic (28 billion microorganism count in two divided doses), and
- electrolyte powder (most of the refractory diarrhea was analyzed to be secondary to disturbed microflora and electrolyte imbalances)
- at least 12 8 oz glasses of fluid daily, 8 of which should be electrolyte-enhanced

brought the rate of diarrhea-related drug omission or dose reduction down from 22% (MONARCH 1 and 2) to under 1 - 2% in the cohorts run by my research teams in India and the Middle East.
NOTE: We found that the adjunct interventions of Big Pink, high-dose probiotic, electrolyte rebalancing, and assured fluid intake were at least important as the conventional agents, and in cases that seem intractable, converted to success, given that therapy-driven diarrhea inevitably causes GI tract flora, and electrolyte, imbalances, aggravated by inadequate hydration. Also critical was "through-and-through" loperamide dosing: 4 mg at each episode, but NOT de-escalating - as current protocols do - down to 2 mg after first (that de-escalation regimen we found indifferently effective, with large numbers of failures.

And although not reported to date, I note that in the MONARCH 3 trials the incidence of ANY grade diarrhea dropped to just 2% (courtesy of data provided by Levi Garraway at Lilly).

ACTIVITY IN LOBULAR CARCINOMA
The trials largely fail to report to date differential invasive-type stats, but the impression from conversations with some principals is that lobular breast cancer subjects are unlikely to experience significant decrement, and I also extrapolate from some hints surrounding the PELOPS (Palbociclib and Endocrine Therapy for LObular Breast Cancer Preoperative Study) Trial another CDK4/6 inhibitor palbociclib (Ibrance), as well as from some molecular considerations (the p27 gene is a key regulator of certain types of progression (G1 to S-phase) and it appears that lobular carcinomas tend to have higher p27 which in a complex way under contextual effects can have either positive or negative effects on phase progression), but we have to await sub-group analysis to report on this issue explicitly. I am cautiously confidant of little differential outcome, which I think may be confirmed across the general class of CDK inhibitors. In addition, both the lobular and the ductal groups appear to have benefited from the addition of palbociclib (Ibrance) in the PALOMA-/TRIO-18 Trial, but I note that the difference observed in PFS in that trial is likely to be an artificial artifact of the small patient in the subgroup with lobular carcinoma arm (n = 18/19) compared to n = 117 in the ductal subgroup, so this is a small sample size effect not a robust finding, an impression in agreement with that of the principal investigators (Richard Finn and UCLA and colleagues). As we learn more about lobular BC and abemaciclib in particular, I will offer further clarifications.

DEGREE OF DIFFERENCE - IBRANCE v VERZENIO
Given the dramatic 14-fold (!) greater CDK4 activity in abemaciclib (Verzenio) compared to palbociclib (Ibrance) and ribociclib (Kisqali), as MONARCH 3 lead author Angelo Di Leo has established and noted in interview, and other consequent fundamental molecular pathway differences, I view these as only shared-class (CDK), but therapeutically distinct, agents, more like the difference between third-generation capecitabine (Xeloda) versus first-generation 5-FU although these are both fluoropyrimidines.

So: More different than same as witness also the high degree of relative invariance of efficacy and durable response in later-line treatments for Verzenio compared to that of Ibrance (see my original posting, above). These differences are sufficient warrant for me to classify palbociclib (Ibrance) as a first-generation CDK inhibitor, and abemaciclib (Verzenio) as a second-generation CDK inhibitor. The devil - as always - is in the details.

CNS (BRAIN) ACTIVITY
We have preclinical data [Raub et al. Drug Metab Dispos. 2015] of the cross-BBB (blood-brain barrier) capability of Verzenio, as witness the remarkable benefit in GBM (glioblastoma, being even non-inferior to temozolomide (TMZ), the standard of care in cross-BBB activity, and this although not a human clinical, was an in vivo, not just in vitro, study. And the Dana-Farber JPBO human clinical trial (I3Y-MC-JPBO) under Sara Tolaney is investigating single-agent abemaciclib in patients with ER+/HER2+ brain metastases, where I fully expect clinically relevant CNS benefit to be confirmed, with first phase interim results reported in June at ASCO 2017 showing 2 patients (8.7%) out of 23 having confirmed partial response (PR).

I should point out that there has been some provisional data on palbociclib (Ibrance) having potential cross-BBB activity in brain metastasis, but I hasten to note that strong in vivo data show a 10-fold greater cross-BBB activity for abemaciclib than palbociclib, with abemaciclib brain levels being more efficient at substantially lower doses than palbociclib and also active for longer duration, and finally abemaciclib was active as monotherapy, palbociclib was not.

Finally, as to leptomeningeal metastases, no explicit data bears on this question directly, but as to date all agents active in brain metastases have also been active in leptomeningeal metastases, activity would be expected.

THE ISSUE OF SWITCHING
It remains an open question whether patients who have progressed on or after another CDK inhibitor like palbociclib (Ibrance) may derive significant benefit from continuance of CDK4/6 inhibition by using a following CDK inhibitor like abemaciclib (Verzenio), with many in-progress trials like TRINITI-120 (and NCT0185719319 and NCT0263204521, among others) exploring the issue. But there is some plausible extrapolation from some preclinical data which has suggested non–cross-resistance among CDK4/6 inhibitors. A Barts Cancer Institute study reported at SABCS 2016 found that some palbociclib(Ibrance)- and ribociclib(Kisqali)-resistant cell clones were sensitive to abemaciclib (Verzenio).

For patients now on Ibrance (or Kisqali) but who have NOT PROGRESSED , is it motivated to switch to abemaciclib (Verzenio)? This is an issue that needs to be thrashed about candidly with your oncology team and is a highly individual decision, but my own sense at this time is that it may be more optimal in the long run to stay the course, and consider abemaciclib (Verzenio) for recourse upon progression either off-label until the FDA expands its approval, or on one of the many abemaciclib (Verzenio) clinical trials available.

I would however entertain some specialized exceptions in which a switch now, off of Ibrance or Kisqali, onto abemaciclib (Verzenio), might be motivated; for example:

1. If a patient is experiencing repeated difficult-to-manage neutropenia, occasioning multiple drug interruptions or reductions (neutropenia being dramatically less with abemaciclib (Verzenio)), but the patient must weigh the associated countervailing issue of higher incidence - but still manageable I would argue - diarrhea on abemaciclib (Verzenio).
2. If a patient is in advanced later-line setting (say, more than 5 to 7 lines or so of treatment in the metastatic setting already completed), where it is suspected that abemaciclib (Verzenio) may be somewhat more consistent and durable in response and benefit in such challenging contexts. This is a difficult one to judgment-call, and I would tend to want to weigh each patient's circumstance and their complex treatment history and individual pathology to assist in the decision, since we have no hard data to be dispositive on this decision.

Yes, these are arguable and have to be intensively debated (as in a tumor board setting), but they are not wholly unreasonable. Outside of these exceptions, however, I do not see sufficient motivation to prematurely abandon Ibrance or Kisqali, as these have strong track records of efficacy and should be push to progression.

FDA APPROVAL

Abemaciclib is currently approved ...
1. as combination therapy with fulvestrant (Faslodex) for the treatment of women with HR+/HER2- advanced or metastatic breast cancer who experience disease progression AFTER ENDOCRINE therapy.

2. as monotherapy for the treatment of women with HR+/HER2- advanced or metastatic breast cancer who experience disease progression AFTER ENDOCRINE therapy AND prior CHEMOTHERAPY in the metastatic setting.

(Z) MO's have latitude to prescribe outside of these indications and there are strong arguments for doing so. My MO appears to have wide latitude to prescribe Abemaciclib and get insurance approval in other settings.

EXPANDED ACCESS:
Abemaciclib continues to be available through Lilly's attractive Expanded Access Program (EAP):
https://clinicaltrials.gov/ct2/show/NCT02792725?term=abemaciclib&rank=24
which is active and recruiting currently in several US locations (California, Florida, Minnesota, Missouri, Texas, and West Virginia), more being added. However that is for patients who have not as yet progressed on a previous CDK inhibitor like palbociclib (Ibrance), that is, for "switchers" who may want to explore the improved benefits of abemaciclib (Verzenio) over Ibrance (assuming the patient meet the other trial criteria); but not for patients who have already progressed on Ibrance.

RECHALLENGE

In several cases I have known, I counseled that although someone progressed on Ibrance, to reintroduce it after a hiatus of 3 - 6 months, and in many cases this washout appeared to resensitize the tumor cells to Ibrance, which upon re-introduction was newly effective. It is a variant of a trick I have counseled and seen working not infrequently with other agents like capecitabine (Xeloda) where after progression on it, I advised a trial on a new metronomic schedule (low-dose, continuous, daily, capecitabine) and seen again it newly effective despite previous progression, just by this shift I schedule (there is some provisional data for this, but not decisive). But these are beyond convention and reserved for highly special circumstances.

MARKERS THAT PREDICT RESPONSE TO CDK 4/6 INHIBITION
I am not convinced that there is any biomarker - protein or otherwise - that reliably identifies responsivity to CDK inhibitors, and Fabrice Andre of the Institut Gustave Roussy and colleagues, as reported in their presentation at ASCO 2017, were unable to identify any such biomarkers of response: neither Rb levels, p16 protein levels, Ki-67 cell proliferation, CDKN2A, CCND1, nor even ESR1 gene expression, all the usual suspects, and others, had any response-predictive value whatsoever. To date the only established biomarker for response to CDK4/6 inhibitors, remain hormone receptor positivity (HR+). Of course not everyone responds, but response rates remain historical high - and higher than any other treatment to date - and as long as one is HR+, one has the potential to benefit from a CDK inhibitor.

Constantine Kaniklidis
Director, Medical Research, No Surrender Breast Cancer Foundation (NSBCF)
Oncology Reviewer, Current Oncology [journal]
Society for Integrative Oncology (SIO)
Member, European Association for Cancer Research (EACR)

Ibrance/Letrozol Feb '16 -Sep '17. Adoptive Cell Therapy Oct 2017. Jan 2018 SBRT to sternum met and liver mets. Jan 2018 start Faslodex. Dx 12/28/2015, IDC, Left, 4cm, Stage IV, metastasized to bone/liver, Grade 3, ER+/PR-, HER2- Hormonal Therapy 1/16/2016 Femara (letrozole) Targeted Therapy 2/2/2016 Ibrance (palbociclib)
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Dec 14, 2018 09:02AM WorkingMom10 wrote:

I haven’t posted here in quite a while. I’ve been on Verzenio (150 mg twice a day) an LY3300054, a form of immunotherapy since March 2018. Disease has been stable so far. TMs are at 22. Still have a tough time with diarrhea and nausea every couple of days. These are usually controlled by using immodium and zofran. I have my next set of scans on 27 Dec and am hoping for more good results.

Dx 4/26/2011, DCIS, 6cm+, Stage 0, Grade 3, 0/1 nodes, ER+ Surgery 7/17/2011 Mastectomy: Left, Right; Reconstruction (left): DIEP flap; Reconstruction (right): DIEP flap Dx 11/1/2016, Stage IV, metastasized to bone, ER+/PR+, HER2- Chemotherapy 11/22/2016 AC + T (Taxol) Radiation Therapy 12/5/2016 External: Bone Hormonal Therapy 5/4/2017 Tamoxifen pills (Nolvadex, Apo-Tamox, Tamofen, Tamone) Targeted Therapy 3/14/2018 Verzenio
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Dec 14, 2018 12:54PM luce wrote:

workingmom10, it would be really interesting to know much more about your trial and side effects. i googled it and it looks like it is a keytruda-like checkpoint inhibitor but not actually keytruda? do you have any autoimmune symptoms as a result of the checkpoint inhibitor? what TM are you referring to? does it keep dropping or being stable?

Dx 12/12/2016, ILC/IDC, Left, Stage IV, metastasized to bone/lungs/other, Grade 2, 0/3 nodes, ER+/PR+, HER2-
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Dec 14, 2018 01:23PM cure-ious wrote:

Ditto to Luce's questions, workingmom!! How interesting to hear from someone on this trial- can you tell us more of how you decided to get in to the trial, did you start on tamoxifen and then Ibrance-Femara? and then progress, or what is your history since diagnosis? Still bone-only disease? was it a few spots or widespread (f you don't mind sharing all that stuff). And for the immunotherapy, what side effects?! And Luce, are you on Verzenio alone?

Also, I was reading that some doctors are concerned that leaving femara and moving to faslodex should be a transition, ie for 3-6 months you might want both drugs. The idea is that removing femara too fast leads to estrogen increase and faslodex cannot degrade the estrogen receptor immediately, so by combining the two you give the faslodex a 'head start' before removing the femara= has anyone heard about this?

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Dec 14, 2018 08:50PM - edited Dec 14, 2018 08:50PM by Chemokaze

Pajim, I am sorry to hear about the progression. I have heard that these CDK 4/6 drugs sometimes take several months to really kick in, so I guess I am wondering how does one know how long to give it a chance to work....even with some progression? I'm just thinking out loud and sending The Force.

And thank you Luce, Cure-ious, Working Mom

10/2018: NEAD; 7/2018: Onward to Verzenio, Zometa, Faslodex, & CyberKnife to single met to L4 spine. Dx 9/1996, IDC, Left, Stage IB, Grade 3, 0/21 nodes, ER+/PR+ Dx 5/2016, IDC, Right, Stage IIIC, Grade 2, 14/21 nodes, ER+/PR+, HER2- Dx 6/2018, Stage IV, metastasized to bone
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Dec 14, 2018 09:11PM Chemokaze wrote:

Quick story that makes me want to get 2nd radiological opinions when there is concern about progression.

I found out that my original L4 lesion on my 5/2018 MRI...the scan that first revealed my met was under measured.

This was discovered after 2 follow up MRIs after CyberKnife treatment in 8/2018....showed the lesion was larger by 50% in one dimension. Lesion was same measurement on both of those scans. All MDs scratching their heads because my PET scan was ok in Oct.....so they sat down and looked at ALL imaging including the more precise MRI I had for CyberKnife planning at that facility....and that’s when it was found the tumor was under measured in May.... so I had not progressed after all.

So, still on Verzenio/Faslo/Zometa.....diarrhea is manageable most of the time, hair is thinning, eyes sometimes suddenly leak!......still wondering about the efficacy of the Verzenio at a lower dose....will ask next month

10/2018: NEAD; 7/2018: Onward to Verzenio, Zometa, Faslodex, & CyberKnife to single met to L4 spine. Dx 9/1996, IDC, Left, Stage IB, Grade 3, 0/21 nodes, ER+/PR+ Dx 5/2016, IDC, Right, Stage IIIC, Grade 2, 14/21 nodes, ER+/PR+, HER2- Dx 6/2018, Stage IV, metastasized to bone
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Dec 15, 2018 07:39PM luce wrote:

hi, cure-ious: yes, monotherapy, by my own choice. anti-estrogen therapy is indicated but i have never wanted to go that route, even before i went into premature menopause from chemo. i don't like life without estrogen. chemo-menopause has been hell (i wouldn't even have done it had i known it would destroy my ovaries. long story): i wake up from nightsweats up to 15 times a night.

i never tried adding keytruda. too worried about autoimmune issues. have you heard any updates from the JPCE trial from san antonio?

Dx 12/12/2016, ILC/IDC, Left, Stage IV, metastasized to bone/lungs/other, Grade 2, 0/3 nodes, ER+/PR+, HER2-
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Dec 15, 2018 08:44PM - edited Dec 15, 2018 08:45PM by cure-ious

Hi Luce, No news on JPCE, WTF?! they just didn't show up, and nothing reported since SABCA2017!! So are we to infer that the trial is not going well? It's super-frustrating when these trials just disappear, absolutely no idea.

It sounds like Faslodex is working great for you- its been awhile, hasn't it? The PFS of Faslodex alone is supposedly only six months, but there are people on these boards who took faslodex alone for YEARS.

I'm thinking its time to try adding Faslodex to the Ibrance-Femara, why not? My onc will probably say that is not an approved protocol, but I see some people doing it here..

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Dec 15, 2018 11:14PM JFL wrote:

Chemokaze, very disturbing about the scan measurements being off and that you hadn't actually progressed when the report said you did. Scary. I do see my own PET-CTs with my DH, which makes me feel a bit better. My scan before my last one had stated that I progressed until my MO called the IR. If my MO didn't call, my DH was going to do so. The IR ignored the note I just had a Y90 radioembolization procedure on my liver mets and indicated I had progression when it was only post-Y90 changes - swelling around the tumors (all mets were inactive in one lobe and had a significantly decreased metabolic uptake in the other). He revised the report to state that it appeared the Y90 was working.

Cure-ious, odd that there was no news on JPCE. You are probably right re that not being a good sign as far as the study results go. I took Ibrance/Aromasin/Faslodex and had no issue getting it past by insurance. My MO did that for me because I was pregnant when diagnosed and he said the AI would not do anything for the circulating estrogen that was raging around my body at the time. I would say from observation that once people fail Ibrance, there seems to be a major explosion of the cancer. If that could be prolonged, that could be a good thing. I lasted 15 months on that combo although I didn't start the Ibrance until about month 7 or 8 when it was approved in combination with Faslodex. I suspect I would have lasted a longer on that regime had I been taking Ibrance from the beginning. I may be lucky to have made it that long because I had numerous aggressive genetic mutations / amplifications that indicated that I should be resistant to hormone therapy at that time.

Chart your own course. Dx at 30. Dx with mets at 38 while pregnant - extensive liver & bone involvement. Currently on Enhertu & XGeva. ER+/PR+, HER2-low (IHC equivocal, +2/FISH negative). Y90 liver radioembolization in 2018. Dx 9/2006, IDC, Right, 1cm, Stage IIB, Grade 3, 1/16 nodes, ER+/PR+, HER2-, Surgery 9/22/2006 Mastectomy: Left, Right Chemotherapy 11/5/2006 Adriamycin (doxorubicin), Cytoxan (cyclophosphamide), Taxotere (docetaxel) Hormonal Therapy 3/15/2007 Tamoxifen pills (Nolvadex, Apo-Tamox, Tamofen, Tamone) Dx 12/2014, IDC, Stage IV, metastasized to bone/liver/other, Grade 3, ER+/PR-, HER2- Surgery 12/26/2014 Prophylactic ovary removal Hormonal Therapy 12/26/2014 Aromasin (exemestane), Faslodex (fulvestrant) Targeted Therapy 6/18/2015 Ibrance (palbociclib) Chemotherapy 3/10/2016 Xeloda (capecitabine) Hormonal Therapy 5/13/2017 Aromasin (exemestane) Targeted Therapy 5/13/2017 Afinitor (everolimus) Chemotherapy 8/17/2017 Abraxane (albumin-bound or nab-paclitaxel) Chemotherapy 3/22/2018 Doxil (liposomal doxorubicin) Chemotherapy 4/25/2019 Navelbine (vinorelbine) Hormonal Therapy 4/25/2019 Tamoxifen pills (Nolvadex, Apo-Tamox, Tamofen, Tamone) Chemotherapy 11/26/2019 Gemzar (gemcitabine) Hormonal Therapy 8/24/2020 Faslodex (fulvestrant) Targeted Therapy 8/24/2020 Piqray (alpelisib) Targeted Therapy 10/1/2020 Enhertu (fam-trastuzumab deruxtecan-nxki)
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Dec 16, 2018 05:30AM sandibeach57 wrote:

Hi Cure-ious. I follow this thread because I might request Verzenio/Fas as my next treatments. Why are you thinking of adding Faslodex while still on Ibrance/Letrozole? Do you suspect you are progressing and Faslodex is next anyway? Or do you just want to make sure all estrogen paths are blocked?

DCIS (06&07)HR+Gr 3 Bil mx-rad-tamox. Oct 2016 Stage IV liver mets IDC ER+PR-HER2- Gr 3 AC then I/L 01/17- 03/20. Liver mets 03/20 ER+PR+HER2- Gr 3 Xeloda until 06/21. Liver mets June 2021 ER+PR+HER2-Gr 3 Taxol.(IHC 1+, FGFR1amp, ATM inver)
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Dec 16, 2018 06:18AM pajim wrote:

Cure-ious, back in the day (maybe 8 years ago) there were two trials of letrozole alone versus letrozole plus Faslodex as first line therapy for ER+ MBC. This was in the pre-Ibrance days.

When I was diagnosed I chose Femara/Fas as my first line. And it appears I was right as the paper just came out showing an overall survival advantage. Not a large one but still.

When F/F started to fail me, Ibrance had come on the market. MO suggested we just add it on. Gave me another year on the treatment. Insurance paid. I don't recall any wrangling about it either.

Dx 4/20/2008, IDC, Right, 4cm, Stage IIIA, Grade 2, 1/15 nodes, ER+/PR+, HER2- Dx 2/1/2013, IDC, Stage IV, metastasized to bone, mets, ER+/PR+, HER2- Hormonal Therapy 2/26/2013 Femara (letrozole) Hormonal Therapy 4/21/2013 Faslodex (fulvestrant) Targeted Therapy 2/24/2016 Ibrance (palbociclib) Chemotherapy 6/18/2017 Xeloda (capecitabine) Targeted Therapy 8/14/2018 Verzenio Chemotherapy 1/1/2019 Halaven (eribulin) Chemotherapy 12/29/2019 CMF

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