Topic: Abemaciclib Verzenio for Stage IV

Forum: Stage IV/Metastatic Breast Cancer — 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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Jan 9, 2018 08:10AM cure-ious wrote:

Some progress is being made on identifying biomarkers for response to CDK4/6 inhibitors (and luce-there is no way only 14% of luminal A cancers respond to drugs like Ibrance, don't know the number but it would have to be waaaay higher to get a doubling of response in the trials)

Here is a recent paper showing that certain mutations in Cyclin D1 gene, in breast and other cancers, can cause it to get amplified and those cancers respond particularly well to Abemaciclib.

https://www.ncbi.nlm.nih.gov/pubmed/29232554


Dx 10/2003, IDC, Stage IIB, ER+/PR+, HER2- Dx 7/2015, Stage IV, metastasized to bone, ER+/PR-, HER2-
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Jan 9, 2018 10:06AM - edited Jan 9, 2018 10:10AM by luce

Zarovka: Thanks for your informative reply regarding monitoring! Yes, I agree on the immune system stimulation and involvement, and that it is the key. That's why it greatly concerns me what abemaciclib is doing to the gut microbiome, where the immune system presumably resides. One of my doctors (an MD, not an ND) believes that generally, the gut microbiome is the key to being, becoming, and staying healthy and alive. He recommends a high-dose bifidobacteria supplement. (Not that that is a cure at this time, of course.) Abemeciclib riding roughshod over the GI tract might ultimately not keep us alive longer, nor offer any chance of an actual cure, I worry.

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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Jan 9, 2018 02:59PM zarovka wrote:

Luce - It is interesting that you mention Abemaciclib's effect on the gut. My primary treatment is immunotherapy at the moment so anything I do needs to complement the immunotherapy (enhance not depress the immune system). I've seen strong arguments in favor of Abemaciclib because of the PDL-1 inhibition ... takes the breaks off the immune system. I considered doing it as a single agent through the treatment. However, the gut issue is a concern. For the moment I am watching and waiting.

Probiotics are one way to go. The problem is that the bacteria are never really going to set up shop and thrive in your got with the constant armageddon going on. Same problem with chemo. I take a Japanese product called Chitsu which is basically lactus bacteria broken down by enzymes found in soy. Basically the product is broken down bits of bacteria. It gives you some of the effect of these good bacteria even if your gut cannot support the ecosystem.

Viome is an interesting test. The provide the most comprehensive profile of the gut that I have seen. Something to consider if you want to know if your gut is getting in the way of your health. You may find you have a healthy biome in there despite the diarrhea. That may give you some piece of mind.

I have had mild to extreme diarrhea for 3 months, ever since September and I haven't been on an standard of care. I haven't had time to figure out what is going on. Will be doing a Viome test soon.

It would be interesting to study what Abemaciclib is doing to the gut lining and how that might effect absorption and the immune system. So many things I would like to study ...

The truth is that we often don't see improvements in overall survival from treatments that are pretty good at getting rid of lesions. Like you, I suspect that the side effects are one reason for that.

>Z<

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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Jan 9, 2018 03:24PM aem65 wrote:

Thanks so much for creating this post! I'm new to Abemaciclib (started a few days ago) after progressing on Faslodex/Zometa. I was bone-only for a decade until a recent scan showed a few small spots in my liver...hence, the med switch. I consulted with an IR at City of Hope yesterday who has requested an additional MRI to assess the full extent of the mets. That said, he recommended giving the Verzenio 6-8 weeks to determine efficacy before exploring localized treatment (I'm hoping for RFA). Upon the first dose of Abemaciclib, I had extreme nausea/headache/dizziness that was akin to motion sickness. I was fully expecting diarrhea based on the data from the Monarch-2 trial and I have an rx for Lomitil on hand. Didn't need it initially but I was sidelined by the nausea so took a couple days break and now I'm reattempting today with Zofran. My gut (pun intended) is telling me that this med may not be optimal as I too am underweight and not thrilled about compromising the microbiome. I'll be following this thread faithfully and will keep you posted on my SEs.

Dx 1999 IDC Stage 2, ER/PR+, Her2- Dx 7/09 Stage IV mets to bone
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Jan 9, 2018 03:41PM cure-ious wrote:

Luce- The most recent studies show that Abemaciclib works synergistically with immunotherapy, and that immunotherapy in turn is very dependent on good gut bacteria and strongly stimulated by probiotics that have bifidobacterium, so your ONC sounds right. Apparently, we will hear updates from the first year of Abemaciclb-Keytruda next month, but for anyone taking immunotherapy its probably a good idea to add probiotics as well .

Dx 10/2003, IDC, Stage IIB, ER+/PR+, HER2- Dx 7/2015, Stage IV, metastasized to bone, ER+/PR-, HER2-
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Jan 9, 2018 04:04PM luce wrote:

This is the probiotic my doctor recommends and I use: http://www.customprobiotics.com/five-strain-bifido...

I've looked but not found anything comparable anywhere. (I had been hoping to order at cost through my ND friend from one of her suppliers, but haven't found a brand that combines that many strains of bifidobacteria, or anywhere near that potency.)

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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Jan 9, 2018 06:14PM cure-ious wrote:

interesting, Luce! Are you taking Abemaciclib now? Because the probiotic/Bifido in preclinical studies had the same effect as a low dose of immunotherapy- and if Keytruda were also added, that combo might be very effective. Is your doctor part of a clinical trials hospital?

One question is whether we will even be allowed to take Abemaciclib after failure on the Ibrance-Femara combo, I'm certainly hoping so



Dx 10/2003, IDC, Stage IIB, ER+/PR+, HER2- Dx 7/2015, Stage IV, metastasized to bone, ER+/PR-, HER2-
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Jan 9, 2018 06:15PM cure-ious wrote:

Z- What is up with you?! Still in Siena? When do you go back to Japan, world traveler?!!

Dx 10/2003, IDC, Stage IIB, ER+/PR+, HER2- Dx 7/2015, Stage IV, metastasized to bone, ER+/PR-, HER2-
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Jan 9, 2018 06:30PM cure-ious wrote:

Also, Luce, did you notice any increase in neutrophil levels when taking the probiotic?

Dx 10/2003, IDC, Stage IIB, ER+/PR+, HER2- Dx 7/2015, Stage IV, metastasized to bone, ER+/PR-, HER2-
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Jan 9, 2018 07:04PM cure-ious wrote:

Here is one of the 2015 papers that identified bifido as tumor fighting- note however it is for melanomas, which respond well to immunotherapy whereas MBC does not.

https://www.ncbi.nlm.nih.gov/pubmed/26541606


This shows bifido bacteria stimulate immune system function, including tumor killing activity, and helps patients get more benefit out of immunotherapy. Might do the same thing in combination with Ibrance/Abemaciclib, and all three could be better?


Dx 10/2003, IDC, Stage IIB, ER+/PR+, HER2- Dx 7/2015, Stage IV, metastasized to bone, ER+/PR-, HER2-

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