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Responding to IMiD and proteasome inhibitor may be game changer

Home/About Pat, Supplements/Drugs, Therapy, Transplants/Responding to IMiD and proteasome inhibitor may be game changer

Responding to IMiD and proteasome inhibitor may be game changer

Friday I left everyone hanging when I wrote:  Monday I am going to explain how this seemingly mundane result–a 0.2 M-spike–may have been the most fateful news I have ever received as a soon to be six year multiple myeloma survivor.  I know I said Monday.  But I couldn’t resist yesterday’s fun and frivolous, self indulgent look at our fun St. Patrick’s Day.   But now the barking dogs and bagpipes are only a fading memory.  Time to get back to work!

Let me reproduce more copy from Friday’s post as a review to help get us started:

Even a small M-spike can be dangerous for me.  After my first relapse, I began to experience bone involvement and damage at a low M-spike of 0.5.  So even an upward creeping 0.2 number was concerning.

Since I had never used Velcade until my induction therapy prior to my auto stem cell transplant 20 months ago, I had asked Dr. Alsina before we started consolidation therapy, after my transplant, if we should experiment with Velcade and dex alone.  After all, I had been using Revlimid for the better part of five years.  But RVD (Revlimid, Velcade, dex) worked so well for me during consolidation she didn’t want to mess with it.  And in her defense, it had worked much faster post transplant than it had before.

But following that report, she had decided it was time to stop cold-turkey.  “Let’s drop the Revlimid.”  Said my doctor of few words.

So Thursday’s appointment was key.  After three months, could Velcade and dex alone do the trick?

YES!  Results from last week’s PET scan remained stable, with the only questionable area my already damaged right hip.  That single hot-spot could be written-off as layer upon layer of lesion-laced decay.

And my M-spike.  A wonderfully stable 0.2.  Weekly Velcade and 20 mg dex had done the trick and held the line.  Better yet, my Kappa/Lambda quantitative free light chain ratio had dropped below the magic value of 1.0; now 0.93.

So what is the significance of all of this for me–and more importantly for you?

We all dread the lab work analysis we get from our doctors.  Whether it’s monthly, every two or three months, we wouldn’t be human if we didn’t sit-down in that exam room with trepidation.  We’ve all be there, right?  “Am I still in CR?”  “Am I still stable?”  “Has the new therapy helped slow things down?”

Month in and month out.  Always the same.  Of course, if our myeloma is “gone” or stable it helps us feel a bit less apprehensive with time.  But invariably, that sense of uncertainty or dread returns–and so does our myeloma.

I received good news from Dr. Alsina last Thursday.  My myeloma had remained stable for three months.  So what?  What made this news so fateful for me?

It proved Velcade and dex alone are capable of keeping my myeloma at bay.  I wasn’t in remission–that had only lasted a short ten weeks.  But stable at a low 0.2 M-spike works for me!

More importantly for my long-term prognosis, this proved that my myeloma will respond to a proteasome inhibitor as well as an IMiD. 

Let me back-up a sec.  Like Thalomid (thalidomide) and the newly FDA approved drug, Pomalyst (pomalidomide), Revlimid is an IMiD; an acronym for immunomodulatory drugs.  Revlimid worked for me–on and off–for five+ years.  This makes it likely that I will respond to Thalomid and/or Pomalyst.

Now Velcade is working for me.  Velcade is a proteasome inhibitor, a second class of anti-myeloma drugs.  Newly FDA approved Kyprolis, and the experimental, intriguing new drug, MLN9708 are both also proteasome inhibitors.

What makes last Thursday’s news a game changer?  Now that we know my myeloma is responding to Velcade and dex alone–like IMiDs–I am more likely to respond to Kyprolis and/or MLN9708, too. 

With all the news circulating about new drugs, one stark fact remains clear:  IMiDs, proteasome inhibitors and high dose melphalan (used just prior to a stem cell transplant) are (so far) the only three ways to achieve remission.

Depending which expert you ask, there are theoretically six or seven pathways doctors might use to attack myeloma.  Researchers are feverishly pushing to establish additional therapy options that utilize new pathways with mixed results.  If and when they are successful, they may be able to box myeloma in and achieve what I call a “chronic cure.”

More about all of this on Thursday.  Tomorrow I’m going to run a promo about this month’s Myeloma Cure Panel broadcast.  I can’t put it off, since we air live Wednesday night!

In the meantime, feel good and keep smiling!  Pat