I had the opportunity to participate in another Myeloma Panel hosted by Cure Talk and the wonderful Priya Menon. Last week’s guest was Dr. Asher Chanan-Khan of Mayo in Jacksonville.
Dr. Chanan-Khan was speaking about monoclonal antibodies (elotuzimab, daratumumab, etc.) which are emerging therapies that didn’t exist even a few years ago. They’re exciting because most of the developments in Myeloma over the past five years — chiefly Carfilzomib and Pomalyst — have been continuations of existing families of drugs. Carfilzomib is a proteasome inhibitor, like Velcade, and is essentially a more effective version of the same drug. Pomalyst is next generation Revlimid, which itself was next generation Thalidomide — all immunomodulatory drugs. And like Carfilzomib vis-a-vis Velcade, it’s more effective and is easier to tolerate. Because Velcade and Relimid are themselves so effective against Myeloma, and because Carfilzomib and Pomalyst / Pomalidomide are effective in patients that have MM with resistance to Velcade and Revlimid, Car and Pom are usually used as “salvage” therapy to extend the lives of people who have otherwise run out of options. This is all good and fine, and 18 months may be a lot of time to somebody who is otherwise looking at packing bags (not to be overly morbid).
But 18 months isn’t long enough for somebody that wants to live many years. And so new drugs that are whole new ways of attacking MM have special interest. There are others (believe it or not, one is called a hedgehog inhibitor) but the ones that are now “in market” so to speak (meaning in Phase III trials) are monoclonal antibodies.
I knew very little of these prior to the call, so I was excited to learn a bit about them.
Essentially, myeloma cells express certain proteins — these have names like CD138, CD38, CD27, CD45, etc (the CD stands for, I think, “cluster designation” since the proteins are in clusters). Monoclonal antibodies attach themselves to these proteins and allow the body’s immune system to attack them, killing or weakening the cells. Consequently, these are effective both on their own and in conjunction with other therapy (e.g., Velcade, Revlimid, etc.) that kill cells. As a result, adding an antibody to treatment with Velcade can reduce drug-resistance to Velcade.
Because not all MM cells express these proteins, and because the key is still getting a weakened immune system that wasn’t particularly good at getting rid of MM in the first place to respond and kill the targeted cells, this is not a perfect therapy and it’s not a cure. But it does represent an advancement and, combined with other therapies, could make a significant impact.
Looking at my MRD test, UAMS tested for the presence of seven proteins in my marrow (CD138, CD38, CD45, CD56, CD81, CD27, CD20 and CD19, for those playing the home game). Of the 3,562,010 cells analyzed, none exhibited any of these proteins. That sounds good!
On December 16th, there will be another panel conversation and the guest physician will be Dr. FVR, who works for BB. I will have some specific questions for him about the current “cure curves” for Total Therapy 3 and 4, now that there has been 10 years of follow up for the first group and five for the second. I will also be asking about residual monoclonal protein, per my last post.
If any of you have other questions, feel free to post them in response to this, or email me and I’ll see if we can’t get some of them answered.
Meanwhile, for those that celebrate the holiday, let me extend a hearty Happy Thanksgiving to you and your families!