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Understanding our future: immunotherapies

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Understanding our future: immunotherapies

I just listened to one of the best and easiest to understand videos I’ve found, explaining how the new monoclonal antibodies (elotuzumab and daratumumab) work.

Dr paul richardson 2My good friend and long lived myeloma survivor, Jack Aiello, is interviewing Dana-Farber’s Dr. Paul Richardson on a Patient Power broadcast. It’s short and to the point. Give it a listen:

There are a number of other related videos available, too. You may need to join Patient Power; a good idea and it’s free:


Honestly, I have mixed feelings about the immunotherapy approach. Like I’ve often said, it’s hard to hit a moving target. For example, daratumumab targets a protein common to most myeloma cells, CD38. Note I wrote, “most myeloma cells.” Maybe the fact drugs like these aren’t all inclusive leads to those disappointing 30% success results in experienced, late stage patients like me.

To pause and review, monoclonal antibodies are part of a broader category known as immunotherapies. For our purposes we can use the terms interchangeably, referring to new compounds that enlist our own immune system to attack and weaken unwanted cancer cells. Elotuzumab and daratumumab are first in class attempts to do this. But researchers are confident that building off these basic models, more sophisticated alternatives will be available very soon.

Now, there are three or more new monoclonal antibodies being developed which target CD38. And like drugs in existing classes (IMiDs and proteasome inhibitors), sometimes a similar drug succeeds when the first one fails. So if daratumumab doesn’t work, maybe SAR650958 will. Similarly, if Velcade (a proteasome inhibitor) stops working, maybe its new oral cousin, MLN9708 (Ixazomib) will.

That’s the best part as new immunotherapies are developed. You can add them to combination therapies with little risk of additional side effects. This will allow doctors to bracket our myeloma, hitting it from a number of different directions, with drugs seeking out and destroying different targets.

Using traditional chemotherapy only, toxicities mount as each new drug is added to the mix. But with new immunotherapies, additional toxicity is low. So I can envision the day when more than one immunotherapy is used at the same time, or possibly a pulsing approach, using a number of different drugs in sequence.

Mind blowing, isn’t it? The key is the targets. If CD38 doesn’t get it done, the next group of immunotherapies will hopefully target other protein types, expanding the numbers of patients that can be helped.

Of course there are still major hurdles to climb. For example, how do researchers get a new immunotherapy–or any myeloma drug–to last longer. Being one of the lucky ones that respond to elotuzumab or daratumumab is great, but the response may only last ten months or so. Someway, somehow the response time needs to be extended, don’t you agree?

But I’m not here to rain on anyone’s parade. I can see why myeloma specialists are so excited about the promise of immunotherapies, in this case first generation monoclonal antibodies. And you can bet the drug companies are all over the concept. That’s a great thing!

Plenty of room for optimism, especially for myeloma patients near the start of their difficult journey. For late stage patients like me? The researchers better start peddling faster!

Feel good and keep smiling! Pat