Okay, I finally got Checkpoint inhibitors
After reading Ted’s summary about three times, I finally figured it out. I admit I never understood what a checkpoint inhibitor was before. Here’s how it goes (simple version):
When foreign or tumor cells arrives in the body, immune cells, especially T-Cells, multiply and go out and kill the foreign or tumor cells.
But it’s no good if the immune cells just keep multiplying because they’d clog everything up and cause a lot of problems. So the body has some molecules called CTLA4 and PD-1 that turn off the immune response when appropriate. We call these molecules checkpoints.
The T-Cells (immune cells) kill most cancer cells, but occasional cancers are successful because they happen on a way of using the body’s CTLA4 and PD-1 molecules (checkpoints) to suppress the T-Cells and stop the T-Cells from killing them, the cancers.
So drug companies have developed drugs that inhibit the checkpoint molecules (CTLA4 and PD-1) that are being used by the cancers to protect themselves from the T-Cells. And, natually, these are called checkpoint inhibitors.
And what’s IL-2?
It stands for interleukin-2 (brand name Proleukin). It’s a medication molecule that stimulates T-Cells like mad. But it has two problems: it’s quickly destroyed so it has to be given very frequently, and it goes all over the body and causes T-Cells to go wild throughout the body instead of just in the tumor, so it was incredibly toxic, and it never caught on.
And how would be NKTR-214 better?
If NKTR-214 is proven to do all it’s supposed to do, it will be prove to be delivered specifically to tumors, bind preferentially to cell types that fight tumors, and specifically activate them to start killing off the tumor cells. This means preferential activity and little or no toxicity.
I hope that this simplified version helps some of you understand this better. Figuring it out helped me! And a big, BIG, thanks to Ted, for explaining it so I could finally understand it.
Best,
Saul