The tumultuous history of the drugs that helped cure Jimmy Carter

[n2doc]

Immunotherapy can be an effective treatment against cancer. But over the past 30 years, research into immunotherapy has nearly been abandoned several times. And if no one had ever picked it back up, it might have been bad news for former US president Jimmy Carter.

Last August, Carter announced he had stage IV metastatic melanoma, and that it had spread to his brain. When he first got the diagnosis, he thought he might have only “a few weeks left,” he said, but by the time of his press conference, he was more optimistic.

Carter would soon undergo surgery and radiation treatment, and would also receive regular doses of pembrolizumab, an immunotherapy drug that had been approved by the Food and Drug Administration (FDA) to treat melanoma less than a year earlier.

And four days ago, after about three and a half months of treatment, Carter announced that his cancer was gone.

The former president, who is now 91, said in a statement: “My most recent MRI brain scan did not reveal any signs of the original cancer spots nor any new ones. I will continue to receive regular three-week immunotherapy treatments of pembrolizumab.”

more

http://qz.com/566948/the-tumultuous-history-of-the-drugs-that-helped-cure-jimmy-carter/

[eppur_se_muova]

1. A key to some of those strange drug names ...

n contrast to traditional chemotherapeutic agents that affect rapidly dividing cells, targeted agents are more precise in the way they fight cancer. Presently, two main families of targeted therapies exist—monoclonal antibodies and small molecule inhibitors. The ending letters (stem) of the generic names are like surnames that tell what family the drug is from and how the drug works to kill cancer cells. Monoclonal antibodies end with the stem “-mab” and small molecule inhibitors end with the stem “-ib”. The “-mab” family of targeted therapies has three distinct methods for interfering with cancer cell growth.
***
The sub stem of the generic names of the “-mabs” identifies the source where the antibodies were generated or cloned. The three most common sources are

Chimeric human-mouse—drugs ending in “-ximab” (i.e., rituximab)
Humanized mouse—drugs ending in “-zumab” (i.e., bevacizumab)
Fully human—drugs ending in “-mumab” (i.e., ipilimumab).

Finally, both “-mabs” and “-ibs” contain an additional stem to describe the targeted therapies bullseye. For example, the “tu” in rituximab indicates the target is the tumor, the “ci” in bevacizumab designates the circulatory system, and the “li” in ipilimumab identifies the immune system target. Some of the intracellular targets for the “-ibs” include:

Tyrosine kinase inhibition—sub stem “-tinib” (i.e., imatinib)
Proteasome inhibition—“-zomib” (i.e., bortezomib)
Clyclin-dependent kinase inhibition—“-ciclib” (i.e., seliciclib)

The prefix of the generic names and the drug market names are where researchers and pharmaceutical companies—like the parents of the young dancers—take creative liberty.
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more: http://connect.ons.org/ons-connect-blog/the-names-of-targeted-therapies-give-clues-to-how-they-work#sthash.t50QdkrI.dpuf

[Jim Lane]

2. Thanks! I always thought the names were completely made up. Interesting to know the system. (n/t)