Coney Island Roller Coaster
In the roller coaster of life that is oncology R&D, molecules come and molecules go… a rare few reach blockbuster heights while many others are quietly packed off to dog drug heaven, never to be seen or heard of again.
This is also very true of targets as well…
What about the in-between space?
Unfortunately, that’s where most molecules and cancer targets end up – into a deep black nothingness where we seek the high affinity targets with low grade side effects – and fall short in some way. It’s a frustrating place to be, to be sure.
One of these conundrums is compounds against CD123 (IL3Rα), which have been in the spotlight on and off this year and are turning out to be a rather mixed bag.
After our recent update on Cellectis and their CD123 direct CAR T cell therapy (UCART123), I wasn’t expecting to write any more on this until ASH in mid December. How wrong that prediction turned out to be!
Today we have quite a few things to discuss on this topic, so if interested in CD123 in hematologic malignancies and going beyond that to find better targets in AML then this is the poster for you…
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This morning, like many folks, I woke up to the latest immuno-oncology news on the bispecific front that Xencor, a Los Angeles based biotech, announced their latest collaboration, this time with Novartis.
Over the last few years, we have seen a surfeit of bispecifics emerge that are focused on stimulating the immune system, particularly with regard to T cells and natural killer (NK) cells, as well as antigen targets on the surface of tumours. The first one approved was Amgen’s blinatumomab (Blincyto), a CD19 targeted bispecific for the treatment of acute lymphoblastic leukemia (ALL), which we have written extensively about.
The Xencor/Novartis deal has a number of interesting implications that are well worth exploring in more depth that go far beyond the information provided in the press release.
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One of the most important challenges in cancer immunotherapy is overcoming immune resistance. For example, even with the high response rates seen in acute lymphoblastic leukemia (ALL) with CAR – T cell therapy, a significant number of patients relapse after an initial response.
Chinatown, Honolulu 2016
Could immune resistance be reversed or prevented by the addition of appropriate checkpoint blockade? Which ones matter though, that is the critical question? Rather than randomly picking ones to try, we need scientific evidence regarding these choices.
This post explores some of the latest data presented at the BMT Tandem meeting on the role of T cell immunoglobulin mucin–3 (TIM–3) and PD–1 upregulation in causing resistance.
If you’re not already a sub and want to read our coverage of ASH, BMT Tandem and the forthcoming AACR 2016 annual meeting, you can purchase individual access below. This week only – inspired by the story of Eddie Aikau in Hawaii – we have a special offer that we’ve never done before (and may never do again) of $75 off a quarterly subscription. The deal ends tomorrow Friday March 4th at 12 noon HST. Check it out!
Subscribers can login to read more about the latest data on how alternative checkpoint inhibitors may have a role to play in cancer treatment. Welcome to the new folks who signed up this week, good to see y’all!