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.
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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!