Biotech Strategy Blog

Commentary on Science, Innovation & New Products with a focus on Oncology, Hematology & Cancer Immunotherapy

Posts tagged ‘TIM-3 Checkpoint Inhibitor’

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

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!

Over the last couple of years we have heard much about targeting various checkpoints that exert an inhibitory effect on the immune system and the T cells, in particular.  The main targets where we have a growing body of evidence to date are CTLA-4, PD-1 and PD-L1, but there are others including LAG-3, TIM-3, ICOS etc.

Earlier this year at AACR, we saw new evidence that combining two checkpoints (anti-CTLA4 and anti-PD1) was superior to monotherapy in metastatic melanoma, albeit with a concomitant increase in toxicities.

What about the other inhibitory signals though?  Are they bystanders, much like passenger mutations that have little effect, or do they matter, at least in some tumor types?  If so, which ones?

We took a look at some of the emerging data associated with targeting TIM-3 – the results may well surprise some observers.

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