Biotech Strategy Blog

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

With all the heightened interest in checkpoint inhibitors of late, I wanted to continue my series on what did we learn from the updated data at ESMO that was different from ASCO? Last week we discussed gastric and bladder cancers, this week it’s the turn of lung cancer, or more specifically, non-small cell lung cancer (NSCLC).

By chance, some interesting announcements have also happened since ESMO with the third quarter earnings calls going on from the main players in this space, which also add colour to the developments in this niche. BMS, for example, announced that they expect their rolling NDA for Opdivo in lung cancer to be completed before the year end and will be presenting the CHECKMATE 063 data this week, while Merck announced their Breakthrough therapy designation for Keytruda in lung cancer this morning.

All in all, this makes the lung cancer space a lot more exciting than it was at ASCO, where the response to the data was fairly muted.

To learn more about the updated ESMO data and the impact of the recent announcements in lung cancer, you can log-in to read our insights.

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2 Responses to “Update on PD1 checkpoint inhibition in lung cancer”

  1. David Miller

    How about this hypothesis… Smokers have more mutations, which the immune system at some point probably tried to attack the mutations. The damage persisted so long, the immune system probably shut itself down on those mutational — or mostly, anyway. Using a checkpoint would remove the brakes/press the gas and perhaps reconstitute a prior “failed” immune response.

    This probably isn’t sufficient for big responses, under this hypothesis, but might give the immune system enough regulatory “breathing room” to keep pace. Hence why we’re seeing more impressive swim plots than waterfall plots.

    Just a hypothesis…

    • maverickny

      An interesting hypothesis, David.

      Part of the problem is that cancer cells are ‘self’ not ‘foreign’ cells, so I suspect the immune system doesn’t really see them as something to attack in the first place. Plus the cancer cells lock onto the T cells and hold them down in place, a bit like an armlock. It’s only when they are unlocked that they can be primed to welly the cancer cells.

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