A path through the CD47 wilderness?
Continuing the third part of our ongoing CD47-SIRPα mini-series, we move on from the science and the competitive landscape to look at what CEOs in this niche have to say. There are many different approaches being evaluated at present, mostly in preclinical development, which makes it an intriguing area to potentially follow over time as new data emerges.
Not all of these molecules will be successful and the target is certainly not the easiest to attempt, although not as diffcult as MYC or RAS either!
When all is said an done, what do key players in this field think when they are developing compounds and how do they see the emerging challenges?
In this latest post, we have not one, but two CEOs, who were willing who share their candid thoughts and perceptions on the CD47-SIRPα space…
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When an oncology R&D landscape starts getting crowded and highly competitive, how do you go about working out clinically meaningful differences between compounds in development?
After all, there are often a myriad of small differences and nuances in the preclinical approach that may or may not be useful when it comes to the clinic.
Sometimes design matters, whether this be in the way the molecules are built or function, perhaps in tumour types that are selected for study, while at other times trial design can impact outcome. In short, much like a 3D chess game it can get complicated pretty fast.
One such area that has been receiving increased attention lately and also has a lot of complexity to consider is the CD47-SIRPα pathway.
Last week we covered some of the key basics in a primer exploring the science in Part 1 of this mini-series.
Tomorrow we will post Part 3, which focuses on candid comments from researchers and CEOs in this niche, but before we get there it’s time to look at key clinical perspectives, as well as some of the nuances from related pathways that may be important factors to consider.
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As we move from monotherapies to combinations in the immuno-oncology space, we start to see some intriguing ideas being explored from additional checkpoints to vaccines to neoantigens to immune agonists to oncolytic viruses. There are numerous ways to evaluate how to boost or jumpstart more immune cells upfront in the hope of seeing better efficacy.
One way to do this is to better understand the tumour microenvironment.
Wall of people at ASH16 in San Diego
If we know what’s wrong under the hood, we might be better able to make the immune system get going… more gas, faulty starter motor, dead battery, loose wire, broken fan belt? All these things and more might be a problem so you can see that diagnosing the issue up from from basic and translational work might be instructive for clinical trials.
If you don’t know what problem you’re trying to fix or repair then you might as well be throwing mud at the wall. Just as we don’t expect a car mechanic to suggest changing the battery or starter-motor without first diagnosing the issue, so understanding the tumour microenvironment in each different cancer or disease might also be a helpful strategy.
At the recent American Society of Hematology annual meeting (#ASH16), there was a fascinating sceintifc workshop that focused on this very concept – what’s going on under the hood and how do we go about fixing it?
Here we explore these ideas via an interview with a thought leader and specialist in the field. What he had to say was very interesting and candid indeed.
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The abstracts (apart from the late-breakers) for the 2016 annual meeting of the American Society of Hematology (Twitter #ASH16) went live at 9am ET today. Link to 2016 ASH Abstracts.
ASH16 takes place in San Diego from December 3-6.
In this initial post, I’m sharing my first impressions of what may be some hotly contested trials at ASH16 in San Diego, as well as a few intriguing abstracts with combination data that caught my attention.
With over 3,000 oral and poster presentations, all typically of a high quality, this by post by definition, is a highly subjective one.
After we’ve had more time to process the data, further ASH16 Previews will roll out over the next few weeks highlighting more key abstracts to watch out for by tumour type or treatment modality.
In-depth commentary and analysis will follow after we’ve heard or seen the data presented at the meeting.
I’ll be flying to ASH from the EORTC-NCI-AACR Molecular Targets meeting. Do say “hello” if you have plans to be in Munich or San Diego.
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