September 1st… as the hot summer floats away from London town and cooler autumn days draw in, it’s time to think about the upcoming fall cancer conference season – it’s quite a busy one this year!
In the coming weeks, I will be rolling out our series on the ESMO 2016 Previews (Twitter #ESMO16) and taking a more in-depth look at various topics of interest. The Copenhagen meeting is later than usual and also more compressed, with numerous sessions now held simultaneously. It used to be that you could take a break between key sessions, but not any more – there’s a lot going on this year.
One of the things that jumped out to me from a preliminary review of this year’s hectic ESMO program is an interesting novel target that had some early preclinical data at AACR, but that sadly got lost in the tsunami of data there.
It is good to have that reminder and be able to return to it in the context of broader data because overcoming barriers to drug resistance with targeted therapies is still an important issue that is worth researching.
You likely won’t see it in many analyst reports or previews, however, although it’s a hidden gem of great interest and well worth exploring in terms of what we know so far. This means that readers will be both prepared and intrigued – don’t be surprised to hear about some BD&L deals in this niche in the future.
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Last month’s Biotech Strategy mailbag – where we answer questions from subscribers – turned out to be rather controversial with strong feelings running in several camps on Puma Biotech’s neratinib in breast cancer.
This time around we have a bunch of questions on completely different topics and compounds to cover:
- BRAF plus MEK and/or immunotherapy in BRAFV600 metastatic melanoma
- Immunogen’s IMGN853 – now known as mirvetuximab soravtansine – in platinum resistant ovarian cancer
- AbbVie/Genentech’s ABT–199/GDC–0199 venetoclax
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After the recent raft of posts on immunotherapy, it’s time to turn our attention back to oncogenic addiction. A couple of key topics have dominated colorectal cancer over the years, namely what causes EGFR resistance and why don’t patients with the BRAF V600 mutation do as well with RAF monotherapy compared to melanoma patients?
In today’s post, we take a more detailed look at BRAF mutant colon cancer in terms of what we’ve learned so far and what the potential therapeutic solutions are, which could influence patient outcomes in a positive way.
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The ASCO 2014 season kicks off with the release of the embargo on main abstracts (other than the late breakers and plenary sessions) yesterday evening. Over the next week, I’m planning to cover some of the highlights (positive and negative) that I found interesting or worthwhile discussing. While there was nothing particularly earth shattering or new in the press briefing at lunch time yesterday, that’s not to say there aren’t some important data this year buried amongst the 5000+ abstracts.
Today I’m driving to Orlando and on Friday will be at the American Urological Association (AUA) meeting, so a lighter post will appear here on BSB regarding my initial topline highlights and lowlights tomorrow.
I decided to kick off the ASCO Previews first and focus on an altogether different topic, one that we’ve covered longitudinally on either PSB and BSB – originally with some scientific and translational data – and now with some initial clinical trials that look pretty encouraging thus far. The bench-to-bedside transition is often fraught with many challenges, but occasionally, they actually turn out quite well in practice.
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For the third part of the series on the AACR Previews, I wanted to switch directions and take a broad look at five completely different approaches in cancer research that we haven’t discussed on Biotech Strategy before and look at how they are doing and which ones might be promising going forward. Some of these scientific developments could potentially impact existing compounds in development.
Companies mentioned: Exelixis, Roche/Genentech, GSK, Clovis, AstraZeneca, Oncoethix
Compounds discussed: cobimetinib, DEDN6526A, ipatasertib, dabrafenib, trametinib, OTX015, JQ1, CO–1686, AZD9291
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Every year at AACR meetings there seems to be a new update on how researchers are doing with their work on overcoming resistance in metastatic melanoma. We’ve seen some stunning photos where targeting the BRAF V600E mutation with a specific kinase inhibitor such as vemurafenib (Zelboraf) or dabrafenib (Tafinlar) results in dramatic reduction, and sometimes even complete disappearance of the lesions, only for resistance to set in and the melanoma sadly comes back with a vengeance. Adding a MEK inhibitor such as trametinib (Mekinist) was originally thought to be a rather promising strategy, until it became clear that this only gave a few extra months with exactly the same result.
Over on Pharma Strategy Blog, I’ve written a lot about the fascinating research on various mechanisms of resistance in this disease. They range from specific mutations emerging to activation of COT or MEK and others in response to therapy. There are a number of questions we can ask that need to be addressed:
- Do we need a better/more potent BRAF inhibitor?
- Do we need a better/more potent MEK inhibitor?
- What other combinations and targets can be explored?
- Is timing and dosing important? (e.g. continuous vs. intermittent dosing)
- And many others…
At the recent AACR Molecular Targets meeting in Boston I chatted with Dr Bill Sellers, who is the Global Head of Oncology Research at the Novartis Institutes for Biomedical Research (NIBR) and oversees the drug discovery efforts in this space for Novartis.
Yesterday we highlighted NIBR’s work with CDK4/6 inhibition in breast cancer, but this compound may have surprising utility in metastatic melanoma.
Novartis also have several other melanoma agents in their pipeline in the clinic, including a BRAF inhibitor (LGX818), a MEK inhibitor (MEK162) and more recently, an Mdm2 inhibitor (CGM097) in preclinical development.
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