Biotech Strategy Blog

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

Posts from the ‘Multiple Myeloma’ category

Shining a light on hidden gems in the myeloma niche

If we want to go beyond the proteasome inhibitors, IMiDs and anti-CD38 antibodies in multiple myeloma, there are plenty of emerging candidates these days.

This is excellent news, but how will it all fit together, and which gems were under-rated at the recent ASH meeting?

The latter may catch a few people by surprise when the clinical aspects are considered in the totality of what needs to be done and in which patient subsets.

We discuss near and medium term aspects, which may have a lasting impact and also talk about why they matter.

To find out, the final part of our myeloma mini-series offers an engaging and thoughtful fireside chat with a global thought leader in this niche…

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With all the time and attention surrounding the BCMA-based products in multiple myeloma, including ADCs and CAR-T cell therapies, it’s easy to forget there are other approaches coming down the pike.

Building new mosaics and novel regimens in myeloma is coming

Beyond the hullabaloo there are various bispecific antibodies and T cell engagers in early stage development – not only is the modality different, but the targets might differ too.

How are all of these novel approaches doing in the clinic and how might they all fit together in future regimens? The myeloma world as we know it of proteasome inhibitors and IMiDs may not yet be a thing of the past, but the landscape is certainly changing.

In our third installment of the myeloma mini-series, we tackle these issues and look at near and medium term strategic directions, which can be considered and how these might impact different combination approaches and lines of therapy in order to further improve outcomes in this disease.

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As part of our latest mini-series focusing on multiple myeloma, yesterday we looked at the BMS approach to tackling multiple myeloma with a variety of different modalities against BCMA and other targets.

Today it’s the turn of J&J’s Janssen to be in the BSB hot seat.

In the first part of the company interview today, we take a look at their current and strategic directions in CAR-T cell therapies, including some thought leader reactions. In the second part tomorrow morning we discuss what they are doing with their T cell engagers against different targets in multiple myeloma.

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All aboard the BCMA train – or not?

No matter, this was an interesting one with a few twists in the tale. It also offers some additional context as to why GSK’s experimental BCMA ADC therapy, belantamab vedotin, missed out on a late breaker at ASH.

When you read the briefing documents you can quickly see why this might have been the case.

In the latest installment of this story – the last one was the late breaker than wasn’t at ASH19 – things turned out to be rather more intriguing than many may have initially realised…

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The annual ASH Dash often ends up with crowds waiting for the poster halls to open up – a daily scene captured from ASH19

With coronavirus and COVID–19 pretty much dominating attention and space in the global news on a daily basis lately, I am vividly reminded that not too long ago in December we attended the annual meeting at ASH in Orlando to experience busy scenes like the one on the right…

Imagine those packed crowds now in the current context – it doesn’t bear thinking about!

Which is why all of the oncology conferences we had been planning to attend this year are one-by-one postponing or outright cancelling their events until next year. This is going to create a lot of challenges for companies in terms of data release and presentations, to be sure, but what matters more is reducing the risk of the infection spread in order to limit the risk of serious cases developing.

The good news is that we do have a huge backlog of oncology data – novel targets, new agents, and emerging companies – to write about and share with our audience. There’s always a silver lining to be had if you look carefully enough.

Here’s one such example – a novel cancer target, agents in development, and an emerging company to highlight too…

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What do cancer drug development and Sherlock Holmes have in common?

The simple answer is that sometimes you can gain insights by looking at what did not happen.

Will belantamab mafadotin stand out in the crowded BCMA space?

In 1892 Sir Arthur Conan Doyle wrote a short story about the disappearance of a famous racehorse the night before a race. What was curious about the incident was that there was no barking from the watchdog when you might otherwise have expected it, suggesting the dog knew the thief…

Can we follow the same inductive reasoning when it comes to cancer drug development? Are there things we would expect to see, but don’t? If so, what inferences can we draw from them?

In this post we’re taking a closer look at the latest data for GSK2857916 (now belantamab mafadotin), which in many ways was “the dog that didn’t bark” at ASH19.

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We have been following the progress of various classes of molecules in the myeloma space here on BSB since 2010. These include traditional approaches (e.g. HSCT and proteasome inhibitors/IMiDs and various antibodies or ADCs), as well as immunotherapy (checkpoint blockade, CAR T cell therapy, oncolytic viruses etc).

Brick Lane Grafitti

There’s much going on in this space and it’s not only becoming extremely crowded and competitive (akin to 1L NSCLC), but there is a gradual trend towards convergence on many fronts, be they targets or modalities.

In our latest look at the myeloma space, we focus on several key areas of development – antibodies, CARs, and also highlight a new target that may be of interest…

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The B-cell maturation antigen (BCMA) is an oncogenic protein target relevant to multiple myeloma that we have been following for a while on BSB, including an expert interview with a global myeloma KOL at ASH last December as part of a wide ranging discussion and deeper look at the Future of Multiple Myeloma.

San Diego

This weekend I was following a myeloma workshop where quite a bit of teasing early data was presented that may give us clues about what’s likely to be interesting at ASH18.

I wasn’t the only one doing this judging by a raft of reader questions that came in, particularly on the topic of BCMA and other emerging targets in this disease.

Is one BCMA better or worse than another? Will antibodies take a BiTE out of the CAR-T cell therapy noise? We take a careful look at these issues to explore what’s what and what really matters in this niche.

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Happy New Year!

Immunotherapy treatment for multiple myeloma has been around for several decades, first in the form of stem cell transplantation, then augmented by the addition of IMiD immune modulation drugs such as thalidomide, lenalidomide or pomalidomide. In due course, along came immune checkpoint blockade in solid tumours and it was only a matter of time before they would be evaluated in hematologic malignancies, albeit with mixed results.

The proteasome inhibitors and IMiDs are unlikely to go away any time soon, but other targets have also emerged including CD38, SLAMF7/CS1, BCMA/APRIL, PD–1/L1 and a few others that are being currently investigated in the clinic.

Where does this leave us and what looks really promising?

In our latest thought leader interview undertaken at the recent American Society of Hematology (ASH) meeting in Atlanta, we asked a global expert for his candid views and were not surprised at some of the hard hitting comments that emerged from the in-depth discussion of several key issues…

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Much of the focus in multiple myeloma over the last decade has focused on two key drug classes – proteasome inhibitors and IMiDs – with some recent approvals for monoclonal antibodies targeting key proteins on the surface of malignant myeloma cells such as CD38.

#ASH16 in San Diego

Combinations of these core therapies have lead to a noticeable improvement in outcomes for people living with the disease – from 3-4 years over a decade ago to now approaching 10 years post diagnosis.

If we want to continuously beat the status quo and improve on the chronicity, however, it is likely that several things will need to happen:

  • Better understand mechanisms of resistance that induce relapse
  • Develop predictive biomarkers of response
  • Identify novel therapeutic targets

Here. we focus on the latest preclinical findings that were recently presented at the American Society of Hematology (ASH) in San Diego and explore where the future might be headed in this disease.

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