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Alzheimer's Disease

Amgen and Neuroscience

So Amgen has exited the neuroscience area, with a good-sized round of layoffs at their research site Cambridge. The company has a migraine drug (Aimovig) that they’ll continue to support, and they’ll stick with their existing clinical programs, but it looks like all the early-stage stuff is gone. What does this mean?

Not as much as you might think. Neuroscience is indeed hard, and Amgen’s not the only company to rethink its commitment to it (Eli Lilly did something similar last month with their neuro efforts in the UK). But there are still plenty of participants, large and small – it’s not that the field is being totally abandoned by pharma. It’s just being abandoned by Amgen, because they have other areas that look a lot more promising for them. And let’s face it, Amgen is a bit of an oddity, anyway – it’s not for nothing that they get referred to as a law firm with fume hoods. Enbrel is what pays a lot of the bills over there, and Enbrel is (and has long been) a patent-court story, not a research one.

Inflammation, cardiovascular disease, and oncology are going to be the focus there, and given the company’s portfolio, that makes a lot of sense. It looks like the only neuro programs going on will be the ones that intersect with the larger inflammation area. One interesting thing that came out of the company’s statements was that management felt that a lot of the neuroscience landscape is focused on what their CFO David Meline called “orphan or niche diseases”, and that the company wants to work on things that will have a broader impact. Now, it’s not like there isn’t a neuroscience disease with a huge health impact, and it’s one that even has some inflammation and cardiovascular connections. So one of the things that Amgen is saying is “No Alzheimer’s research for us, thanks”.

Unfortunately, that’s a pretty defensible stance, too, at least as portfolio management goes. Alzheimer’s has been and remains a brutal field to make any progress in. We don’t know the molecular basis of the disease, the most well-founded hypothesis has wiped out over and over again in the clinic, the trials are large, long, and expensive, and the companies that have nonetheless kept at it have thus far been feeding their time and money into a giant shredding machine. Unless you have a really terrific idea, it’s easy to make the case that you should throw some money at the people doing basic research in this area and go spend the rest on something else – and frankly, there aren’t any really terrific ideas in the field right now. Even the Gates Foundation is having trouble finding places to put investments.

So I see Amgen’s move as just an attempt to become even more Amgen-like than before. They’ve been fighting to keep Enbrel going for as long as possible, while at the same time trying to erode competitors by coming up with their own biosimilars, and they have a lot going on in oncology and CV. All that looks to be the Amgen story for a long time to come.

19 comments on “Amgen and Neuroscience”

  1. Curious says:

    So … is chemistry ending at that site, or just the therapeutic area?

    1. Anon says:

      Med chem is being closed in Cambridge and being consolidated in California

      Amgen told FierceBiotech: “We made the difficult decision to end our research in neuroscience, which is largely based in Cambridge, Mass. We are consolidating our U.S.-based Research presence primarily in Thousand Oaks and San Francisco. While not all changes are happening immediately, we anticipate that approximately 180 roles will be impacted.

      “We recognize that Cambridge is a vibrant life sciences community that enables access to external innovation and top talent. The site remains a center of excellence for Operations, with a significant Process Development presence, dedicated to advancing the pipeline and developing next-generation technologies.”

      1. Anon says:

        Are you sure? They just posted a MedChem job in Cambridge that I applied to. Although maybe I’ll blame my inability to get an interview on the fact that they are consolidating/closing MedChem there..

  2. Anonymous says:

    “…a law firm with fume hoods…” Harsh but fair! LOL

    1. CMCguy says:

      Unlike the rest of Pharma that is either a Banking or Sales Group with a few token fume hoods…

  3. name says:

    well after biogen solved alzheimers theres not much left

    1. Sken says:

      Hey, maybe if you looked through your data hard enough you could too!

    2. Cynic says:

      I chortled.

  4. Anonymous says:

    The linked FierceBiotech article begins, “As Amgen rides the wave of hype and hope for its early-stage KRAS effort …”. I thought that there are many good inhibitors of Ras but none that work therapeutically. Although common to many cancers, inhibition of Ras is circumvented by alternate survival and proliferative pathways. Or has something changed in the past 30 years?

    (Not considering multidrug therapies to hit Ras and other targets for that argument.)

    (AMG 510 looks interesting: a chiral methyl on the piperazine and a possible atropisomer on the methyl, isopropyl pyridine.)

    1. Anonymous says:

      it is an atropisomer, but the rotational barrier is high enough that the compound is stable to racemization at room temperature…

    2. Fuh Dhge says:

      I think AMG 510 is the first clinical candidate that hits Ras directly. The previous drugs that didn’t pan out in clinical trials all modulated Ras activity indirectly (e.g. by inhibiting enzymes that stick lipids onto Ras to anchor it to the membrane). K-Ras doesn’t have any traditional hydrophobic pockets that are amenable to small molecule inhibition. AMG 510 and Mirati’s compounds get around this by targeting a specific K-Ras mutant, G12C . The compounds have a warhead that forms a covalent adduct with the cysteine in the G12C mutant to gain appreciable affinity – as pioneered by the Shokat group in 2013.

      While it’s fascinating that they got the compound to work on the G12C mutant, it needs the cysteine for efficacy. Given that there are plenty of oncogenic Ras mutants that lack a cysteine at that position, it’s very easy to see how resistance would develop.

      Regardless of whether or not mutations will arise, it is working in clinical trials already. A Phase 1/2 trial posted a clinical profile that either produced stable disease or a partial response in 90% of patients with non-small cell lung cancer – which is pretty wild response rate (although it’s disappointing that there weren’t a lot of complete responses).

      I think it’s a big deal regardless because, while there is a mountain of genetic/preclinical evidence linking mutations in Ras to cancer, this is the first evidence that inhibiting Ras in humans is therapeutically viable approach to cancer therapy. So while these compounds can only be used on a small percentage of patients with Ras mutations, it de-risks investment in making Ras inhibitors with broader efficacy – regardless of earlier clinical failures in the area.

    3. Wavefunction says:

      The major development has been covalent inhibitors targeting the G12C mutant of Ras which is frequently mutated in a broad range of cancers. It won’t be a magic pill but it could show modest effects, especially in combination with other inhibitors targeting the Ras-Raf-MEK-ERK pathway.

  5. Klagenfurt says:

    A perfectly sound decision: no brain, no headache.

  6. Anon says:

    PFE also disbanded neuro, so not as AMGN specific as the article suggests.

  7. loupgarous says:

    “Unless you have a really terrific idea, it’s easy to make the case that you should throw some money at the people doing basic research in this area and go spend the rest on something else – and frankly, there aren’t any really terrific ideas in the field right now.”

    It’s hard to explain this to people outside Pharma. Presidential candidates blithely talk about “moon shots” for difficult diseases, but Alzheimer’s has turned out to be impervious to the sort of massive technical effort that gave us Project Apollo – half a billion dollars spent on just one of several promising drug candidates just showed that the beta-amyloid hypothesis, which was a very plausible theory, wasn’t the answer to “Why?”.

    Actual Moon shots largely are well-understood objectives – getting lots of mass out of Earth’s gravity well and over to the Moon and back as economically and safely as possible. Clinical entities such as Alzheimer’s and the other prion-like encephalopathies are, we found, not well-understood in the way they destroy lives; without something as clear as orbital mechanics with which to work, moon shots for medicine will just be tragic boondoggles. Basic research is needed to find out what’s happening in the AD disease process before the next human wave of effort and tsunamis of spending..

    1. John says:

      Argumentum ad Apollum: “If we could go to the moon, why can’t we cure cancer?”

    2. Ian Malone says:

      A certain Derek Lowe has written about this exact philosophy:

      If I can steal the best part:
      “Trying to cure cancer in this way would be like trying to go to the moon without really knowing how rocket engines actually work, without being quite sure if Newton’s laws of motion would hold up, and with some real uncertainty in the position of the moon.”

      1. metaphysician says:

        Honestly, I’d go further. Its more like trying to shoot to the moon without knowing whether the moon is a rock in orbit, or a painting on the celestial dome above a flat Earth.

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