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Bind’s Attempts To Remake Chemotherapy

There’s a lot of effort (and a lot of money) going into targeted nanoparticle drug delivery. And that’s completely understandable, because the way we dose things now, with any luck, will eventually come to seem primitive. So you used to just have people eat the compound, did you, or just poke it into their bloodstream with a sharp stick, and let it float around wherever it would and hope that it made it to the target without doing too much else? Quaint.
The nanoparticle idea, on the other hand, is to encapsulate the drug somehow in the layers of these tiny particles which will release it only under the right conditions. The outermost layers, meanwhile, are meant to be coated in ways (recognition peptides, usually) that send the payload to only the right cell types. Imagine a drug for lung cancer where all of the dose goes to the lungs, and all of it hits only the cancerous cells. You could put in the roughest, toughest chemotherapy agents available, because you wouldn’t be stuck with poisoning the rest of the patient’s body at a slightly slower rate than the cancer, which is how it works too much of the time now.
But that level of control is yet to come. We just got another read on this in the clinical results from Bind Therapeutics, one of the leading companies in this field. Bind is another Bob Langer-derived company – when other parts of the US (or other countries) talk about wanting to have humming biotech hubs of their own, they’d be happy just to have Bob Langer. Bind, under CEO Scott Minick, has deals with an impressive list of big pharma companies to try to apply their nanoparticle delivery systems to existing drugs, although Amgen pulled out of an arrangement with them over the summer.
That didn’t help the stock, and neither did the latest news. This was a Phase II study in non-small-cell lung cancer patients with docetaxel, a widely used chemotherapy drug that could certainly use some targeted delivery. The results were mixed. Investors were clearly hoping for something better, but it could have been much worse. As that FierceBiotech link above details, the company saw some responders when the new formulation was dosed every three weeks, but not when it was dosed every week, an interesting result that’s going to take some thinking about. Inside the every-three-weeks group, the patients with two particular tumor varieties (KRAS or squamous cell carcinoma) seemed to show relatively good responses. But the sample sizes there are small.
The company is planning another round of Phase II, concentrating on those subtypes and dropping the once-a-week dose. That’s exactly what you do in Phase II: the drug has hit the real world with real patients in it, and you do whatever seems to work. It would have been great if they’d seen a bigger across-the-board response, but these are the early days of targeted nanoparticles. There’s a vast amount we don’t know about these things; the odds are huge that no one is going to be hitting any balls over any fences for a while yet. Bind’s next trial should tell them, though, if their current docetaxel particle idea is worthwhile for NSCLC.
That could go either way. The current trial may turn out to have lit up just the sorts of patients who will go on to show impressive benefits, or those effects could just flatten out and slide back into the statistical swamp. Here it is, the absolute essence of drug discovery: there is no way to know in advance. The only way to find out is to round up some more patients, round up some more drug, and round up some more money and try it. Good luck to them!

10 comments on “Bind’s Attempts To Remake Chemotherapy”

  1. Anonymous says:

    Even if Bind does not succeed in improving efficacy and they only reduce toxicity, that itself is a huge, welcome advance for many oncology indications. Imagine patients no longer need to debate whether they should go for aggressive treatment and feel awful through the last months of their lives or forgo treatment for a far more comfortable but shorter time.
    I hope investors/media realize that a safety only outcome is still huge.

  2. Experiencedhand says:

    Been there and done that. My verdict-The science and technology works but the cost ($$) of delivery is a huge barrier. If you thought that the price of cancer drugs already in circulation are expensive, wait until the nano cancer drug delivery arrives! IMHO these delivery systems are only for a chosen filthy rich and not for the ordinary folks! Nano toxicity can also be a huge problem that is not much discussed for these delivery vehicles.

  3. Anonymous says:

    Even though KRAS has been targeted forever now, it seems as though cancer–at least pancreatic– can still come back resistant by avoiding KRAS addiction all together:
    Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer. Cell. 2014 Jul 3;158(1):185-97.
    Also, since I don’t stay on top of the nanoparticle field, wasn’t genotoxicity associated with nanosized particles, or did they sort out those issues/don’t see them with degradable versions?
    For example, this article’s abstract (behind paywall, can’t see) seems to imply that *some* versions of degradable nanoparticles can be genotoxic:
    Genotoxicity and Mutagenicity Evaluation of Polyethylene Sebacate Nanoparticles : Journal of Nanopharmaceutics and Drug Delivery, Volume 1, Number 3, September 2013, pp. 301-310(10)
    Do we have a firm grasp yet of what causes genotoxicity or how to tune the particles to avoid it?

  4. Mo says:

    The BIND results announced yesterday were for a small number (40) of second-line NSLC patients who failed primary chemo treatment. Success has to be measured relative to that starting point. Higher response rate, median survival and decidedly lower toxicity are marked improvements over IV docetaxel. Additional PHII studies will confirm if Bind-014 can be approved as a second-line treatment. Perhaps it will be used additionally as a first line treatment for the same cancer as well as others particularly those that harbor KRAS mutations. Reducing neutrapenia and neuropathy would be huge for patients suffering both cancer and f-in chemo.!

  5. LittleGreenPills says:

    “Imagine a drug for lung cancer where all of the dose goes to the lungs, and all of it hits only the cancerous cells. You could put in the roughest, toughest chemotherapy agents available, because you wouldn’t be stuck with poisoning the rest of the patient’s body at a slightly slower rate than the cancer, which is how it works too much of the time now.”
    Tissue specific treatment would certainly be an improvement over surgery, but still would not solve the biggest problem with cancer, distant metastasis. In someways the lack of selectivity is the biggest benefit of cytotoxic chemotherapeutics.
    But it is a step in the right direction.

  6. Morten G says:

    “The nanoparticle idea, on the other hand, is to encapsulate the drug somehow in the layers of these tiny particles which will release it only under the right conditions. The outermost layers, meanwhile, are meant to be coated in ways (recognition peptides, usually) that send the payload to only the right cell types.”
    Sounds a lot like a virus to me.
    5. LittleGreenPills I think the idea of targeted therapy is that it tracks down the cancer cells for you.

  7. One issue with BIND is that there is already an approved nano-taxane on the market for NSCLC, Abraxane aka nab-paclitaxel.
    But the big improvement with Abraxane over other taxanes is the elimination of the solvent and the need for IV steroid administration, quality of life improvements, not really the big improvements people had hoped for in the past.

  8. anon says:

    just dont get so caught up in the general idea, that you lose track of the ability to judge the efficacy of the actual application they are going for.

  9. Anonymous says:

    look at the xenograft data for their drug . . . notice that nearly their entire effect comes from the retention of the drug and NOT from their “targeted” approach . . .

  10. Anonymous says:

    look at the xenograft data for their drug . . . notice that nearly their entire effect comes from the retention of the drug and NOT from their “targeted” approach . . .

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