Diabecell Research Closes Out (With Comments on Encapsulation In General)

Diabecell is an encapsulated pig beta cell treatment aimed at curing type-1 diabetes. This research started in the 1990s, and was part of a group of encapsulated stem cell cures which were developed at the same time by different companies/research groups. Most of the others ended in the late 1990s and early 2000s, but LCT continued and is still operating today. I’ve blogged many times on this research: https://cureresearch4type1diabetes.blogspot.com/search/label/LCT

The last two running studies on Diabecell were marked as “completed” in October 2017. The most recent clinical trial started in 2011, and published some results in 2016, but they were not strong. Since it has been two years since their last results, and they have not started a new trial in that time, and also because the results of their trials have been lack-luster for years before that, I’m going to drop them from active coverage here.


This should serve as a cautionary tale for all encapsulated beta cell cure research. There were at least 4 companies trying to cure type-1 diabetes this way in the 1990s, and it looks like all of those were unsuccessful. There was another crop of these in the 2000s, and most of those have been unsuccessful as well. (Although Viacyte, founded in 1999 as Novocell, is still in active development and may yet cure type-1 diabetes.) More recently, in the 2010s there has been another batch of start ups in this area (Dr. Melton’s Semma Therapeutics, Beta-O2 Technologies, etc.), and also an even larger batch of new academic research (such as recently reported at Cornell, UCSF, etc.)

I’m positive about all this research. I’m positive about all research aimed at curing type-1 diabetes. I hope it all works. I hope any of it works (because it only takes one cure). However, I do think it is important not to get to overly excited about encapsulated beta cell research (even as it sounds straight forward), because it’s obviously more complex than it sounds.

Especially, it is clear to me that the hard part is the encapsulation part, not the beta cell part. The pig beta cells used by LCT generate the insulin that people with type-1 diabetes injected for decades (from the 1920s to the 1970s). Those cells work just fine, so LCT’s problems are encapsulation. Other companies have used human beta cells from cadavers. Those cells worked just fine for their previous owners, which reinforces my belief that the breakthrough that makes encapsulated beta cells successful is going to be on the encapsulation side, not the beta cell sourcing side.

Recent Clinical Trial Records:

Academic encapsulation research in the news:

Joshua Levy

publicjoshualevy at gmail dot com
All the views expressed here are those of Joshua Levy, and nothing here is official JDRF or JDCA news, views, policies or opinions. My daughter has type-1 diabetes and participates in clinical trials, which might be discussed here. My blog contains a more complete non-conflict of interest statement. Thanks to everyone who helps with the blog.


@joshualevy Josh, thanks for the update.

It’s becoming increasingly clear that encapsulation comes with the problem of immune suppression, the cure being most often worse than the disease.

I have my sights set on what I think is a most novel, and likely to succeed, approach.

If you have influence with investors. SYNER-III would be most worthwhile.


@joshualevy, thanks for a great update!

(I hope you know that many of us follow your blog regularly. We truly appreciate what you contribute to the diabetic community!)

I appreciate your analysis. Encapsulation appears to be what has failed in most of the recent, promising trials I have read.

There is one way in which they may be both intertwined: sourcing exogenous beta cells inherently creates an immuno-suppressant issue that does not exist with homologous transplants. Of course, for T1s (but not for T2s) there still is need for encapsulation (since, in the case of T1s, we would expect destruction of the new beta cells by the immune system)—but possibly it is of a lesser degree?


I’ll reply to the SYNER-III post on its home thread. --Joshua


@joshualevy, I totally agree with you. The good thing about encapsulation, though, is that it may be more an engineering issue than a scientific issue.

Unfortunately, I am on the road right now, but in a couple of days I will be able to put some more words together on a post in this thread. This is a great thread: I am really glad you started it.


I like your view on “playing the field” with regards to T1 research for a cure. I never knock any research because I feel that ALL research is important – even if the research only discovers that it isn’t a viable option for a cure. The more logs in the fire, the better the odds that there is some cure, some day. So I love all R&D and cross my fingers that some day, some cure is achieved.

I feel that whatever “cure”; however, will have to address the most important thing – the Immune system. No mouse cures ever attract much of my attention because they don’t address the immune system issue that exists and really decides whether a cure is achieved or not. Immune suppression has to be attained, I feel, if any cure is ever going to be successful. But I keep my hopes up that my son, Liam, who has just turned 4 (diagnosed at 2 yo) sees a cure before adulthood!


The good thing about encapsulation, though, is that it may be more an engineering issue than a scientific issue.

I am not sure what you mean; the issue is one of biology, predominantly. Sure, the encapsulation is an engineered tissue or some equivalent, but the reason the beta cells die or do not grow has to do with complex signalling factors.

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I feel that whatever “cure”; however, will have to address the most important thing – the Immune system.

I agree a thousand percent. But also am daunted by that fact, as no one has ever cured an autoimmune disease, ever. All we’ve ever come up with are treatments. Some of those treatments are great, to be sure, but none is a cure.


I followed that DiabeCell research for a long time and wondered how that was going? And here you find the answer in the probably best informed community there is.
Here is my question: If encapsulation is the issue but not the production of insulin through beta cells wouldn’t that indicate that we could inject those pig beta cells into human bodies if they are cloned to the recipients DNA? Meaning, avoid the rejection not through encapsulation but assimilation to the DNA of the recipients body? Wouldn’t something like cloning be the path to go? Interesting read below, the Type1 relevance is in the latter part of that article with Alan Meeker being a Type1.


I don’t know that making beta cells which share DNA characteristics of the recipient would work as well as one would think. The original beta cells which were destroyed by the immune system were of course, already “self”, and they still got destroyed.

Now, if we made changes to some of the genes involved in the onset of T1D, such as genes for the cell surface human leukocyte antigen (HLA) proteins, which are involved in signaling to the immune system whether something was self or non-self, producing beta cells that are unique to a person’s DNA would possibly be more effective. But there are a wide range of variations in the HLA genes which can confer either protection against T1D or susceptibility to T1D depending on the specific variation. About 40-50% of familial aggregation of T1D has been associated with HLA variants though!

There are also about 50 other genes which have been linked to possibly being related to T1D, and it would be challenging to custom design new beta cells for every patient based on which genes needed changing, and the exact function of some of these genes in the disease mechanism hasn’t been fully made clear.

(I have written a few papers on T1D during my college experience, mostly because I try to find ways to make any open-ended research paper assignment relate to T1D :wink:)


you need to hide the cells from the immune system; that’s the primary challenge. Creating ones that don’t require immune-suppressing drugs is just one issue

I always thought that the destruction of the original beta cells were always the cause of a singular catastrophic event in the immune system? Not an ongoing one. Basically that your own immune system misidentified the cause of an infection and killed your beta cels off? If this is an ongoing event and it continues to happen with every healthy insulin producing beta cell introduced into this body then we would have “no game”. But the disease, T1D would be misclassified as an autoimmune deficiency while actually being a genetic disorder? Or do we look again at T1D as a very individual disease that is different from patient to patient?

And now I do not know enough about cloning and DNA but in my train of thought it was going something like that: you take insulin producing healthy beta cells from a donor which obviously have the DNA signature of that donor which seemed to be the easy part. Now you have to find a way of isolating the function of that beta cell from the DNA signature of that cell and attach to a new DNA signature. And if you can do that, those cells should survive in the patient with that DNA signature and produce insulin as part of those encapsulated beta cells have done before the encapsulation failed. The DRI BioHub people might have solved that problem? Now we would only see a failure rate of beta cells that do have the patients signature if that patient continuously attacks those insulin producing cells. But than we would not have an autoimmune disease but a genetic disorder?

Maybe those DRI Biohub people, who supposedly can place the implant safely, should get together with those Diabecell people, who can supposedly produce enough beta-cells, and sit down with those cloning people, for better protection and production, and put the pieces of the puzzle, everyone seems to have, together?

But that one thing that actually ■■■■■■ me off more than anything are sentences like this: " Some DRI islet transplant recipients have been living without the need for insulin injections for more than a decade, but this life-changing cell replacement therapy remains limited to the most severe cases of T1D."
What are “the most severe cases of T1D”? If you manage your T1D, you are not a a severe case? It sends the wrong message and a false promise.

Hi @John, no there is an ongoing destruction of beta cells. The body does actually make new ones all the time (not a lot, but a few) – but the immune system is systematically killing them off. The immune system has essentially a “most wanted list” of specific epitopes, or a part of a cell that’s recognizable to the immune system, and that is kept in the immune system memory long after an initial attack. That’s why beta cell function continues to decline for years after initial diagnosis. Around 7 years after first diagnosis the number seems to plateau and it’s thought that’s because there are populations of beta cell “stem cells” which seem to be resistant to such killing, but they represent a tiny fraction of what you need to prevent diabetes.

The idea of genetically modifying the beta cells to be invisible to the immune system is logically a good one; the trouble is we don’t know what part of the beta cell the immune system is recognizing and using for attack. we have antibodies to multiple things associated with type 1 diabetes, but we don’t know if those are bystanders or what. And the antibodies that the immune system uses to reject those cells in a transplant (i.e. the ones that cause all immune rejection) could be different from the ones that the immune system first used to identify them and kill them, at least thats’ my understanding.

However, there is some thought that if you hide the cells in another part of the body, they may become invisible to the immune system in ways that transplants into traditional sites like the liver might not be.


Interesting, that is a new perspective for me.
Essentially we have as T1D’s an overdeveloped immune system that by memory association defends the body from perceived bad cells continuously? And the research goes that way with throwing more and more precious cells at those defenses? Wow, that is kind of senseless zombie-desperation tactic in any game.

But anyhow, if I continue to look at that from a MMO gamers perspective, you probably need to identify “50 other genes which have been linked to possibly being related to T1D” as Glitza said and position the cure accordingly. At least it is not an indefinite number and hopefully a constant reaction that is always the same.
I wonder if somebody takes the framework of what we know about T1D and transforms it into an MMO “bad monster” that needs to be defeated in order to progress in the game what results we could get? I believe that this has been done before for different results, looking " helping prevent the spread of infectious diseases ." I think it might have been World of Warcraft or EverQuest that had a “plague” in their games that needed to be cured. That was a long time ago.

What a reminder! A guild mate of mine, way back when, always had that tagline under his avatar " We don’t stop playing because we grow old; we grow old because we stop playing." - George Bernard Shaw

Some more info about the DRI procedure:

It is because it requires anti-reject drugs (immunodepressants) for the rest of your life, a slavery that may be worse than the original disease, and with dire consequences if you miss. It also leaves you prey to many infection risks, since it artificially depresses your immune system. It cannot attack and destroy your “new” exogenous beta cells (because it is so weakened) but it cannot destroy other invaders as well. For the rest of your life you live on a knife’s edge. See what it says here:

At this time, islet transplantation still requires the use of immunosuppression and therefore is indicated in a very small group of subjects that, despite management of diabetes mellitus under the care of diabetes specialist, continue to have life-threatening, severe hypoglycemia

And — it is not that successful, unfortunately:

After two years, 71 percent of participants continued to meet these criteria for transplant success.

Which means that after 2 years 29% of patients do not have a successful outcome, but, worse:

After one year, 52 percent of study participants no longer needed insulin therapy.

Which means that, after 1 year, 48% of patients still need to take exogenous insulin :frowning: . Unfortunately, it is not a cure.

It is physically impossible to do that, although it would be really nice if we could, because it could solve many critical problems in modern medicine. The DNA inside the cell IS the cell.

But, even if you could, you would still have to depress the immune system so that it does not destroy these cells again.

Which is why everyone is working on encapsulation right now, if there is a way to do that. As @TiaG explained, encapsulation, if it can work, would isolate the new cells from the attacks of the immune system.

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I think it is obvious that any research that does include the necessity of anti-rejecting drugs is pretty senseless, replacing one drug with another is not a cure.

“DRI’s goal is to create a BioHub that will not need immunosuppressants”. That glass is still ½ full.

Diabecell seems to have failed or given up with their encapsulation. That glass is ½ empty, except for their ability to produce beta cells.

“The DNA inside the cell IS the cell.” also a ½ full glass with this cloning company who claims to have an 85% rate of live birth of cloned ponies. What do they know? And how do they achieve it and why is the owner even entertaining the idea of curing his T1D and everyone else’s? Obviously again that the need for immunosuppressants are not a cure or an answer. Pipe-dream or do they do something already very successfully that can have an impact?

They are cloning the same organism, with the exact same DNA. That is what cloning is. They are not creating a new cell with different DNA.

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Yes of course, that is obvious. But what else do they know within a self proclaimed very successful operation in this field? An 85% success rate is by far above anything we know. Normal would be 10%. It could be an unfounded claim for various reasons and no oversight to prove anything to enhance their primary business of Polo ponies? This is obviously big money. But why this connection to the owner and his T1D? It would not be necessary to enhance their primary business.

This was the key-sentence in that article to me : “The institute’s scientists have advanced to the point where they have been able to produce insulin-producing beta islet cells from a donor’s non-beta islet cells in a laboratory setting.” What if that donor is you as T1D? And do those cells, essentially a clone, carry the characteristics of your cells that your immune system keeps destroying? If not…
That is why I called this glass is ½ full.

For sure it is good to be optimistic. However, until we see results such as these in peer-reviewed articles, and duplicated, I think it is best to remain healthily skeptical :slight_smile: Otherwise we would be constantly disappointed!

That would have been a miserable 30 years to be constantly disappointed. I rather celebrate this dubious anniversary as being alive and adjusted well enough that I can do whatever I want to. Well, not everything I want to but everything that is reasonable at your mid 50’s.
I just wish that for everyone including Alan Meeker with his Polo ponies and further hopes to become reality. I’ll gladly take a cure for another 30 years of my life even if I manage quiet well without it. But who wouldn’t?

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