Friday, April 29, 2011

Possible Cures for Type-1 in the News (late April)

Alefacept Starts a phase-II Clinical Trial
This study is also called "T1DAL", which I'm sure is pronounced "tidal".

This drug targets the immune system's T cells, and is already approved for treating "plaque psoriasis" which is an autoimmune disease similar to type-1 diabetes.  It has a good safety profile there. The hope is that by giving it to honeymoon type-1 diabetics, beta cells will be preserved.

Because this is an ITN trial, there is a long list of sites where you can participate. For the locals: UCSF is the only California location.  They expect enrollment to take 2 years, but (of course) I hope it fills up sooner than that.  The sooner they finish recruiting, the sooner we learn the results.  The trial is for people within 100 days of diagnosis, and requires weekly injections for 12 weeks, followed by 12 weeks "off", followed by another 12 weeks of injections.

Estimated Enrollment:  66
Study Start Date:  March 2011
Estimated Study Completion Date:  August 2014
Estimated Primary Completion Date:  August 2013 (Final data collection date primary outcome)

Web page:
Recruiting web site:
Clinical Trial:

Artificial Pancreas Trial Handles Dinner and Night

Hovorka's team at Cambridge University continues to make progress on testing their AP. These most recent results are aimed at showing that their AP can deal with dinner and the night after dinner. They tested with both a simulated "at home" dinner (fewer carbs, earlier in the evening) and an "out" dinner (more carbs, alcohol, and later in the evening).  The study was small (12 people) and "cross over" meaning that half used a pump and half used an AP for the "eat in" dinner, and then they switch (previously pumpers do AP, previous AP use their pumps), and have another "eat in" dinner, and then do again for the "eat out" dinner.  Each person was in the test group once, and in the untreated group once, for each meal scenario.
"For the eating-in scenario, overnight closed loop delivery increased the time plasma glucose levels were in target by a median 15 percent," said Hovorka. For the eating out scenario, the average time good blood sugar control was increased was 28 percent on average. And, when combined, the average increase in blood sugar control was 22 percent, according to the study.
Remember, the goal for FDA approval for something like this is as good control as a pump, so 22% better than a pump is more than good enough.  Now, to get insurance to pay for it, it will need to do better than a pump, but this trial shows that it is.  My reading of the study, is that they did tell the pump the number of carbs eaten at the meal, so this is what the JDRF would call a stage 4 AP.  (A stage 5 AP would not need to be told ahead of time about carbs in food.)  You can read my general background for AP research (including stages) here:

I know there has been some interest in how accurate CGMs really are.  This is what the study found:
The accuracy of the sensor, evaluated as the median relative absolute difference between sensor glucose levels and paired plasma glucose levels divided by plasma glucose levels, was 8.0% (4.5-19.3%) in the eating in scenario and 12.0% (6.8-17.2%) in the eating out scenario.
News coverage:
Full paper:   (Thank you BMJ!)

Team Brazil Rolls
In the past, I have blogged about what I call the "Burt" research, which you can read here:
but it was done in Brazil, so maybe that is a better term for it.  This research uses the patient's own hematopoietic stem cells. (remember that)

In any case, it is by far the most successful research aimed at curing honeymoon type-1 diabetics.  Most of the people treated were insulin free for months, many for years.  Some for five years or longer.  These are much better results than anyone else.  But those results came at a cost of safety.  Although no one died or suffered serious side effects, the treatment involves significant risk.  At least one researcher (not part of this team) has estimated that the chance of dying would be "less than 1%" (personal communications with me), but that is way too high for most people to accept.

So the question is, how does this research move forward?  There have been several different answers, as you might expect:
  1. Haller's CSGF+ATG studies are trying a similar treatment, but without the most dangerous drug.
  2. Snarski is replicating the Brazilian trial, and getting similar results (and no serious side effects so far).
  3. Now in this paper: a Chinese group is replicating their work.  University of Naijing (2006) found that of 5 patients treated within 3 months of dx, 4 of them used no injected insulin for a time.  However, of 11 patients treated after 3 months of diagnosis, none became free of injected insulin.  So the good news here is that the replicated the results.  The bad news is that it looks very honeymoon dependent.  In the past, I had hoped that this treatment might also work for established type-1 diabetics, but this trial shows that isn't true.
  4. And also in this paper: the original group is trying to use mesenchymal stem cells (a different type of stem cell than used previously.  This protocol is significantly safer than the current one.  The following paragraph from the paper describes the new protocol:
The protocol includes bone marrow biopsy under general anesthesia in first-degree relatives for the collection of mesenchymal cells. These cells are sent to a laboratory to be stimulated to proliferate for a month and are later infused into the patient ...; there is no need for chemotherapy. The patient is hospitalized for 1 day but only as a precaution. After 1 month, the patient receives another infusion. ... Inclusion criteria are age 12 to 35 years, diagnosis of T1DM less than 4 weeks prior to treatment without ketoacidosis and positive serum levels of anti-GAD. So far [in 2008] , two patients have been included in this protocol and, as soon as we have a proper follow-up, the results will be published.
The paper below is an overview written by this research team.  It describes the background for their original research, the results they got, and continue to get, and (new to me) extentions of their work (items 3 and 4 above).

Full paper:  (Thank you Diabetology & Metabolic Syndrome!)

Another Overview Paper

This is a readable overview paper by Jay S. Skyler and Camillo Ricordi, both very big names in type-1 diabetes research.  The title is "Stopping Type 1 Diabetes: Attempts to Prevent or Cure Type 1 Diabetes in Man".  Thanks to Ellen at CWD for pointing out this paper to me.

Joshua Levy
All the views expressed here are those of Joshua Levy, and nothing here is official JDRF or JDCA news, views, policies or opinions.
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Saturday, April 23, 2011

Roadmap To Curing Type-1 Diabetes

This posting is a draft.  But I've been working on it for so long that I decided to publish what I have while continuing to refine it.  It's not perfect as-is, but I've decided that it is good enough to publish.

I've been posting a lot of narrow updates recently.  By narrow, I mean "treatment X passed milestone Y" kind of thing: a lot of detail on a very specific treatment.  This posting is the opposite, it is my attempt to put all those narrow postings into context. It is an overview of how we can cure type-1 diabetes using the research that is going on right now.  That cure is still a long way off, but this posting describes the possible paths between here and there.

Please remember that this is a posting about possibilities!  By listing a line of research here, I'm not saying that I think it will work.  All I'm saying is that researchers are actively working on it.  I'm sure that in the end most of the research listed here will fail.  That doesn't matter.  If one succeeds, then it doesn't matter how many fail.  Also, I fully understand that not everyone thinks that all the "cures" listed below are legitimate cures for type-1 diabetes.  Feel free to ignore the ones that you don't consider cures.

First, A little terminology:
Pancreas is the organ that contains specific structures called isletsIslets contain beta cells, which are the exact cells that generate insulin. 

When the immune system mistakenly attacks cells of it's own body, that is called autoimmunity.  If the attacked cells are beta cells, that creates a disease called type-1 diabetesAutoimmunity can target other cells, in which case the disease will have different names and different symptoms.

The immune system attacks beta cells with killer T-cells.  Those specific killer T-cells which attack beta cells are often called "bad" killer T-cells or autoreactive killer T-cells.  Killer T-cells in general are held in check by regulatory T-cells, which are often called T-regs.  Also within the immune system are B-cells (not to be confused with beta cells, which are in the pancreas), and those cells communicate between T cells to encourage them to attack certain cells.

There are many different types of T-cells and B-cells, and they are often identified by CD numbers.  So a T-cells might be described as a CD3 T-cell or a CD8 T-cell.  B-cells might be CD20.  A cell is not limited to one CD number, you could have CD4+CD25+ T regulatory cells (for example).

How to Cure Type-1: Overview

Type-1 diabetes is caused by the body's own immune system mistakenly destroying beta cells in the pancreas.  These beta cells would normally create the insulin the body needs.  Current research is following five basic paths to try to cure it (labeled A-F below) and many of those basic paths have different sub-paths, which I've numbered. 

A. Replace the Beta Cells
Replace the patient's beta cells with ones that can not be attacked by the immune system, so the are not effected by autoimmunity.   Simply replacing beta cells is not likely to be a cure, since the autoimmune attack will destroy the new ones same as the old ones.
  1. Encapsulated islet cells.  Wrap the cells in a membrane which allows nourishment and sugars in, waste products and insulin out, and also prevents immune cells from attacking the beta cells on the inside.  LCT is in phase-II trials and has permission to sell this in Russia but the current results are not a cure, and there are separate phase-I trials in Belgium and Australia.
  2. Elecro-mechanical pancreas (Artificial Pancreas).  Build a pump and sensor replacement pancreas that can measure blood glucose and dose insulin.  The term "Artificial Pancreas" usually refers to using current pump and current CGM sensor technology, so both of these things use external hardware, and the sensors measure BG levels just below the skin, not in blood veins.  There are at least three groups in phase-I or phase-II trials.
  3. Sertoli cells.  There are cells in a human body which are not genetically the same as the rest of the cells, and yet are not attacked by the body's immune system.  An example are sperm cells; which only contain half the genetic material as regular body cells.  They are quite different than regular cells, yet are not attacked as foreign by the immune system.   This is because there are special cells, called Sertoli cells, which block the immune system.  A possible cure for type-1 diabetes it to combine beta cells and Sertoli cells in a transplant that would not need immune suppressive drugs.  Not in clinical trials, although has been in the past. Sernova is doing animal trials in Canada.
  4. Implanted elecro-mechanical.  Similar to the artificial pancreas described above, except that implantation means that the blood glucose sensor can be put directly into a blood vein, and resupplying with insulin and new batteries is more of a problem.  Also, this is internal, so not visible outside of a person.  At least one was in phase-I trials in the past; not sure if any are now.  (Dr. Rennard's work in France is with an implanted pump, not an implanted artificial pancreas.  So is headed in this direction, but not quite here, yet.)
  5. Non-pancreatic beta cells.  In the last decade we have learned a little bit on how to take adult stem cells and program them to become other types of cells.  So a possible cure for type-1 diabetes would be to take adult stem cells or even just normal cells from the liver, and program them to produce insulin in response to glucose.  The hope is that since they started out as liver cells, the autoimmune attack would not target them, but they would still generate insulin in response to blood glucose.  Not in clinical trials.
  6. No Moving Parts Artificial Pancreas.  This is similar to "self dosing insulin" (described below), except that there is a chemical barrier that is sugar sensitive, and the insulin is stored behind the barrier.  If the sugar level in the blood is too high, the barrier becomes more permeable and more insulin leaves the reservoir.  Conversely, if the sugar level goes low, the barrier becomes less permeable and less insulin gets out.  Not in human trials; may not even be in animal trials.
I don't consider a classic pancreas transplant or beta cell transplant a cure, because they will require a lifetime of immune suppressive drugs and related complications and side effects. But there is a lot of research going on to improve these procedures.
      B. Stop the Autoimmune Attack
      Stopping the body's immune attack on it's own pancreas is another way to cure diabetes.   Some refer to this as curing the underlying cause of type-1 diabetes, as opposed to replacing the pancreas which they view as curing the symptoms.

      I divide this research into different groups based on how they attempt to stop the autoimmune attack.  Since the immune system is very complex, there are many ways to try to get it to stop, and so many different ways to categorize this research.  The division below is my personal taste.  Different researchers do it differently.

      Any treatment that stops the immune attack on beta cells needs to be focused, so that it does not stop the immune attack on foreign cells.  A "cure" that hobbled the immune system's beneficial functions would be worse than than type-1 (in my opinion), and I would not consider it a cure at all.
      1. Antigen specific targeting
        • GAD65.  GAD65 is one of the proteins on a beta cell which is (mistakenly) attacked by the immune system, and this treatment is an attempt to teach the immune system not to attack that exact protien.  In phase-III trials.
        • Insulin B chain.  Finished phase-I trial.
        • Insulin.
      2. Targeting specific "killer" T-Cells. Modern technology can create monoclonal antibodies which specifically target specific T-cells. 
        • Anti-CD3s.  CD3 are a type of immune cells which are involved in the attack on beta cells.  These treatments target that cell type.  There is currently one (NI-0401) in phase-II trials.  (Two more just failed phase-III trials.)
      3. Targeting communications cells.  Monoclonal antibodies have also been created to target CD20.  Finished phase-II trials. 
      4. Heat Shock Protein 60 (HSP60) is a small protein that might help teach the immune system not to attack it's own body.  Diapep277 is based on this, and in phase-III trials.
      5. Polyclonals.  
        • ATG.   **need more info here**  In phase-II trials.
      6. Raising the level of TNF.  BCG.  TNF is a naturally occurring substance that kills of certain types of cells (especially tumor cells).  If TNF kills off "bad" killer T-cells specifically, then raising TNF levels might put type-1 diabetes into remission or even cure it.  Since BCG is known to raise TNF levels, it is a possible cure for type-1 diabetes.  No results from a phase-I trial.
      7. Reinforcing T regulator cells.
        • Dendric cells. **need more info here** In phase-I trials.
        • T-regs.  **need more info here**  In phase-I trials.
      Note that this path may require that we replace the lost beta cells (see section C), or those cells may regrow without outside help, once the autoimmune attack is stopped.

      C. Create new beta cells to replace those that were lost.
      If the autoimmune attack is stopped by a cure from group B, then it may still be required to regrow, improve, or replace beta cells in order to have a cure.  
      1. Drugs that trigger regrowth.  There are several drugs which might trigger regrowth of beta cells.  These include Human Growth Hormone and Exsulin, which have done some clinical trials, and CureDM, which has not yet.  Exsulin is in phase-II trials.
      2. Stem Cells could be used to grow new beta cells.  Many different techniques, some you can get in a clinic now, some in phase-I, and others still doing animal experiments.
      3. Temporary beta cell replacement.  Any of the cures in group A could also be used to provide new insulin, especially if only needed temporarily while the body's beta cells naturally regrew.
      4. Type-2 drugs. Many of the drugs given to type-2 diabetics work by getting more insulin out of existing beta cells, or having that insulin used more efficiently by cells, so any of them might be helpful here as well.  Several in phase-II trials.

        D. Stop inflammation to stop type-1.
        Most researchers believe that as the immune system attacks the beta cells, it causes inflammation:
                Autoimmunity -> Kills Beta Cells -> Causes Inflammation
        But some researchers believe that the inflammation itself kills the beta cells.
                Autoimmunity -> Causes Inflammation -> Kills Beta Cells
        This difference is important because the second group of researchers believe that if you could stop the inflammation, you could stop type-1 diabetes.  There are a large number of anti-inflammation drugs out there, and new ones are being worked on all the time, so I'm only listing those that are being tested on type-1 diabetes specifically: Anakinra is in phase-II, Lisofylline and Xoma 052 are in phase-I. **need more info here**
          E. Self Dosing Insulin.
          Create a substance that contains insulin, but only makes that insulin available when the blood glucose level is too high.  SmartInsulin, SIA-II, and BIOD Smart Basal are examples of research into this type of cure. Smart insulin is probably in clinical trials now.  (I'm trying to confirm this.)  The other two are not.  **need more info here**

          F. Gut Permeability
          Most researchers believe that gut permeability has nothing to do with diabetes.  But some researchers believe that heightened gut permeability causes the autoimmune response that causes type-1 diabetes.  When more and larger molicules move out of the intestine and into the bloodstream, that over activates the immune system which attacks the cell of the body.   These researchers believe that if you could lower gut permeability, you could prevent or stop type-1 diabetes.  Right now, there are no drugs based on this theory in clinical trials, although in the past Alba Therapeutics talked about testing their AT-1001 drug on type-1 diabetes.  (It is currently only being tested for Celiac disease.)

          Combining Therapies

          Basically A, D, E, and F cures are "one step" if they work, we're done.  But B and C are a little more complex.  B might require C to be a cure, or maybe not, or maybe B will work by itself, but take a very long time, so a practicle cure would still require both B and C.  In any case, it seems unlikely that C alone could cure type-1.  Certainly, we have tried Exsulin, Human Growth Hormone, and many types of beta cell transplants, and none of those have led to a cure.

          Please do remember that this posting is a work in progress, and I do hope to improve it over time.  Please email me with specific parts that are hard to understand, or need more explanation.  This is a case where I think publishing this information now, is better than waiting for perfect, refined information to be ready in the unknown future.
                Joshua Levy
                All the views expressed here are those of Joshua Levy, and nothing here is official JDRF or JDCA news, views, policies or opinions.
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                Sunday, April 17, 2011

                History of Exsulin and AAT

                Based on my last couple of posts, I got the two following questions:

                How is the phase-II Exsulin study that is currently underway, different from the phase-II Exsulin study that was reported on in 2009?

                The first trial gave one day's dose in one injection.  In the current trial, one day's dose is spread over three injections over the course of the day.  On one hand, the researchers think this will lead to better results, because they think that Exsulin does not stay in the system very long, so putting it in repeatedly over the day should lead to better results.  The drug will be more consistently in the system the whole day through.  On the other hand, they also think this will lead to fewer "injection site side effects".  In the earlier trial, some patients complained about pain, redness, itching, and other problems right around the injection site.  Since the second trial will only be injecting 1/3 of the dose at once, they are hoping there will be far fewer of these side effects.  They are also changing the exact formulation to try to minimize this discomfort.

                Also, the first study lists the doses as 600 and 300, while the second lists them as 200 and 100.  I'm assuming that is per injection, and the daily dose was the same for each study.  But it is possible that is not true and the second trial is using a much lower dose.  If so, this would be another big difference.

                The purpose of most phase-II studies is to find the best dose, the best format for that dose, and to test the treatment on a larger population than in phase-I.  So this study is testing improvements to the dosing and formulation; just what you would expect in phase-II studies.

                What is AAT used for today?  Is that disease like type-1 diabetes?

                AAT (Alpha 1-antitrypsin) which is also sometimes called A1AT, is approved for treating Alpha 1-antitrypsin deficiency.  Makes sense: your body doesn't produce enough AAT, so AAT is approved as a treatment.  This disease is not an autoimmune disease, and is nothing like type-1 diabetes.  It is genetic, and comes in different severities depending on if you have one or two of the bad genes .  It is estimated to affects 1 out every 2,500 people in the US, although only about 10% of the people affected are actually diagnosed.  Here is a note on the most common symptoms from the Alpha-1 Association:
                The most common indicators of Alpha-1 include shortness of breath, a chronic cough, and abnormal liver test results. If you have any of these symptoms there is a simple blood test that can detect alpha-1 antitrypsin levels. This test is also recommended if you have relatives, especially siblings, who have been diagnosed with alpha-1, or if there is a family history of early emphysema, with or without smoking.
                You can read about it here:

                And here are some support groups:

                Joshua Levy
                All the views expressed here are those of Joshua Levy, and nothing here is official JDRF or JDCA news, views, policies or opinions.
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                Tuesday, April 12, 2011

                Possible Cures for Type-1 in the News (mid April)

                Exsulin's Phase-II Trial is Data Complete 

                The exact update I got on the Exsulin phase-II trial is this: "We have finished recruitment for this trial. We are still in the process of finalizing the results".  I interpret this to mean, not only have the finished recruting all their patients, but they have all their data, and are now working on the data analysis / paper writing part of the research.  This is great news, because I'm hopeful that we will hear the results in a few months.

                Rituximab Starts another Phase-II Trial

                Rituximab targets the CD20 part of the immune system's B cells (different from the pancreas's beta cells) to try to prevent the autoimmune attack. B cells are part of the body's immune system and communicate with the T cells, which actually attack the body's beta cells in the pancreas. By targeting the B cells, it is hoped this treatment will stop or lower the attack of the T cells.

                Comment: Most treatments aimed at stopping the autoimmune attack are very focused on stopping the "bad" T cells which directly attack the beta cells in the pancreas. This treatment (if successful) opens up a whole 'nother way to stop the attack: by targeting the immune systems communication and support system, the B cells.

                The current research (which I consider phase-II, although the researchers list it as phase-IV) is very similar to the a previous trial which I blogged on before (link below).  The current trial has already started enrolling 50 people at First Affiliated Hospital, Nanjing Medical University (Nanjing, Jiangsu, China). If you are interested in enrolling, contact Tao Yang, PhD at phone 86-25-83718836 ext 6466 or email  There is no placebo group in this trial: everyone is treated.  They started in July 2010, and hope to complete it by December 2013.  This is for people with type-1 diabetes for less than one year.

                clinical trial record:

                A Sad Note to the Previous CD20 Research
                The previous Rituximab research was led by Dr. Mark Pescovitz who died in a car crash at the end of last year.  That work was published by the prestigious New England Journal of Medicine, and was just one part of a distinguished research career.

                My previous blogging on Rituximab is here:

                Sitagliptin Completes Enrollment on a Phase-II Trail (as a Treatment)

                This is a large (140 person) trial which started in late 2010 and is the follow on to a trial which I've blogged about before.  The goal of this is to lower A1Cs for type-1 diabetics by about 0.3, by lowering BG levels more quickly after a mean than is done now.  The 0.3 number is pretty close to what they did in an earlier, smaller trial. Sitagliptin is already approved for type-2 diabetes.  It's trade name is Januvia.

                They completed enrollment in February 2011, I think.  The record is not 100% clear, and it might have been earlier.  If they did complete enrollment in February, then they will finish collecting data about June.  The clinical record says the trial will complete in July 2011, so I think it is reasonable to see results by the end of this year for this research.  This same group published their previous results very quickly after the study was done.

                Clinical trial:
                Previous trial:
                Results from related trial: (but this was combining this drug with another)

                Extra Reading

                Dr. Skyler has written a wonderful summary of some of the more interesting clinical trials in type-1 diabetes done between June 2009 and July 2010:
                One of the things I particularly liked about this paper, is that for each clinical trial, there is a summary of the abstract and then Dr. Skyler's comments.  These comments often put the research into context, discuss next steps, or give his opinions on it.  That perspective is missing from the raw scientific papers.  (Although he wrote this before the two anti-CD3 treatments had failed in phase-III trials, so those are discussed here, although they are already dead as cures.)

                Here is part of his summary of the whole year:
                That negative studies continue to dominate the field, and that the positive ones still show decline in β-cell function over time, has led to more calls for combination approaches. When I [Dr. Skyler] have advanced such prospects at meetings of paediatric diabetologists, I hear groans. Yet when I have advanced these prospects at meetings of immunologists and transplant surgeons, I hear cheers.

                Joshua Levy
                All the views expressed here are those of Joshua Levy, and nothing here is official JDRF or JDCA news, views, policies or opinions.
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                Saturday, April 2, 2011

                Possible Cures for Type-1 in the News (early April)

                Canakinumab Completes Enrollment
                Canakinumab is a monoclonal antibody, which is designed to lower inflammation.  It targets IL-1β (interleukin-1 beta) which causes inflammation.  The drug was approved in 2009 (both US FDA and EU EMEA) for a collection of rare autoimmune based inflammatory diseases.  (And type-1 is an autoimmune disease which causes inflammation, but it is not clear how important the inflammation is to the symptoms of the disease.)  Good results have been seen in people with type-2 diabetes, and it has been used in children as young as 3.

                They have completed enrollment of their phase-II clinical trial (66 people) as of March 2011. Because this drug is already FDA approved, there was not a phase-I trial in people with type-1 diabetes.  So the results from this trial will be the first type-1 results that we see.

                Why is completing enrollment important? For two reasons.  First, because it is now possible to predict when they will finish collecting data.  This study runs for 2-4 years, so they should have data collected by March 2015 at the absolute latest, and might have some early data by March 2013.  Second, because much of the uncertainty that surrounds clinical trials, is involved with recruiting participants.  It is often unclear how hard it will be to recruit people, and long it will take.   But that this point, all that uncertainty is behind the researchers.  From now on, it is just gather data, then analyze data, and then publish data.  Researchers have a lot more control over those later stages, then over recruiting people in the first place.

                Clinical Trial:
                Wikipedia entry:

                Xoma 052 Fails (Mostly) in Phase-II for Type-2

                Xoma 052 is a monoclonal antibody which is a broad anti-inflammatory, and works by blocking the IL-1 inflammation pathway.  The news is that Xoma announced that their Xoma 52 phase-II trial for type-2 diabetes had missed it's primary end point (which was better BG control).  They are still hopeful that it will lower bad cholesterol and be marketable for that purpose.  But that's a big come-down: they were hoping to lower BGs which is a big, sweeping treatment for type-2, but now they are hoping to help one particular symptom.  Plus, there are already other drugs that lower bad cholesterol.

                Why is this important? Xoma is also testing this drug on type-1 diabetics.  That trial is ongoing and results are not expected until around October 2011.  But obviously, this is not good news.  However, since the mechanisms behind type-1 and type-2 are very different, we really need to wait and see what happens in their type-1 clinical trial.

                Reminder About The Blog
                This blog generally only covers research results.   Occasionally related topics are discussed.   However, I generally don't discuss funding issues, stock issues, new hires (such as presidents, new board of director members, etc.)  patient issues, mergers and acquisitions ("M&A"), director or C-level resignations, etc.  These are all news worthy, but they are not the kind of news that I cover here.

                Joshua Levy
                All the views expressed here are those of Joshua Levy, and nothing here is official JDRF or JDCA news, views, policies or opinions. 
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