Friday, October 23, 2009

Possible Cures for Type-1 Diabetes in the News (October)

Living Cell Technologies Starts Phase-I Study in New Zealand

LCT is developing an encapsulated pig cell cure for type-1 diabetes. They have completed a phase-I study in Russia which resulted in one patient being off insulin for a few months, and another for a few weeks. They finally got approval from the New Zealand government, and have now treated their first patient. This clinical trial is very similar to the one they completed in Russia, but half the patients will get twice the dose that the Russians started with, and the second half will start out with three times the dose. Eight people total. This trial is scheduled to complete in January 2011.

Commentary
This research has already shown that their encapsulated cells can have good effect for short periods of time. The big question they need to answer are these:
1. Will larger doses of encapsulated cells results in less need for injected insulin?
2. How long will the encapsulated cells continue to work?
This trial will directly address question 1. By using higher doses, they will see if they get more generated insulin, and a higher percentage of people who are off insulin entirely. Unfortunately, question 2 can only be answered by time. By following the patients from the Russian trial and from this new trial for a year or two. Although it may be that they'll learn more about duration by starting with a higher dose.

Another issue for me is this: is this a phase-I study or a phase-II study? That's a big difference because a phase-II study moves them closer to general availability, while a second phase-I study doesn't. Officially the study is "Phase-I / Phase-II". It's size is 8 people, and that's on the small size of phase-I. However, it's goal is to try different doses, and that's a phase-II type of goal. (Phase-I is more focused on basic safety.) The real measure is how the US FDA views it, and I don't know the answer to that question.

Sources
http://www.clinicaltrials.gov/ct2/show/NCT00940173
http://www.lctglobal.com/downloads/cms_latest_news/2009-10-06-LCT%20NZ%20Implant%207%20Oct%2009%20.pdf
http://www.nzherald.co.nz/nz/news/article.cfm?c_id=1&objectid=10601771

LCT also issued their yearly report
which is here:
http://www.lct.com.au/downloads/cms_latest_news/2009-10-19-LCT%20Annual%20Report%202009.pdf

There are a couple of pieces of meaty news buried in this report.
On page 10 there is a list of KEY TARGETS. Nothing about any US trials, but (in addition to finishing their current trials) they list these two items:
  • Commence pivotal trial in Russia.
  • Commence DIABECELL® commercialisation [sic] – initially in Russian market.
And that makes it sound like whatever they are doing, they are going to do it in Russia first. They have a wholly owned subsidiary there, already.
Their clinical trials are described on pages 14 and 15.

Osiris Therapeutics Announces Preliminary Results For Prochymal Phase III GvHD and COPD Trials

Osiris is running two phase-III trials for their Prochymal treatment, for diseases other than type-1 diabetes. Both of these results are in and both were failures. They have several separate phase-II trials going on, and one of these does target type-1 diabetes. So having all their phase-III studies fail is bad news, but what really matters is the results of their type-1 diabetes clinical trial. Those results are expected in mid-2010.

press release: http://www.bioresearchonline.com/article.mvc/Osiris-Therapeutics-Announces-Preliminary-Res-0001?VNETCOOKIE=NO
http://www.clinicaltrials.gov/ct2/show/NCT00690066

Effects of Sitagliptin (Januvia) in Adult Patients With Type 1 Diabetes

This is a 20 person study which started in September and is expected to finish in December. It is trying a drug already in use for type-2 diabetics to see if it helps type-1 diabetics. This is aimed at helping type-1s use less insulin, not curing them. Based on my quick read of how this class of drugs works, I don't see why it's expected to work on type-1 diabetics. It helps the body create more insulin. I understand how that would help type-2s, but not type-1s. Anyway the proof is in the results, and we will not need to wait long. The research is being done at the
Barbara Davis Center in Denver (which is top-of-the-line.) The good news is that we will have results very soon, and if they are positive, the drug is available right now.

http://www.clinicaltrials.gov/ct2/show/NCT00978796
http://en.wikipedia.org/wiki/Sitagliptin

Sernova's Animal Studies Continue


Sernova published results from some animal studies. You can read the links below for details. No date to start human trials was announced. This work is a follow on to Valdez's work in Mexico years ago, which was very controversial at the time it was done. He didn't do animal trials before going straight to people, and was eventually shut down by the Mexican government. It was also unclear if he was really getting as good results as he claimed. Sernova is trying to use the same ideas, but do the animal studies first, and then get Canadian or US FDA approval to do a clinical trial. So this treatment has been in clinical trials in the past, although not right now.

The basic trick was to get porcine beta cells, mix them with sertoli cells, and then implant the mix. Sertoli cells block the immune system, so the idea is that the immune system will not attack the new beta cells. So it's similar to encapsulated beta cells (LCT), but a little different.

http://www.genengnews.com/news/bnitem.aspx?name=65911061
http://www.benzinga.com/press-releases/m26601/sernova-s-cell-pouch-system-tm-and-sertolin-tm-preclinical-efficacy-presented-

Tuesday, October 20, 2009

Wilson's Pioglitazone Phase-I Study is half way enrolled

Dr. Wilson was kind enough to tell me that his Phase-I study of Pioglitazone is about half way enrolled. They are hoping to enroll 15 people total. The study is a pilot one, being done at Stony Brook, NY, USA. Pioglitazone has been approved for use in type-2 diabetes for about 10 years. Pioglitazone is part of a larger drug family called thiazolidinediones which have been shown to preserve beta cells in animals with type-1 diabetes, and to reduce death of beta cells in petri dishes.

This study is also unusual in that it will enroll children as young as six. I assume that is at least in part because they are working with an already approved drug with a known safety profile. Open to patients within 4 months of dx.

For those of you who are near Stanford University, the Dr. Wilson doing this trial is different than the Dr. Wilson who is at Stanford.

Joshua Levy

Thursday, September 24, 2009

Two Possible Cures go to the Boneyard

It's never good news when possible cures "go to the boneyard", but it is part of research. Some treatments work and many don't. Here is a little discussion of two treatments, one of which has not worked out (for type-1 diabetes), and the other is on hold, with no clinical trials in sight:

Transition Therapeutics's TT-223 goes to the Boneyard

Transition Therapeutics is researching using a combination of two drugs to cause beta cell regrowth in an attempt to cure type-1 and type-2 diabetes. As of May 2009, they had officially marked their phase-I human trial for type-1 diabetes as closed. I haven't seen any published results for it, but I'm still looking. However, actions speak louder than words, and Eli Lilly (working with Transition Therapeutics) started a clinical trial in February 2009 using Transition Therapeutics's TT-223 product, but only for people with type-2 diabetes.

Also, in May 2009 they announced that JDRF and Transition Therapeutics had agreed that JDRF would stop funding clinical development of TT-223. Transition Therapeutics and JDRF terminated their agreement. Eli Lilly is taking over support for TT-223, but is applying the technology only to type-2 diabetes.

So the news from Transition Therapeutics for type-1 diabetics is not good. I will move Transition Therapeutics to my "boneyard" of research that has not panned out if there is no good news in the next 6 months.

Discussion

This result is not too surprising, and is similar to previous results with INGAP: because type-1 diabetes is an autoimmune disease, simply regrowing new beta cells can not cure it. The immune system attacks the new beta cells the same as the old ones. This type of treatment has more direct applicability on type-2 diabetes, where more beta cells are more likely to be helpful. Of course, if any of the treatments currently being developed succeeds in ending the autoimmune attack, then treatments that regrow beta cells will suddenly be in high demand. Unless the body regrows beta cells naturally without intervention.

A few months after stopping the funding of TT-223, JDRF started funding a large, general program (together with Genomics Institute of the Novartis Research Foundation) to test generic drugs for their ability to help regrow pancreas cells. Although I don't have visibility into JDRF's decision making, I think it is reasonable to say that since TT-223 did not pan out, JDRF is putting money into other research with similar goals. Unfortunately, that research is not in human trials yet, so I won't be following it.

These are records for Transition Therapeutics's phase-I studies:
http://clinicaltrials.gov/ct2/show/NCT00239148 (type-1)
http://clinicaltrials.gov/ct2/show/NCT00239187 (type-2)

And here is the clinical trial record for their phase-II study (which is type-2 only):
http://clinicaltrials.gov/ct2/show/NCT00853151

I'd like to thank Susan Mohr for some of the information used here.

Alba's Lazotide (previously AT-1001) goes to the Boneyard for type-1 diabetes, but not Celiac Disease

I recently moved Alba Therapeutics's Larazotide (previously known as AT-1001) from my "preparing for clinical trials" section to my "boneyard" for treatments that are no longer under development as cures for type-1 diabetes.

I did this before reading the following Scientific American article:
http://www.scientificamerican.com/article.cfm?id=celiac-disease-insights
That article (written by a founder of Alba Therapeutics) says that the FDA approved human trials for Larazotide for type-1 diabetes. However, I can not find any references at the company's web site that they are planning such a clinical trial, and there is nothing in www.clinicaltrials.gov, either. So therefore it is staying in the boneyard for now.

If you read the article linked above, remember that the author did some of the original research into Larazotide and founded Alba Therapeutics, so is not an unbiased source! In particular, this quote:
Surprisingly, essentially the same trio—an environmental trigger, a genetic susceptibility and a “leaky gut”—seems to underlie other autoimmune disorders as well. This finding raises the possibility that new treatments for CD may also ameliorate other conditions.
This is the author's opinion, however I don't think it is general consensus among researchers. Most researchers believe that autoimmune disorders are built on a foundation of a genetic susceptibility and an environmental trigger. The idea that "leaky gut" underlies autoimmune disorders is a minority opinion. Of course, if Larazotide works the way Alba hopes it will, that might change.

All of the above comments pertain to using Larazotide for type-1 diabetes, not Celiac Disease. The situation for Celiac is much different: Alba is running human trials. There are several listed at www.clinicaltrials.gov, and I think some of them are phase-II. (But I don't follow Celiac closely so am unclear on the details. Also, there appear to be two different drugs called "AT-1001" and "AT1001" so don't get confused.)

Joshua Levy

Saturday, September 19, 2009

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

This is an experiment in "quick hits". I will provide a paragraph or two of information on recent news items about possible cures for type-1 diabetes. So, in no particular order, here we go:

Andromeda Completes Patient Recruitment in Phase III Trials for DiaPep 227

Andromeda has announced that their phase-III clinical trial of DiaPep277 is fully enrolled. This is an important milestone, because it now means the end of the study can be predicted. Since their protocol is 2 years long, they will be data complete around September 2011. They have also said that they will have results at end of 2011, which makes sense.

DiaPep277 is the oldest Phase-III clinical trial that I know of. Previous news has not been good. Their intermediate results were lackluster and they changed their experimental design and recruited more patients. I've never gotten around to reviewing their Phase-II results (which were published prior to my interest in clinical trials), but maybe I should.

Press release: http://www.pipelinereview.com/index.php/2009090929254/Proteins-and-Peptides/Andromeda-Biotech-Successfully-Completes-Patient-Recruitment-in-Phase-III-Trials-for-its-Lead-Drug-DiaPep277-for-Type-1-Diabetes.html

4-Year Follow-up of Diamyd(r) Phase II Study Shows Clear Positive Trend

Diamyd got permission to extend their Phase-II trial, and continue to follow the same group of patients for a total of 7 years. They talked about 4-year data in this way:
Initial analysis of new data shows, that patients treated with the Diamyd(r) vaccine early after diagnosis have a clearly better diabetes status compared to the corresponding placebo group, still 4 years after the injections.
Since there are no actual numbers here, I wouldn't read too much into it. "Clearly better" is pretty vague. There is no reference to anything published, so there is no place to look for more details or actual numbers.

press release: http://www.reuters.com/article/pressRelease/idUS86571+03-Sep-2009+GNW20090903


Diamyd to include children over 10 yrs in US phase III study with Diamyd diabetes vaccine

Diamyd got FDA approval to lower the minimum age of enrollment in their US Phase-III study down to 10. That's young for a clinical trial, and a sign that the FDA thinks that Diamyd's treatment is very likely to be very safe. For comparison, ToleRx can accept people as young as 12, and MacroGenics down to 18 (and even 8, but only with special approval).

press release: http://www.pharmabiz.com/article/detnews.asp?articleid=51470&sectionid=

Faustman is Data Complete, Results by early 2010.

In 10-February 2009, the Nathan/Faustman group officially reported that they had enrolled the last patient into their Phase-I trials. They also updated their clinical trial record to show that they would be data complete in July 2009. (This makes sense, since the protocol only requires 3 months of data gathering after a patient starts.)

So, as of now, they should be working on analyzing the data, writing the paper, and getting it published. (And if we are lucky, getting reporters or bloggers to write about the results!)

They also have a facebook page which contains this quote:
"We hope to have all of the Phase I data submitted to our biostatistics center in November 2009", and their lab web pages talks about having results by early 2010, so I think we are close to hearing about their results. Their just-released newsletter also has the "early 2010" date.

Joshua Levy

Saturday, September 12, 2009

Background for the Artifical Pancreas

In the past, I have not posted updates for the artificial pancreas (AP) as a possible cure for type-1 diabetes. But I'm now going to spend more time on this area of research. This post provides background for how to follow progress on an Artificial Pancreas. At the end is a section on why I'm posting in this now, when I have not in the past.

Components of an Artificial Pancreas (AP)
I'm going to discuss an AP built out of the technology that we have now, so an "off the shelf" pump connected to an "off the shelf" CGM, with some extra software on the pump to handle the control functions. A successful artificial pancreas is going to involve several different components that can be developed and tested separately. Understanding these components will help help track progress toward the final goal. The components are:
  • A pump that can deliver small enough doses of insulin.
  • A continuous glucose monitoring system (CGM) that is accurate enough.
  • Insulin which acts quickly enough.
  • Software that can take the data from the CGM and do a good enough job of automatically calculating the commands to send to the pump.
  • Government approval of all of the above.
To create an implanted artificial pancreas (IAP), one that can be put inside a person,, there are three more required components:
  • Higher density insulin, so that a longer supply can be stored inside a person.
  • Enough miniaturization so that the pump, CGM, software, and insulin can fit inside a person.
  • And government approval of all these components.
Where are We Now? (what is "good enough")
Part of the uncertainty in the status I describe below, is that these components work together. So imperfections in one might or might not be overcome by advances in the others. For example, if CGM were perfectly accurate, that would make the control software much easier to create. Similarly, the faster acting the insulin that can be used, the easier the control software is to write, because it does not need to take into account the delay in the insulin or build up of insulin in the body. So the question is not do we have good enough CGM. It is more complex than that: do we have a good enough pump, CGM, software and insulin, so that together then can form an AP. And the same is true for all the major components.

For pumps and fast acting insulin, we are in good shape. Today's mass produced pumps are likely precise enough to support the first generations of AP, and currently available insulin is likely fast enough.

For the computer control of an AP, we are very close. There are several computer algorithms which have been tested in different clinical trials, and which seems to work well. The biggest hurtle remaining is to get the software good enough to work with the current generation of CGM.

For CGM, we are not there yet. There are two problem areas for CGMs, both important. First there is accuracy. BG meters in general are only accurate within 20%, but CGM are not even that accurate. No CGM has been approved as a replacement for regular BG meters for exactly that reason. One of the problems with CGMs is that the interstitial liquid that they measure sometimes has higher glucose levels than the blood which standard meters measure (and it is blood glucose levels that really matter). This means that the current generation of CGM devices can sometimes measure higher glucose levels than really exist (which would cause an AP to put in more insulin than it should).

But there are also non-accuracy related issues, which may be a larger problem. Many CGMs are not comfortable to wear, often fall off, have calibration problems, need to be replaced often, etc. My memory of comments in brave buddies, from people who tested CGMs, and from those who now use them, is that there are occasional worries about accuracy, but much more complaining about replacement, falling off, skin space, pain, recalibration work, etc. The bottom line is that no AP will be successful if the CGM component of it is constantly falling off, etc.

As for an implanted artificial pancreas:

There have been European tests of U-1000 insulin (which lasts ten times as long as the U-100 insulin commonly used). And this insulin was enough to operate an implanted pump for 3 months between refills. So I think we have the insulin needed, although it is not yet FDA approved in the US. There are currently clinical trials in the US on U-400 insulin, also.

Also, there have been clinical trials of an implanted pump in the US, including a pump produced by Minimed. So that too, is within sight, although not yet US FDA approved.

For a technical review of where we are, especially in terms of CGM systems, here is a whole journal issue focused on that question:
http://www.liebertonline.com/toc/dia/11/s1

Six Stages to an Artificial Pancreas

The JDRF framework for a pump is based on six stages as described below. Note that stages 1 and 2 are more of emergency shut off functionality than artificial pancreas functionality, but you need to start somewhere! Indeed, I think it is fair to say that only at stage 4 is there a limited AP, and stage 5 is a full AP:

Stage 1. An emergency shut off when the patient experiences too-low BGs.
Many of us live in fear of extreme lows in the middle of the night which lead to seizures. In the worst case, type-1 diabetics occasionally die in the middle of the night from too-low BG. So a straightforward safety improvement which could be made to a pump, if it was attached to a CGM system would be to shut down the pump if the patients BG levels were too low for too long. Research has shown that most (although not all!) night time seizures are preceded by several hours of low BG numbers. So by simply telling the pump to stop putting in more insulin into the patient, many of these seizures could be prevented. Also, this plays into the strengths of the current CGM technology (the accuracy problems usually effect high BG measurements, not low ones). No any complex software is needed, and if the AP is wrong, BG may go up more than it should, but that is a relatively minor problem. The problem it solves ("dead in bed") is real (if rare) and terrifying. Finally, the FDA can view it as a simple safety interlock, for approval purposes.

Stage 2. A shut off when the patient is heading to a situation where they will have too-low BGs.
This is similar to stage 1, except that it uses software to predict when a low BG situation is likely to happen in the future, and causes the pump to dose less before the low BG situation occurs, hopefully avoiding it. This is much like stage 1, except that it requires more complex, predictive software.

Stage 3. Improving BG levels at all times (avoiding both too-low and too-high BG levels).
The goal of this stage is limit the time the patient spends with either too-high or too-low BG levels. This stage is not trying to keep the patient at ideal BG levels, rather it is just trying to avoid unhealthy BG levels.

Stage 4. Limited control with meal announcements ("overnight control")
At this stage the AP can control BG, aiming at optimum levels in the relatively undemanding time while the patient is asleep. And if it is notified ahead of time about eating. This stage does not need to worry about exercise, or emotional changes, or unexpected eating.

Stage 5. Fully reactive control of insulin.
This is what most of us consider to be an artificial pancreas. It keeps BG levels in the healthy range without having to do separate blood checks or counting carbs.

Stage 6. Fully reactive control of insulin and other hormones.
Beta cells produce other hormones besides insulin, and a better AP will provide those hormones as well as insulin, so this stage is icing on the cake.

Basically, steps 1 and 2 are designed to prevent serious low BG events, especially at night.
Steps 1, 2, and 3 are really focused on avoiding bad BG numbers, rather than keeping the patient with good BG numbers. They are fundamentally trying to avoid mistakes, rather than create a better system.
Steps 4, 5 and 6 are trying to improve what we've got.
Step 4 is sort of a night time AP, while 5 is an all the time AP.
Step 6 is a complete solution for multiple hormones.

How I Plan to Cover Artificial Pancreas Research
Except for this posting, I don't plan to cover each component separately, because that would be a lot of work, and I don't think it would be very useful. Instead, I will cover human trials of complete APs as they are tested, noting which components are in use for each test. I don't think it is useful to report of every trial of U-400 insulin, and U-500, and U-1000, etc. Instead, I will just note if an advanced insulin is used in a specific test of an AP.

Also, I'm probably going to limit my coverage to clinical trials where each patient uses the AP for at least 24 hours (not 24 consecutive hours, but 24 hours total), at least to start. There are a large number of clinical trials aimed at gathering data on a very specific algorithmic questions, and I don't plan to report on all of those. They are very important to the end goal, of course, but there are to many of them, and each one is individually such a small step, that I don't plan to cover them. These advances get incorporated into the longer studies which I will cover.

One problem that I have already hit, is how to name these studies. I don't want to name them after the company or institution running them, because one of those could be running many AP trials at the same time (Minimed, is running more than one right now.) Many of them have one researcher who developed the software being tested, and another who is running the clinical trials. Which one should I use? And what if several people worked together on the software, or in running the trials? I could name them all based on their Clinical Trial number, but that seems so sterile. I'll figure something out. (Maybe they will all get code names or something. :-)

In the next 2-3 weeks I will post a summary of clinical trials posting, which will give a very short status of a large number of current clinical trials involving APs. After that, I'll make follow up postings covering trials, much like I do with non-AP clinical trials.

Why I have not posted about the Artificial Pancreas before; Why I will Now
I have not previously posted about an Artificial Pancreas, for three reasons:
  1. Many don't consider it a cure at all.
  2. There was not that much news on it.
  3. I didn't have a framework to measure progress, in the same way I had a framework for drugs.
However, recently all three of these issues have resolved themselves.

First, I was particularly worried that a posting referring to an AP as a cure would trigger a long a pointless argument about weather an AP was a cure or a crutch. If you gave someone a new heart valve, have you cured their heart condition? If you gave someone a brace, had you cured their withered leg? It is a philosophical question and different people will have different answers. Even worse (for this discussion) I doubt one side could convince the other they were right, because it really is a philosophical difference, so the email discussion could last forever.

Personally, I had always considered an IAP as a cure, but I was not sure if an AP was a cure or not. However, in the past I also thought that this was a minority opinion, and that most people felt that APs were not cures, not even IAPs. However recent discussions with other parents of children with diabetes has convinced me that many people consider APs to be cures, or at least important enough to be very valuable even short of a cure.

The one thing that I don't want to happen, is a long email argument about if an AP is a cure or not. There is no doubt in my mind that some people will consider it a cure, while others will not. Therefore, I'm posting on it's progress for those who consider it a cure, and people who don't should ignore those posts.

Second, in the last four months or so, there has been several reports of progress toward an AP. I think that Weinzimer's work at Yale has been generating much of this press coverage, but others are moving forward in this area as well.

Third, the JDRF has published a framework for evaluating APs. These are the stages that I've discussed above. This framework is based on APs working in progressively more and more realistic (and difficult) situations. It is not based on progress in individual components of an AP, and so it is perfect for me to use as I report on progress.

In the past I have thought about covering APs by covering progress in each major component of an AP. However, this tended to scare me off because of the work involved in covering several different components all of which are making many small, incremental improvements all the time. By limiting my coverage to complete AP testing, I'm hopeful that it will be a reasonable amount of work, and our kids will end up using a complete AP anyway.

Thanks to Dr. Mary and Dr. Steve (both at Bearskin Meadows) for getting me to think about these issues, and providing some of the information used here. All mistakes are my own.

Joshua Levy

Sunday, September 6, 2009

JDRF Funding Research for a Cure

In the US, we are starting the "Walking Season" when JDRF asks us to walk to raise money for cure. So I'd like to do my part, by reminding you all how important JDRF is to the human trials of potential cures for type-1 diabetes, which I track.

Let me give you the punch line up front: 69% of the treatments currently in human trials have been funded by JDRF. (And the number is 86% for the later phase trials!) This is an amazing impact; one that any non-profit should be proud of.

Cures in Phase-III Human Trials
Summary: there are 4, and all of the treatments have been funded by JDRF.
  • GAD65 (several different studies)
  • TolerRx's CD3 (several different studies)
  • MacroGenics's CD3 (several different studies)
  • DiaPep227
Cures in Phase-II Human Trials
Summary: there are 10, and 8 of them have been funded by JDRF, either directly or indirectly through ITN. Here are the treatments that have been funded by JDRF:
  • MMF/DZG by Skyler
  • PROCHYMAL by Osiris Therapeutics
  • Rituximab by Pescovitz at Indiana
  • Thymoglobulin (also known as ATG) by Gitelman
  • Abatacept by Orban at Joslin Diabetes Center
  • Umbilical Cord Blood Infusion by Haller at University of Florida
  • Exsulin (previously INGAP) by Exsulin
  • Kineret / Anakinra by Mandrup-Poulsen at Steno Diabetes Center
Not funded by JDRF:
  • Atorvastatin (Lipitor) by Willi at Children's Hospital of Philadelphia
  • Brod at University of Texas-Health Science Center

Cures in Phase-I Human Trials
Summary: there are 12, and 6 of the are funded by JDRF and 6 are not. Here is the list funded by JDRF:
  • BHT 3021 by Bayhill Theraputics
  • Trucco at Children’s Hospital of Pittsburgh
  • IBC-VS01 by Orban at Joslin Diabetes Center
  • CGSF by Haller at University of Florida [*]
  • Proleukin and Rapamune by Greenbaum at Benaroya Research Institute
  • Lisofylline by DiaKine
Not funded by JDRF:
  • ATG and autotransplant by Burt at University of Sao Paulo
  • Diabecell by Living Cell Technologies
  • NI-0401 by NovImmune
  • Etanercept (ENBREL) by Quattrin at University at Buffalo School of Medicine
  • CGSF and autotransplant by Esmatjes at Hospital Clinic of Barcelona [*]
  • Pioglitazone by Wilson at Stony Brook [*]
The studies marked with a [*] are ones which I have not yet blogged about, but hope to in the next few weeks, as I work through my backlog. This summary does not include Artificial Pancreas research, which I will discuss more in a future posting.

Summary of all Trials
26 in total
8 not funded by JDRF
So 68% of the human trials currently underway are funded (either directly or indirectly) by JDRF. Everyone who donates to JDRF should be proud of this huge impact; and everyone who works for JDRF or volunteers for it, should be doubly proud.

It is important to remember, however, that although there are four treatments in Phase-III trials, we are not close to a cure for established type-1 diabetes. All of the clinical trials in Phase-III and Phase-II are targeted at honeymoon type-1 diabetes; none at established cases. Even with that restriction. None of the treatments in Phase-III trials resulted in cures during their Phase-II trials. They all extended or increased the honeymoon phase in some way.

We have a long way to go, and that is where JDRF comes in.

Compared to Last Year

In 2008 there were 3 treatments in Phase-III trials, in 2009 there are 4 (growth of 33%).
In 2008 there were 5 treatments in Phase-II trials, in 2009 there are 10 (growth of 100%).
In 2008 there were 10 treatments in Phase-I trials, in 2009 there are 12 (growth of 20%).

I do think that a little of this "growth" is because I have gotten better at finding clinical trials, so last year I missed some trials which I'm not missing this year. But I also think that most of the growth is real. There really are more clinical trials going on now.

Discussion
  • I give an organization credit for funding a cure if it funded that cure at any point in it's development cycle.
  • I use the term "US Gov" for all the different branches and organizations within the United States of America's federal govenment (so includes NIDDK, NIAID, NICHD, etc.)
  • The ITN (Immune Tolerance Network) has JDRF as a major funder, so I count ITN as indirect JDRF funding.
  • I have made no attempt to find out how much funding different organizations gave to different research. This would be next to impossible for long research programs, anyway.
  • Funding of research is not my primary interest, so I don't spend a lot of time tracking down details in this area. I might be wrong on details.
  • I don't work for the US Gov, JDRF, or any of the other organizations discussed here. I'm not a member of JDRF or any of the other organizations discussed here. I do own stock in several of the companies discussed here.
This is an update and extension to a blog posting I made last year:
http://cureresearch4type1diabetes.blogspot.com/2008/10/jdrf-funding-of-cure-research-phases-ii.html

Joshua Levy

Saturday, August 29, 2009

Update on Gitelman's ATG Phase-II Clinical Trial

Dr. Gitelman at UCSF has started a Phase-II human trial aimed at using ATG to cure (or lessen) type-1 diabetes. The goal of this study is to preserve remaining beta cells for people within 100 days from diagnosis. This study started in August 2007, and is expected to run until June 2011. So far it has enrolled 11 out of an expected 66 patients. It's a four day treatment (in hospital), and 12 follow up visits over a 2 year period. They are recruiting at a total of 9 sites (growing to 13), which are listed in the clinical trial page linked below.

Here is a quick summary of how they hope ATG (Thymoglobulin) will work:

Type 1 diabetes is caused by destruction of insulin-producing beta cells by T cells, part of the immune system. Thymoglobulin is a mixture of different antibodies that target T cells. This mixture includes the anti-CD3 antibody (and anti-CD3 treatments are in Phase-III trials already, having completed successful Phase-I and II trials). The researchers hope that this multi-faceted approach will be even more successful and have a longer lasting effect than with anti-CD3 alone, and may treat diabetes by several mechanisms. First, it lowers the number of T cells, so there are fewer to attack the beta cells. It also seems to alter the T cells remaining behind, rendering them less likely to be destructive. Following this depletion, the T cells that grow back in the following weeks may be reset and have a healthier balance (meaning that a special type of T cells, called regulatory T cells, will help keep the destructive T cells in check).

Using ATG to cure type-1 diabetes is an idea that flows from two sources. The first source is a line of clinical trials aimed directly at curing type-1 with ATG. Eisenbarth's work of long ago, a Phase-I trial done in Europe, etc. But it also has another source, which is Burt's Brazilian research as described below.

Discussion: How to Follow Up Burt?

One of the questions that I'm occasionally asked is this: when will there be a follow up to Burt's Brazilian research? When will there be a Burt, phase-II? This is a natural question, because Burt has -- by far -- the best results of any one. Many patients on that trial went years without using external insulin. No other study comes close. So an obvious question is: how do you move forward with that research.

Burt's research is the opposite of most. Most researchers use the smallest possible doses during phase-I. Phase-I is targeted at safety, so they use small doses to assure safety even at the expense of effectiveness. So for most studies, for phase-II studies, they move forward by raising the dose to try to make a safe treatment a more effective one. But Burt's research is the opposite. The effectiveness is the strongest yet, but there are real questions about safety. So you would NOT follow it up by raising the doses!

One way to follow up Burt's relative success, is by turning down the dose. Trade off a little effectiveness for added safety. Oversimplified a little: Burt's research involves using three drugs (ATG, GCSF, and cyclophosphamide), and reinjecting the patient's own precursor bone marrow cells (previously removed). Dosing with just ATG can be viewed as a "kinder, gentler" Burt. Especially since the cyclophosphamide is the most risky drug of the bunch. (I'll be posting on two GCSF clinical trials in the coming weeks.)

Since I'm a software engineer, I'll use a software analogy: Burt is doing a "hard reboot", Gitelman is trying for a "soft reboot".

Notes

One of the complexities of following the research, is that ATG is referred to by many different names by different groups. For example: Thymoglobulin, rATG, hATG, ATGAM, antithymocyte globulin, etc.

The cells that Burt is removing and then reinjecting are sometimes called "precursor bone marrow cells" and other times "adult stem cells".

The lead investigator for this clinical trial is Dr. Gitelman at UCSF. For those of you at Bearskin Meadows: yes, this is the same "Dr. Steve" who is often up there. I'm indebted to Dr. Gitelman for his insights into Burt's research and how it relates to other research, including his own. All mistakes, opinions, and oversimplifications are my own.

Patient oriented information on this trial:
http://www.type1diabetestrial.org

Previous Blog postings on this
http://cureresearch4type1diabetes.blogspot.com/search/label/ATG (blog on ATG)
http://cureresearch4type1diabetes.blogspot.com/search/label/Burt (blog on Burt)
http://cureresearch4type1diabetes.blogspot.com/search/label/Gitelman (blog on Gitelman)

Web pages (but these need updating):
http://joshualevy.pbworks.com/DiabetesCureReadyForHumanTrials#ThymoglobulinalsoknownasATGbyGitelman (Gitelman)
http://joshualevy.pbworks.com/DiabetesCureReadyForHumanTrials#ATGandothersbyBurtatUniversityofSaoPaulo (Burt)

Clinical Trial records for this study:
http://www.clinicaltrials.gov/ct2/show/NCT00515099 (Phase-II ATG)
http://www.clinicaltrials.gov/ct2/show/NCT00190502 (Phase-I ATG)
http://www.clinicaltrials.gov/ct/show/NCT00315133 (Burt)

Joshua Levy