Type 1 Diabetes Drug "Teplizumab" Successful in Clinical Trial
August 8, 2013 2:39 PM
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It's mainly for pre-diabetics who don't have an advanced version of the disease
A new drug could give pre-diabetics the chance to combat the onset of full-blown
type 1 diabetes
The drug is called teplizumab, and it helped pre-diabetics maintain their current level of insulin production for two full years without the condition worsening. The drug seemed to be most beneficial for pre-diabetics rather than those with advanced type 1 diabetes.
The drug was developed by Jeffrey Bluestone, PhD, an immunologist at UC San Francisco, and Mary Clausen, Distinguished Professor at UC San Francisco. The clinical trial was led by Kevan Herold, MD, PhD, a professor of immunobiology and deputy director for translational science at Yale University.
Teplizumab works by using an antibody targeted against a molecule called CD3. The antibody binds to the immune system's T-cells and stops them from attacking beta cells. This is effective because the disease is caused by the body's immune system destroying insulin-producing beta cells in the pancreas.
"The benefits of treatment among the patients who still had moderately healthy insulin production suggests that the sooner we can detect the pre-diabetes condition and get this kind of drug onboard, the more people we can protect from the progressive damage caused by an autoimmune attack," said Bluestone.
Those who have advanced type 1 diabetes, however, didn't seem to benefit in the clinical trial. Some even lost half or more of their ability to produce insulin, which was likely due to differences in the "metabolic condition of the patients and in the severity of their disease."
For those who are past the point of pre-diabetes, don't fret. Just earlier this year, researchers from the Universitat Autònoma de Barcelona significantly improved the
blood glucose levels
of dogs with type 1 diabetes through a gene therapy that consists of a single session of multiple injections. These injections presented adeno-associated vectors (AAV) that both expressed the insulin gene, and also glucokinase (an enzyme that regulates an uptake of glucose from the blood). When both genes were expressed, the excess of blood sugar in type 1 diabetic dogs was controlled over a long-term period.
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RE: Makes sense
8/9/2013 6:40:00 PM
That's right, but presumably at that point the monoclonal antibody therapy discussed in the article could be set in and achieve the same results (by stopping the autoimmune process) as in an early-stage patient who has not yet had progressive autoimmune destruction of their own islet cells. In other words, there would have to be a combination of these two novel therapies in late-stage diabetes type I patients in order to achieve, hopefully, a cure - whereas patients diagnosed at an early stage and with islet cells still intact would only need monoclonal antibodies and not stem cells to regenerate them.
Like I said, there is also the option of transplantation where islet cells that do not even have to be autologous (i.e. they could come from for example a pig) are implanted, shielded by seaweed or other material that blocks immune cells from entering and encountering the islet cells and thereby sparing them from an autoimmune process that could still be left active.
"The whole principle [of censorship] is wrong. It's like demanding that grown men live on skim milk because the baby can't have steak." -- Robert Heinlein
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