In a recent study published in the British Journal of Pharmacology, researchers at the University of Georgia found that the therapy triciribine could be able to reverse or stop pulmonary hypertension and pulmonary fibrosis progression.
Pulmonary fibrosis occurs when lung tissue becomes damaged and scarred. This thickened, stiff tissue makes it more difficult for the lungs to work properly. As pulmonary fibrosis worsens, patients become progressively more short of breath. According to the Coalition for Pulmonary Fibrosis, the condition affects 130,000 people in the United States.
Pulmonary hypertension is a type of high blood pressure that affects the arteries in the lungs and the right side of the heart. According to the Centers for Disease Control and Prevention, the condition is rare and affects 15 to 50 cases per million people.
“The average life expectancy for people with these diseases is only about five years after diagnosis, and while the drug treatments we currently have may help improve quality of life, they don’t reduce mortality,” said Somanath Shenoy, co-author of the paper and associate professor in UGA’s College of Pharmacy. “Our tests show that treatment with triciribine can halt disease progression and may even reverse some of the damage to lung tissue.”
The team used pulmonary hypertension and pulmonary fibrosis mouse models to assess the effect of triciribine, a drug agent that is able to inhibit the production of the Akt1 protein.
Results from previous studies showed that Akt1 is partly responsible for the development of myofibroblasts, cells that migrate to the sites of injury to aid in wound healing. When there is an unregulated production of these cells, they cause scarring, leading to loss of functional blood vessels and fibrosis in the lungs.
In the study, when mice had the disease symptoms, the researchers injected them triciribine once per day for three weeks, with results showing a slowing in the scarring and loss of lung vasculature. They even found that tissue in the mice’s lungs returned to normal.
“To our knowledge, this is the first direct evidence that Akt1 causes disease onset and progression of pulmonary fibrosis and pulmonary hypertension,” Shenoy said. “We have also tested this process in human cells taken from diseased lung tissue, and we see very similar results.”
The team then examined mice genetically modified with the Akt1 pathway absence, with results showing that these mice did not develop any symptoms of the disease. Based on the results, the researchers suggested a new direction for the cause of the disease. However, these findings are still preliminary, and more studies are needed before the researchers can examine the efficacy of triciribine in humans. A human version of triciribine could be administered orally, eliminating the need for daily injections.
“We still need to identify the downstream effects of Akt1 inhibition to see if there are any negative side effects,” Shenoy said in the news release. “But if these tests go well, we hope to begin human trials within the next three to five years.”
Hello,
I am interested in the clinical trial study of Triciribine. As an individual who suffers pulmonary hypertension and pulmonary fibrosis progression, I would like to be considered for the first human trial. Is there a potential pre-candidate list for the inclusion and exclusion based on certain heath and procedures one might have had. I want to make sure to steer clear of any diagnostic test which might disqualify me. Thank you
Why will it take 3 to 5 years for human studies. That is a lifetime for people with ipf.. Can’t you speed things up a bit?
What I’d like to know is how much the manufacturer is going to price gouge us. There are currently two drugs used in the treatment of IPF, but only the Bill Gates and ted Turners can afford them.
Please keep me informed on when human clinical trials start.. my father in law has pulmonary fibrosis and would like to be part of the trail.
I m interested in clinical trial for my father as soon as possible. He is 77 yrs old and a doctor too. He has just started taking oxygen concentrator just few days back @ 2 lpm. I m from India
I am interested too for my wife to be a part of the clinical trials for triciribine. Earlier the better. She is an IPF patient.
I m interested my mother is suffering from pulmonary fibrosis.i m from bangladesh
My husband is only 46 and just been told he has pulmaryfibrosis need to try anything so would be interested in the clinical trails triciribine thankyou .
A dear friend was just diagnosed with pulmonary fibrosis as well, he is 67. It’s surprising I can’t find anything about triciribine that seems to be current. Does anyone know what’s been going on with this drug the last 2 years? Please let me know when the clinical trials begin.
Thank you.
My husband would like to be considered for this human trial for Tricibine. Grady Ayers he tried Esbrit and could not continue because of the side effects.
I am interested in to be a part of the clinical trials for triciribine. I am IPF/Hypersensitive Pneumonities Patient.
I have had chronic sarcoidosis for 15 years. My lungs are steadily headed towards PF. Is this something that could prevent further scarring r/t pulmonary sarcoidosis?
Thank you.
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I have scarring of the lungs from Sarcoidosis. Is this something that could help me?
I have difficulty breathing, fatigue, asthma, cough (productive and non-productive) and susceptible to upper respiratory infections.
I live in Atlanta Ga, but from Athens Ga.
i’m 71 years old would i qualify for the clinical trails
I read the comments but don’t see replies as these people are serious about participating in a clinical trail. Whoever manages this website should provide answers to those who are inquiring. This is sad to put information and failed to respond.
Has anyone responded to your comment?