Posted on 04/27/2025 8:04:53 PM PDT by ConservativeMind
A drug candidate, previously successful at treating severe fatty liver disease, reduces atherosclerosis—a primary driver of cardiovascular death worldwide—in large mammals, a study suggests.
DT-109 limited the formation of atherosclerotic plaques in both the aorta and coronary arteries of nonhuman primates.
This glycine-based tripeptide also stopped critical processes that lead to vascular calcification, a significant catalyst of arterial stiffening and plaque instability.
Said Eugene Chen, M.D., Ph.D., "DT-109 has demonstrated a remarkable ability to counteract the progression of atherosclerosis, an achievement that holds immense therapeutic potential."
Chen's team developed DT-109 in 2019 after it was discovered that impaired glycine metabolism can cause non-alcoholic fatty liver disease.
In a 2023 study, the compound reversed fat buildup and prevented scarring in the livers of mice and nonhuman primates that had developed the most severe form of fatty liver disease, nonalcoholic steatohepatitis.
NASH—renamed metabolic dysfunction-associated steatotic liver disease in 2023—affects nearly 7% of the global population.
The condition is strongly associated with an elevated risk of atherosclerosis, which increases the likelihood of life-threatening events like heart attack and stroke.
During the 2025 study, researchers fed nonhuman primates a cholesterol-rich diet for 10 months before treating them with oral DT-109.
In addition to suppressing the formation of atherosclerotic plaques, DT-109 quelled chronic inflammation that is associated with calcification of the arteries.
This occurred in part by reducing signaling from the NLRP3 "inflammasome" protein, which plays a necessary role in vascular calcification.
"These results are of particular importance because they suggest that DT-109 could not only reduce atherosclerotic lesions but also prevent the vascular calcification that exacerbates arterial stiffness and plaque vulnerability in advanced atherosclerosis," Chen said.
"This presents an opportunity to address the root of the issue, rather than managing complications as they come up."
(Excerpt) Read more at medicalxpress.com ...
This compound, or glycine by itself, may be helpful at preventing artery plaques.
I was thinking about taking 10 grams/day of glycine anyway for glynac and general longevity reasons (plus it helps improve the skin); now I definitely will be doing so.
TRI methyl glycine is available now as a supplement. You can purchase pharmaceutical grade on Amazon. It’s been used for years as a liver detoxifier.
How is this different from what this study was using?
The supplements I’ve seen that are sold for detoxifying the liver are using 650 to 1500 mgs of tri-methyl glycine.
Article a bit misleading. It prevents or blocks further atherosclerosis. It does not reverse the process.
I like the fact that it reduces inflammation.
It makes sense that if it does this is in the liver maybe it does it elsewhere.
I recently had a CRP test that showed some elevation, indicating inflammation. Which is the cause of heart disease, not cholesterol etc. Sugar is the biggest culprit.
Would ge interesting to go on the trimethyl glycine in a supplement dosage of at least 650mg or more per day, and redo the CRP after 90 days.
Your body pretty much detoxifies within 90 days, esp the GI lining providing that you stop any pollutants, including alcohol.
Interesting article. Thanks.
Is your concern reversing arterial plaques?
No one has discovered a medical treatment to remove hard plaques
There are ways to so this, and I did so.
I take both glycine/NAC because they have both individual roles which I dimly understand and because together they create —in just the right amounts—glutathion which is a big antioxident. I also take TMG—originally because I was takin NMN or B3 or niacinimide...and its said that these supplements deplete TMG. But I have cycled off all of them for now. And I still take TMG. Now for no reason except habit. It would be nice if TMG did reduce or prevent arterial plaques. But its not clear that TMG is an analog for the peptide mentioned in this article.
It would seem the new tripeptide used leucine, but the paper itself doesn’t validate that.
Turns out, not always.
That does not seem fair.
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