New Study on BAM15

Happy Wednesday!

A landmark study was just published on BAM15 in April.

I’ve been cycling BAM15 and SLU-PP-332 for 6+ months now, so I know it works personally.

This study may be the strongest evidence yet for why BAM15 deserves a seat at the table as a serious contender for metabolic, cardiovascular, and anti-inflammatory optimization.

Why is this a big deal?

The results are nothing short of jaw-dropping, and they open up new possibilities for those of us who want powerful results without the risks or side effects of more conventional drugs.

Let’s break down exactly what was studied, what it means, and how YOU could benefit from the BAM15 protocol.

Here’s the link if you want to read the study yourself.

The Study

Let’s get nerdy for a second, because understanding the experimental design is key to appreciating why these results matter.

Researchers used ApoE(−/−) mice.

If you’re not familiar, these are genetically engineered mice designed to develop rapid and severe atherosclerosis (arterial plaque).

Why? Because their ApoE gene is “knocked out,” making them a perfect model to study what goes wrong in human arteries over years of poor lifestyle, but sped up to a few weeks in a mouse.

All animals were fed a Western diet—think high fat, high cholesterol, and high sugar, essentially the standard American diet that clogs arteries in humans.

The treatment protocol:

• BAM15 group: 85 mg/kg/day, orally (by mouth), 6x per week, for 12 weeks straight

• Positive control: Atorvastatin (Lipitor), 2 mg/kg/day, to benchmark against the world’s most prescribed cholesterol drug

• Endpoints: They measured everything—plaque in arteries, blood lipids (including cholesterol, triglycerides, LDL, and HDL), liver histology, inflammatory markers, and a comprehensive analysis of gene expression and protein signaling using RNA-seq, molecular docking, and dynamics.

The Results

The numbers say it all.

Mice treated with BAM15 saw a dramatic reduction in atherosclerotic plaque compared to the untreated group.

In fact, BAM15 outperformed atorvastatin on specific markers, most notably lowering cholesterol and triglycerides, while also reversing liver damage and lipid buildup—a result that atorvastatin failed to achieve in this study.

Here are the results:

• Plaque reduction: Less plaque in the aorta and the aortic valve region. Less necrotic core (bad, unstable plaque).

• Blood lipids: Lower total cholesterol, triglycerides, LDL; better HDL.

• Liver protection: BAM15 reduced steatosis (fatty liver) and improved liver enzymes (ALT, AST)—a huge win for metabolic health.

• Inflammation: Downregulation of key inflammatory cytokines (IL-1α, CSF3, PTX3), with a boost in SRC (a protective signal for arteries).

• Cellular effects: In cell culture, BAM15 inhibited the differentiation of macrophages into foam cells (the cells that contribute to the formation of arterial plaques) and prevented them from proliferating and migrating.

The gene expression and molecular modeling side of the study showed that BAM15 works by a multi-pronged attack:

• It blocks inflammation right at the molecular level.

• It boosts mitochondrial health and activates AMPK (that’s the longevity switch that metformin and exercise hit).

• It even increases PGC-1α, the gene that drives mitochondrial biogenesis and antioxidant defense.

In other words, BAM15 is a metabolic and vascular optimizer, an inflammation-slayer, and a mitochondrial upregulator all rolled into one.

What Could This Mean for Humans

Here’s where the magic (and some educated guesswork) comes in.

Although this was a mouse study, ApoE(−/−) mice are the gold standard for preclinical atherosclerosis research.

Most therapies that work in this model have a high likelihood of success in humans, particularly for metabolic diseases, inflammation, and cardiovascular health.

However, what really gets me fired up is that BAM15 is addressing the root causes of disease: metabolic dysfunction, mitochondrial health, and chronic inflammation.

Most people—especially those who won’t (or can’t) take GLP-1 injections—have very few options that target this whole spectrum.

BAM15 is orally bioavailable (67% in mice, which is pretty good), targets fat tissue, doesn’t require a prescription, and has a safety profile that, at the right dose, avoids the classic toxicity of older uncouplers like DNP.

Imagine a world where you can get the metabolic, anti-inflammatory, and cardiovascular benefits of a powerful peptide stack—without ever having to inject.

Human Dosage Math

Time for some back-of-the-napkin pharmacology math.

Mouse dose used: 85 mg/kg/day, oral

Standard mouse-to-human dose conversion (using body surface area scaling):

Human equivalent dose (HED) = Mouse dose × (3 / 37)

So:

85 × (3 / 37) ≈ 6.9 mg/kg/day

For a 70 kg human:

6.9 mg/kg × 70 = 483 mg/day

BUT hold on just one second.

Animal studies almost always use “sledgehammer” doses to guarantee effect, while humans generally respond to much lower doses (especially if the compound is potent and orally available).

My real-world recommendation:

Start low, titrate up.

This allows your body to adapt, assess individual tolerance, and avoid any “too much of a good thing” issues.

BAM15 + SLU-PP-332 (Metashred)

If you’re looking for metabolic synergy, it doesn’t get much better than this.

I suggest pairing 50–100 mg of BAM15 per day with 100–200 mcg of SLU-PP-332 per day—which is exactly 1 capsule of Metashred.

As you adapt, you can titrate up to 3–4 capsules.

SLU-PP-332 is a potent mitochondrial enhancer in its own right, helping with further mitochondrial uncoupling, fat loss, and metabolic flexibility.

Want to take it next level?

MetaShred stacks beautifully with:

• Retatrutide or other GLP-1 peptides (if you’re comfortable injecting, this is fat loss on steroids…without the actual steroids)

• BPC-157/TB-500 for gut repair and recovery

• Metformin for added insulin sensitivity

But if you’re needle-shy, traveling, or simply don’t want to mess with injectable peptides, BAM15 is your oral alternative.

Final Thoughts:

We’re on the edge of a metabolic revolution.

This new BAM15 study is the clearest sign yet that targeting mitochondrial uncoupling, inflammation, and metabolic dysfunction is the future for fat loss, longevity, and peak performance.

If you’re ready to ditch the needles, break through your fat loss plateau, and take control of your cardiovascular health from the inside out, this is your green light.

Start low and watch your metabolism shift into high gear.

And as always, listen to your body, track your labs, and keep learning.

Best,

Hunter Williams

References:

• Scientific Reports, 2025, 15:13347 (full text on the latest BAM15 research)