**SLU-PP-915 + SANA + BAM-15 -- three spend strategies, not one stack caption**
People are running these names in the same sentence a lot right now. Fair. They all ask a fat cell or a mitochondrion to **burn more**. They do not share a receptor.
**Three factories**
**SANA / MVD1**
Creatine futile cycle in adipose. Nitroalkene on a salicylate. UCP1 not required. AMPK not required. Creatine depletion kills the effect. Appetite is not the published driver. That is why it is the odd one in the catalog.
**SLU-PP-915**
Pan-ERR agonist. Transcription tool. Turns on the PGC-1α / fatty-acid-oxidation / mitochondrial-gene program. Exercise-mimetic *language* in rodent files. This is a clipboard in the nucleus, not a leak in the inner membrane, not a creatine loop in white fat.
**BAM-15**
Mitochondrial protonophore. Uncoupler. Lets protons slip back without making ATP, so the cell spends fuel as heat. That is why people compare it to DNP and why that comparison is lazy -- different design, different leak, different research question. Still a **membrane physics** tool. Not an ERR program. Not a creatine cycle.
**Why they get named together**
Same research question: raise expenditure without being a GLP-1.
Three answers: **cycle**, **transcript**, **leak**.
A combo in a dish or a rodent protocol is three knobs. It is not proof they complete each other. It is not a human stack. Measure the readout that belongs to the factory you actually touched -- creatine-cycle enzymes, ERR target genes, or uncoupled respiration.
**The mash-up to kill**
“Mito stack.”
No. One is adipose creatine chemistry. One is nuclear receptor transcription. One is a hole in the proton gradient. Put them in one hashtag and you hide the controls.
Simple version: 915 writes the exercise program. SANA wastes ATP on a creatine loop in fat. BAM-15 leaks the gradient. Hot research combo. Three jobs. Three assays.
Educational. Not a protocol. Not a fat-loss stack. Not medical advice.
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For research and laboratory use only. Not for human consumption. Not intended to diagnose, treat, cure, or prevent any disease.
Use code ELEVATE for savings at https://t.co/nY9GP4OYAx on research compounds.
#SLUPP915 #SANA #MVD1 #BAM15 #EnergyExpenditure #ResearchUseOnly #EvidenceBased
Tadalafil started as a heart failure drug. Researchers discovered the "side effects" by accident. Now the amino-modified version is back in the lab
#peptide#cialis#tadalafil#research
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The FDA approved a drug in 1998 that activates estrogen receptors in bone and blocks them in breast tissue simultaneously — same compound, same receptor, opposite effects depending on tissue #estrogenblocker#bodybuilding#fitness#biohacking
if you forget everything all the time, feel like you have to read the same sentence 10 times before it makes sense and want to have memory like Mike Ross from Suits you should look into BPN14770.
BPN14770 makes the signals that store information work longer.
to store information into your brain, the brain uses the cAMP intracellular signal pathway. but this signal gets degraded very quickly by the PDE4 enzyme, thus putting a limit on how much information can be stored at a time.
BPN14770 inhibits the PDE4 enzyme which allows cAMP signaling to continue for longer, this makes it so that more information can be stored and you remember WAY more of what you actually read.
some benefits worth noting:
1) accelerated learning
2) better memory
3) improved working memory
4) better focus during cognitively demanding tasks
5) stronger synaptic plasticity
6) better long-term learning capacity
7) better retention after studying
8) improved language-related cognition
it also doesnt come with the usual PDE4 inhibitor side effects like nausea because of its selectivity for PDE4D.
banger compound.
Join the discord: https://t.co/Xn7LUDpkj5
Retatrutide vs Tirzepatide 🧬
🔵 Tirzepatide activates GIP + GLP-1 receptors.
🟠 Retatrutide adds glucagon receptor activity, making it a triple agonist.
Two vs three metabolic signals. Retatrutide remains investigational.
�� Research purposes only
**The design of SLU-PP-915**
Not a mystery powder. A structure-based ERR ligand.
**Where it starts**
ERRγ already had a crystal pose with an acyl-hydrazide agonist, **GSK-4716** (PDB 2GPP). The Burris line used that pocket as the map and **left that chemotype**.
SLU-PP-915 is a **2,5-disubstituted thiophene** built to sit in the same nuclear-receptor hole with a different spine. The point was occupancy of ERRα and ERRγ with usable in-vivo chemistry, not a new receptor.
**The deliberate handles**
Older ERR agonists liked phenols and anilines. Those get oxidized. 915 puts a **boronic acid** on the A-ring instead. Binding stays. Microsomes calm down (half-life **>60 min** in the stability assays).
That is why oral gavage produces plasma instead of a shrug. It is also why medicinal chemists side-eye boronic acids as electrophiles design always has a second sentence.
Selectivity panels in the papers said ERR over a pile of other nuclear receptors and GPCRs. That is a screen. That is not a lifetime safety file.
**What the curve is**
Pan-ERR. Roughly balanced nanomolar range across α/β/γ in the later write-ups — not an α-only hammer. Downstream: the aerobic program. PGC-1α neighborhood, PDK4, Ddit4 in quad, mitochondrial DNA chatter, treadmill distance and time. Separate lane: TAC heart-failure model with earlier ejection-fraction movement and better stroke-volume / output notes.
Oral plasma in mice is real and short. Proof of design. Not a once-daily human label.
Simple version: 915 is a thiophene ERR agonist drawn from an ERRγ crystal, capped with a boronic acid so the pocket and the blood can both see it.
Investigational ligand. Educational chemistry. Not a protocol.
#SLUPP915 #ERR #MedicinalChemistry #ExerciseMimetic #ResearchUseOnly #EvidenceBased
For research and educational discussion only. Not medical advice.
Can you actually buy the ability to lock in for 12 hours?
Modafinil might be the closest thing we have to a real “Limitless pill”—but the science is a lot stranger than the hype.
We dug into the human trials, dopamine, sleep deprivation, Modafinil vs. Adderall, side effects, and why this drug becomes a completely different animal when you’re running on empty.
The “smart drug” that actually works? Full breakdown 👇
**Why a balanced triple like SAR441255 can beat retatrutide for many people**
Retatrutide is the scale favorite these days. Phase 2 numbers are loud. That is not the same as “best molecule for most bodies.”
**Two different triples**
Both hit **GLP-1, GIP, and glucagon**. They do not hit them the same way.
Retatrutide is a **GIP-forward** peptide with enough glucagon to light energy expenditure. Hierarchy is roughly GIP >> GLP-1 > glucagon. That glucagon slice is why the fat and liver-fat drops look nuclear. It is also why heart rate and the “am I paying for this in lean tissue and pulse” conversation will not die.
SAR441255 was built as a **balanced** unimolecular triagonist on an exendin-4 backbone. Bossart et al. designed it so GLP-1, GIP, and glucagon occupancy stay in the same neighborhood. The GIP arm is there to **buffer glucagon’s glucose-raising habit** while still keeping the extra energy-expenditure ticket. In DIO mice and obese monkeys, weight and glucose moved hard versus a GLP-1/glucagon dual. Single-dose humans: meal-test glucose looked civilized, GI was the usual incretin tax, hemodynamics were watched on purpose. That is a design paper plus Phase 1 — not SURMOUNT. Say it out loud.
**Who “many” are**
If the only scoreboard is percent on the scale at week 48, retatrutide currently wins the published fight.
If the scoreboard is **stay on the drug, keep the pulse boring, keep glucose from yo-yoing, don’t torch the tank for an extra three percent**, a balanced triple is the more interesting hypothesis.
Glucagon is a tool. It is also a chronotrope and a glycogenolysis signal. Stack a lot of it on a person who already runs hot, lifts for a living, or sits near prediabetes, and “more agonist” stops being free. GIP + GLP-1 in equal voice is how you cash the glucagon check without bouncing it. That was the SAR thesis.
**The honest limiter**
Retatrutide has the late-stage file. SAR441255 does not. “Will outshine” is receptor math plus early translation, not a head-to-head Phase 3. Pipelines stall. Ratios on a slide are not a prescription.
Simple version: retatrutide is the aggressive triple. SAR441255 was the polite triple. A lot of people do not need the aggressive one. They need the one they can live with.
Investigational comparison. Not a protocol. Not medical advice.
#SAR441255 #Retatrutide #TripleAgonist #GLP1 #GIP #Glucagon #Balance #EvidenceBased
For educational discussion only.
@VinnieSOfficial interesting stack. is vesugen better than cialis ?
im gunna write a paper on this soon. want to hear your opinion on tis if you have tried cialis before that is.