Favorite compounds/foundations so far that I have utilized.
1. Testosterone
2. HGH
3. Desiccated Thyroid
4. Primobolan
5. Retatrutide
6. FLGR-242
7. Anavar
8. Tesofensine/Dihexa combo
9. BPC/TB/KPV (w/cartalax)
10. MT2
11. Tesamorelin
12. ATX-304
13. SLU-PP 915
14. SS-31
15. Boneless chicken wings 💯 🖕
-Currently researching high-dose SANA in a surplus to see if partitioning benefits with creatine kinase pathway are noticeable.
-Nandrolone is eventually entering the picture here shortly..... hopefully.....
SANA/MVD1
I was working on this yesterday, but in the Telegram today, the guys got me more pumped hearing their results, which unlike me, they actually track. LOL
Currently running 250 mg twice a day on this for a planned 30 days, in a surplus. Goal is simple: see if we finally have an oral fat-loss compound you can actually use while growing, that doesn’t touch muscle repair, doesn’t blunt appetite, and still has a shot at holding some midsection fat off.
Cutting is the obvious use case. The mechanisms also line up for a surplus run, which is the part almost nothing else covers cleanly. No AMPK. No GLP, GIP, or glucagon. No appetite suppression. Creatine kinase pathway.
What it is:
SANA is the lab name. MVD1 is the clinical code. Same molecule: 5-(2-nitroethenyl)salicylic acid. Nitroalkene hung off a salicylate scaffold. Oral small molecule, not a peptide.
How it’s supposed to work:
It drives creatine-dependent thermogenesis in fat.
Mitochondrial creatine kinases, mainly CKMT1 and CKMT2, plus the cytosolic kinase, get upregulated in white and brown adipose. Creatine content in those depots goes up. Gatm, the rate-limiting step in creatine synthesis, comes up with it.
The cycle is futile on purpose. Creatine gets phosphorylated with ATP, phosphocreatine gets broken straight back down, and the energy leaves as heat. Substrate cycling, not classic uncoupling.
Three loss-of-function checks carry the claim. Deplete creatine and the thermogenic effect disappears. Knock out UCP1 and it still drops fat. Knock out AMPKα1 and it still protects against diet-induced obesity. Ckmt1 knockout mice handle a cold challenge worse on SANA, and thermoneutral housing rescues that. So it is not riding brown-fat UCP1, and it is not an AMPK drug.
Food intake in the mouse work did not drop. Activity didn’t explain it. Fat mass fell across depots, lean mass rose as a percentage of body weight, liver fat and insulin resistance improved. Parent salicylate at much higher doses did not do this.
Human data, kept in scalePhase 1 A/B, randomized, double-blind, placebo-controlled. Single doses 200-800 mg in lean volunteers. Multiple doses 200-400 mg/day for 15 days in overweight and obese volunteers.
Primary read was tolerability. Up to 400 mg/day looked clean in that short window: mild headache, soft stools, constipation. Two reversible renal tubular events, proteinuria and glucosuria, showed up at the 800 mg single dose, and escalation stopped there. No accumulation by day 15.
200 mg every 12 hours, about 3% body weight down over 15 days versus placebo, with fasting glucose, insulin, HOMA-IR, and fructosamine moving the right way. One participant in that cohort still saw fasting glucose rise. Diet was controlled and high-carb. Fifteen days is not a cut or a bulk. Treat the weight number as a signal, not a result.
Why the surplus test:
Nothing in the published mechanism suppresses appetite, hits incretins, or switches on AMPK. The energy dump is localized to adipose creatine cycling, and the mouse data did not show a hit to lean tissue. That is the whole reason a growing-phase run is worth doing. If food drive stays normal and training and recovery stay normal, any waist or midsection difference versus a matched surplus is the actual question.
Cutting use is the straightforward one: extra expenditure without the appetite crash or the AMPK tax on growth pathways. Surplus use is the interesting one. Same pathway, different goal. Hold a bit of the fat that usually shows up once calories go up, without paying for it in muscle.
How this run is set:
250 mg twice a day, 30 days, surplus. Slightly above the top Phase 1 multiple-dose arm, still well under the single dose that produced the renal signal.
****Creatine stays in because the effect in animals collapsed when the creatine pool was depleted. ****
@KleosOperator Damn I used to throw Reta in there but that bitch messed me up when I got froggy and tried eating bulk style at 4mg lol...
Tada is just part of us now.. Can we even count it!?
Behind optimized testosterone, there is nothing with a bigger ROI longterm than HGH.
There is so many strategies and benefits (side effects lol), you will likely never find the most optimal way to utilize it, and that imo, is what makes it fun.
I swear you can spend an hour everyday combing the web, reading experience after experience, article after article, study after study, and always learn something new, which may lead to another tweak.
No other compound is quite like this.
It’s never ending.
I’m sure many of you can relate to the GH adjustment lifestyle.
I accepted there is no universal one size fits all way to run GH. Whether it’s time of day or the actual dosing, but damn I will try em all at some point 🤣
🚨DMAA for $36 with an affiliate code🚨
This will be GONE FOREVER tomorrow morning so if this is a research staple I would grab a few
This is utilized in laboratory research for
• Potent stimulant effects via DAT
• Fat loss from classic stimulant pathways (appetite suppression / shaking)
• Extreme mental drive
• Enhanced focus and motivation
• Bronchodilation
Last pic is for nostalgia 😮💨
*Liquid is for RESEARCH only*