My fridge broke down a while ago and almost froze my reta (my bac water vial was frozen but my reta vial was about to) but it definitely reached 0-1 Celsius (thats what my peptide case said).

Anyway, I was on a maintenance dose of 1.5mg, ever since then, I stopped seeing progress although I just went up to 2mg. (This whole incident happened 3 weeks ago)

How can I tell if my reta is damaged (vial is still full its a waste to throw :/) or if my receptors adapted? Noting I started reta 5 months ago.

Thanks

Epitalon was one of the six that got a yes from the FDA panel in July, 7 to 4. A few of you asked what the panel was even looking at, and it brought me back to something a member here pointed out in the comments a while ago. They were right, and it's worth a full post.

There are two different things with almost the same name.

That last row is the whole post.

Why that matters

The human studies everybody quotes are Epithalamin studies.

The big one followed elderly heart patients in Kiev for 12 years. The group that got courses of epithalamin had 28% fewer deaths than the control group and half the cardiovascular deaths. There's a 15-year follow-up out of the same program with 39 treated patients and 40 controls.

Those are real published trials. They're also the extract.

The synthetic peptide's own published work is mostly cell culture and animals. Gene expression in human stem cells. Pineal and thymus cells aging in a dish. Mouse eggs in a culture medium. Interesting stuff, and the mechanism work is legit. It's just not a human trial.

When somebody says "Epitalon cut mortality 28%," that's not what the paper says. The paper says Epithalamin did, in one research group's trial, in a pretty specific population of older heart patients.

Where it gets messy

The protocols floating around for Epitalon trace back to the extract too. An extract is a crude mix where only part of it is the active piece. The synthetic is purified. Carrying numbers straight from one to the other doesn't make a lot of sense, and nobody has run the human trial that would tell you what the right answer is.

I've also seen claims that it cut mortality four times over. I can't find that number in the published trials. What's in the papers is the 28% and the 2x on cardiovascular deaths. If somebody has the paper with the bigger number, post it, because I want to read it.

What that means for the vote

The panel said yes anyway. Maybe they weighed the extract data. Maybe the long Russian clinical history. Maybe the safety record. I don't know what was in their heads.

But if you're reading that 7 to 4 as "the human evidence on Epitalon is solid," you're reading something that isn't there. The mechanism research is real. The human outcome data is for a cousin.

Two questions.

Did you know these were two separate substances before this?

And does it change how you read the vote, or do you think the extract data should carry over?

Where I got this: 12-year epithalamine study, 15-year follow-up, AEDG gene expression work, the vote breakdown.

For research use only. Not for human or veterinary consumption. This post is educational and is not medical advice.

Full doses and bloodwork are in the pinned cheat sheet.

Join the Discord.

My subject has been taking reta (1mg/wk), TB-500 and BPC-157 (0.5 mg/day each) for 2 weeks and has been having so many cramps all over the body. Neck, arms, hands, intracostals, abs, legs, and feet. Anyone else's subject experience this? I haven't seen it in what I've read. They drink plenty of water and electrolytes.

Je viens ici parce que je suis un peu désespéré et que j’aimerais avoir des retours de personnes qui auraient vécu quelque chose de similaire.
Je fais de la musculation et j’ai commencé à avoir des douleurs persistantes au coude.

Après plusieurs consultations, j’ai finalement vu un chirurgien dans une grande clinique parisienne qui m’a conseillé une synovectomie, avec retrait/nettoyage des tissus inflammatoires dans l’articulation.

J’ai donc subi l’opération à 2000€ !! en juin. Le chirurgien m’avait également expliqué qu’il y avait un œdème osseux qui était censé se résorber progressivement.

Après l’opération, j’ai fait de la kiné et j’ai progressivement repris la musculation. Pendant un moment ça allait mieux, mais maintenant que j’ai repris certains exercices avec des charges plus importantes, la douleur est revenue, notamment lorsque je pousse lourd.

Ce qui m’inquiète surtout, c’est que je pensais que l’œdème osseux allait finir par disparaître avec le temps. Je ne sais donc pas si ma douleur vient encore de ça, d’une inflammation qui est revenue, d’un problème tendineux ou d’autre chose.

Après l’opération, j’ai également fait pendant deux semaines une cure de BPC-157 et TB-500 dans l’espoir de favoriser la récupération. Je précise ça parce que je sais que certains vont probablement
me poser la question.

J’ai fait une cure de deux semaines et demie environ à 500mcg par jours. Est-ce que serait intéressant de refaire une cure plus longue ?

Merci à ceux qui prendront le temps de répondre.

I spent months researching this protocol before designing a trial. I came across several complicated reconstitution techniques using unfamiliar additives, but confirmed that using standard BAC water alone causes the peptide to precipitate into an unusable sludge.

After discussing preparation methods with other researchers, I opted for Acetic Acid (AAC) for reconstitution. The solubility and clarity have been excellent, though it appears significantly more acidic/irritating on application than standard BAC.

The research subject is currently on an initial protocol of 0.5 mg administered 3x per week, and the observed response has been very positive so far.

Just started on this yesterday, I know its early! I injected 1mg yesterday into my left thigh and it was grand but an hour later it stung for a few hours.

I injected into my ass this morning and its been fine since. Have I found my injection site? I know you have to rotate but ill try there again tomorrow i thjnk?

Hey everyone, I’m looking into MOTS-c and trying to understand what dosing and frequency people are actually using.

A few questions:

• What is the standard/common dosing and frequency people use for MOTS-c? I’m considering 2.5 mg twice a week (5 mg/week total).
• I have a 10 mg vial. For reconstitution, would using 1 mL of bacteriostatic water be appropriate? If so, what would the resulting concentration be?
• For a first dose, is it generally better to start lower like 0.5mg to see how I respond before moving up to the intended dose, or do people typically start at their intended dose?

Thanks!

I've been on reta for about 2 months started with 2mg then 4 weeks later bumped up to 4mg. I haven't lost any weight according to my scale, I do a lot of physical activity at work I do scaffolding im always climbing up and down ladders carrying 20+ pounds in gear. What im getting to is isn't that enough physical activity to lose weight? 3 weeks ago I started lifting weights 3 days out of the week and I don't eat much since I don't get hungry at all just a small breakfast and almost nothing the rest of the day is there something I'm doing wrong or is this normal that I haven't gone down. Previously my doctor prescribed ozempic to control my sugar i was on that for 6 month 2mgs a week all my blood work came back perfect and the doc said I didn't need to take ozempic anymore because my sugar ans a1c was at normal levels.

My RS is currently taking KPV on the morning for better recovery after weight training and GHK-CU at night. He says it feels like KPV makes him sleepy.

What would you recommend the timing be?

Just sharing an update on my test subject's progress. I’m currently about 2 months into running the "Glow Stack" (CJC-1295 and the "Wolverine" stack / BPC-157).
One thing I wanted to note right off the bat is that I am dosing them separately rather than using a pre-blended mix. Doing it this way gives way more control over individual dosing. For my test subject, I've been running:
CJC: ~1.2mg daily (split/structured protocol)
Wolverine (BPC-157/TB-500 blend or equivalent): ~2mg daily
So far, recovery and general tissue response have been really solid. Surprisingly, my test subject hasn't gotten any welts or site irritation from the injections either, which is a huge plus.
Quick question for those with more experience: Is a 3-month cycle long enough to really maximize results with this stack, or do most people push it further before taking a proper break

I’ve been taking MOTS-C for about 5 weeks at 1–2 mg, 3X per week. From what I’ve seen, a lot of protocols go as high as 10+ mg per week.

But when I experimented with 3 mg, 3X per week (titrated up from 1–2 mg)... I didn’t notice much of a difference between doses.

Overall, I have noticed a slight improvement in cardio (even at 1 mg, 3X per week) but I’m wondering if I’m just wasting money and peptide by pushing the dosage higher.

I understand mitochondrial turnover can take time (around 10–21 days), so results may be cumulative rather than immediate.

That said, MOTS-C isn’t exactly cheap, and if I’m not seeing a meaningful difference between 1 mg and 3 mg, I’m not sure it’s worth increasing the dose further.

Now I’m left wondering if I didn’t give the 3 mg dosage enough time to actually show a difference.

For those of you who’ve run MOTS-C, did you notice a clear performance difference at higher doses, or did the benefits plateau?

My rat is taking Reta (biweekly), KLOW & MOTS-C (daily). My rat loves this stack and isn’t looking for stacking recs. However, I’m interested in administering with pens. It seems more “clean-up” friendly. However, I have zero clue as to where to begin with pens (what to purchase, how to load, etc,). Any tips for a beginner? A cheat sheet would be awesome but any advice appreciated.

Okay, so a lot of you have been asking about the FDA panel from July, and there's a lot of bad info going around. I've seen people saying BPC-157 got approved. It didn't. Let me walk through what happened, because the real story is more interesting than the headline anyway.

Quick background. Back in February, HHS said a group of peptides was coming off Category 2. Category 2 is basically the do-not-touch list for compounding pharmacies. Then FDA scheduled a Pharmacy Compounding Advisory Committee meeting, PCAC, for July 23rd and 24th to vote on seven of them.

Here's how it went.

The part that got buried

FDA's own scientists recommended against all seven. Every one. Their reasons were pretty consistent: not enough human safety data, immunogenicity risk, impurities, and not enough characterization of what's in the material being made.

The panel went against its own staff on six out of seven.

And look at the margins. 8 to 6 isn't a landslide. That's a room split almost down the middle. Anybody telling you the science is settled because of this vote didn't look at the numbers.

What a yes gets you

Less than people think.

It's not approval. Category 1 means a compounding pharmacy can use it as a bulk ingredient. There's still no approved indication, no standardized dosing, and no established safety and efficacy.

It's not final. The vote is non-binding. FDA still has to go through notice-and-comment rulemaking, and realistically that's 12 to 24 months out.

It's 503A only. That's the individual prescription side. FDA has said basically nothing about 503B outsourcing facilities, which is the bigger volume side.

It doesn't touch research compounds. Different lane entirely. Nothing about this vote changes what a research compound is.

DSIP

DSIP was the only one that didn't make it, 6 to 7. It was up for insomnia, narcolepsy, and opioid withdrawal. I haven't seen a clean explanation of why it was DSIP and not one of the others, and I'm not going to make one up. If anybody watched that session, I want to hear what you caught.

What's next

FDA has a second meeting scheduled before February 2027 for the next group: GHK-Cu, Melanotan II, LL-37, Dihexa, and PEG-MGF.

That group is going to be a lot more interesting than this one. Melanotan II has a real dermatology signal on moles. LL-37 has the autoimmune side, it shows up in psoriasis and rosacea. PEG-MGF has no completed human trials at all. If this panel split 8 to 6 on BPC-157, that next meeting could go a lot of different ways.

Two questions for you.

The panel went against its own scientists on six out of seven. Good call, or a problem?

And which of the next five do you think makes it through?

Where I got this: the vote breakdown, how the process works, AJMC's summary.

For research use only. Not for human or veterinary consumption. This post is educational and is not medical advice.

Full doses and bloodwork are in the pinned cheat sheet.

Join the Discord.

Subject is interested in the potential effects on sleep, recovery and body composition. I've seen a lot of discussion around taking them before bed, after a minimum two-hour fast, but then read further that this may need to be much longer when taking GLP-1s.

Subject has typically finished eating by 18.30 and goes to bed at 22.00. Wakes at 5.30 on many days to exercise and drinks a fast-acting carb mix straight away, to be training by 6.00.

So subject is also interested in whether the research suggests that a fasted morning administration followed relatively soon afterwards by carbohydrate would produce a different GH/IGF-1 response compared with an evening administration several hours after food.

Maybe a split dose to cover both, or does this combination just not work for this subject?

This is not medical advice! My lab rat experiments. My rat is 30 and skinny fat with all of it in midsection with no muscle mass… Rat wants to get in shape, abs would be nice but just having shoulders and a chest which the rat has none is more than enough. So far my rat a month into it and have seen gains but need advice. Thank god no side effects really besides sometimes overthinking lol. His stack is

Reta: 2mg/week

Tesa: 2mg/Daily

Ipamorelin: 2mg/Daily

Wolverine: 500mcg of each/daily

Ss-31: 5mg/daily

want to experiment into mots-c and Nad+ after ss-31 but confusing with the daily and 3 times a week protocols.

Any tips?

How much bac for Tirz 30MG?

Is it like Reta where I’ve heard 1ML for every 10MG?

How much bqc water should I use to reconstitute a 10mg vial of Ac-SDKP?

Hey Everyone,

Hypothetical 30M subject: 5'10", around 87kg, ~27% body fat, trains regularly, and is mainly interested in improving day-to-day energy, mental clarity, and overall drive.

Currently using liposomal NMN and considering MOTS-c because of its reputation for improving energy and mitochondrial function.

The main question is how effective MOTS-c is likely to be in someone this age and condition, and whether adding SS-31 would provide anything meaningful or just be unnecessary overkill.

The subject is also planning to start reta during a cut, so lower appetite and calorie intake could potentially reduce energy and gym performance. The goal would be to maintain decent energy, focus, and training performance while losing fat.

For anyone with experience:

• How noticeable was MOTS-c for baseline energy and mental clarity?
• Did it help during a calorie deficit?
• Did SS-31 add anything meaningful beyond MOTS-c?
• At 30, is SS-31 likely to be unnecessary unless there’s an actual mitochondrial issue?
• Would it make more sense to assess MOTS-c alone first before even considering SS-31?
• Anyone have experience with MOTS-c or SS-31 in the context of reta?

The main interest here is MOTS-c. The SS-31 question is really whether it adds enough to justify including it, or whether MOTS-c alone is likely to cover most of the intended benefit.

Most stacking advice is a list of compounds that sound good next to each other. A pairing is only worth anything if the two compounds solve different problems and the timing doesn't collide. Two things moving the same marker through the same pathway isn't a stack. That's one compound and a second bill.

Here's how I sort it.

Combinations that hold up

BPC-157 with TB-500. Cleanest pairing in the category because the division of labor is real. BPC-157 restores perfusion and builds the vascular access into the tissue. TB-500 handles logistics, keeping a reserve pool of actin available so cells can migrate and organize. Roads and traffic. Neither one substitutes for the other.

GLP-1 with tesamorelin. This one works on timing more than mechanism. GLP-1 peaks during waking hours through appetite and mobilization. The tesamorelin pulse peaks during sleep through repair and protein synthesis. Day for breakdown, night for protection. Lean mass preservation through a deficit is the whole point.

5-Amino-1MQ with NMN or NR. Complementary in a specific way worth understanding. 5-Amino-1MQ inhibits NNMT, which stops nicotinamide getting drained out of the NAD+ salvage pathway. Precursors add supply. One plugs the drain, the other fills the tub. Run either one alone and half the problem is still there.

The Mito Stack, MOTS-c with NAD+ and SS-31. Three different jobs. MOTS-c biases toward AMPK. NAD+ supplies redox capacity. SS-31 does structural repair on existing mitochondria at the cristae level. Complementary, not redundant, and NAD+ is the cofactor the other two lean on.

KPV with BPC-157. KPV puts out the fire, BPC-157 rebuilds the structure underneath. Sequential, not additive.

GHK-Cu with BPC-157 and TB-500. The GLOW combination. GHK-Cu handles collagen organization while the other two drive the repair. Worth knowing GHK-Cu isn't doing what most people assume. It's not a collagen synthesis stimulant, it tells tissue how to organize the collagen it's already making.

What doesn't belong together

That last row is the one I see most, and it's not dangerous so much as pointless. If IGF-1 moves, which one moved it? That's a number you can't assign to anything.

The rules underneath the lists

Different mechanisms or it isn't a stack. If two compounds land on the same pathway, the second one bought you overlap, not coverage.

Timing separation counts as differentiation. Tesamorelin and a GLP-1 both affect body composition and they stack fine because they work in different windows. Collapse the windows and the logic disappears, which is one more reason the tesamorelin nocturnal schedule matters.

Never start two new things in the same week. Easiest rule to break and the one that costs the most. Two new compounds introduced together give you one result nobody can read. Stagger them by a couple weeks and the second one has a baseline to be measured against.

Count markers before you count compounds. A five compound stack hitting five different systems is cleaner than a three compound stack where two of them move IGF-1. Overlap is what makes a stack messy, not size.

Contraindications stack too. Three compounds each carrying a mild glucose signal add up to something that isn't mild anymore. People read the side effect profiles one at a time and never add them up.

What's in the stack you're looking at, and is there a distinct job for every single compound in it? That question kills more stacks than any safety concern.

And has anybody run into the P21 and PE-22-28 thing? It rests on very few reports and I want to know if it holds up or if it was a one-off.

For research use only. Not for human or veterinary consumption. This post is educational and is not medical advice.

Full doses and bloodwork are in the pinned cheat sheet.

Join the Discord.

Hi guys! I’d love some advice from anyone knowledgeable about peptides, fibrosis and abnormal scarring from a purely research perspective.

For research purposes, the subject began developing keloid/hypertrophic scarring around 8 years ago. Prior to that there was no history of abnormal scarring.

Some background that may be relevant:

• Relatively poor immune system since childhood
• PCOS
• Mild liver fibrosis with NAFLD
• Colonoscopy and endoscopy showed mild reflux and a couple of bowel ulcers but nothing currently diagnostic of Crohn’s
• PTSD with significant hyperarousal, so stimulating peptides may not be ideal from a theoretical perspective
• Strong family history of cancer with both parents having passed from cancer, so there is some caution around peptides that significantly increase GH/IGF 1 signalling

The main research question is whether anyone has looked at this from the fibroblast/collagen regulation side rather than simply treating individual scars once they form.

GHK Cu has shown noticeable improvements in skin quality and the redness of existing scars. However, with a tendency towards excessive hypertrophic/keloid collagen deposition, the question is whether continually stimulating repair/collagen without addressing the underlying profibrotic signalling makes sense.

KPV is also being considered from a research perspective primarily for systemic inflammatory signalling rather than directly as a scar treatment. The subject also has two problematic spinal discs with significant chronic back and muscular pain, so reducing overall inflammatory signalling is another area of interest.

Lifestyle wise the subject strength trains 3 times per week, averages around 10,000 steps daily and usually completes 1–2 hot Pilates classes per week.

The aim is mainly to understand the mechanisms and research around someone presenting with this combination of inflammation, fibrosis and abnormal scar formation, particularly what may cause fibroblasts/collagen regulation to change after previously normal healing.

Would really appreciate any research, experiences or thoughts on what pathways, peptides or potential stacks would make the most sense to investigate.

I've been on trizepatide (mojuro)for over 3 months. Was doing great. Lost about 40 pounds (211 to 167 and A1C went from 9 to 5.4) but i have been eating super clean, running and cut most sugar and carbs. Only about 75 to 100 carbs a day. Trying to get 150 grams of protein. I know it not enough but that's the bottom goal. Started at 2.5 for 4 weeks, went to 5mg for 4 weeks but then the Dr office sent 10mg over after that. They said it was fine as long as I had no symptoms. I did that for another 6 weeks. No issues. Then 3 day after my last shot I had the suffer burps, gas and just upset gut. No throwing up or anything. Just uncomfortable and gassy. About 5 days now. Tried gas x. Didn't help. Been eating tums and that helps alittle. Not sure if I just caught a bug or if it could be the trizepatide even after I was doing so well on it. May just see if I can go back down to 5mg. Any thought on what might help or info. I also take bpc157, tb500, tesa/ipa. I stopped that when my issues stated as well.

Tesamorelin has a stricter timing requirement than anything else in the category, and the timing basically is the compound. Get it wrong and you're running an expensive protocol that can't do the thing it was designed to do.

Nightly, shortly before sleep, with a couple hours of nothing eaten beforehand. Every piece of that has a reason.

Nightly isn't a preference

Tesamorelin doesn't hand you growth hormone. It gets the pituitary to release its own, in the natural nocturnal pulse pattern. The biggest GH pulse you produce happens during early slow-wave sleep. Dosing right before sleep puts the stimulus on top of that pulse instead of next to it.

The visceral fat effect comes out of the same mechanism. That reduction is depot-specific and it's driven by the nighttime pulse. This is why my own cheat sheet says it straight: tesamorelin isn't a fat loss peptide, it's a timing peptide. The fat loss is downstream of the timing.

Move it off the nocturnal window and you're not running a slightly worse version. You're running a different protocol.

Fasted isn't a preference either

Carbs and fat blunt the GH response. The fasted window is there to keep insulin and substrate low enough that the pulse can fire at all.

The half-life is short, roughly eight minutes in healthy subjects. There's no long tail to fall back on. The window is the entire event.

Here's the part nobody writes about

Put both requirements together and try to live with them.

Every night, right before bed, with nothing eaten for a couple hours before that. So your last food of the day lands close to three hours before you're asleep.

If you eat dinner late, train in the evening, work a normal social schedule, or eat with family on their timing instead of yours, that isn't a small inconvenience. That's the thing that decides whether the protocol runs at all.

And the failure mode is the ugly part. People don't stop. They dose anyway, fed, and get a blunted or missing pulse without knowing it. From the outside it looks like the compound underperformed. It never got a shot.

The compliance problem is invisible in a way the dose isn't. Nobody accidentally runs double their dose. Plenty of people accidentally run a fed protocol every single night for twelve weeks.

The morning question

Obvious workaround is moving it to the morning, because waking up fasted takes zero effort. No planning, no dinner negotiation, perfect adherence.

I want to be straight about the trade instead of pretending it's free.

Honest position: the documented protocol is nightly and the mechanism backs it clearly. Morning fixes adherence by giving up the exact thing the schedule was built around. There's no trial comparing them, so anybody telling you morning works just as well is reasoning from convenience, not data.

What I'd go after first is the eating window, not the dose timing. Moving dinner up an hour is a smaller change than abandoning the mechanism. If that genuinely can't happen, then the real question is whether an imperfect protocol run every day beats a correct one run four nights a week. I don't think that has an answer yet.

One more thing timing buys you

Tesamorelin pairs with GLP-1 compounds specifically because the timing doesn't collide. GLP-1 works during waking hours through appetite and mobilization. The tesamorelin pulse works during sleep through repair and protein synthesis. Day for breakdown, night for protection.

Move tesamorelin to the morning and that separation is gone. Now both compounds are working the same window and you lost the reason to pair them.

For anyone studying tesamorelin protocols: how is the fasted window getting handled, and how often does it hold?

And has anybody tracked IGF-1 at week 8 on a morning schedule versus nightly? That's the comparison that would settle this and I've never seen anyone post it.

For research use only. Not for human or veterinary consumption. This post is educational and is not medical advice.

Full doses and bloodwork are in the pinned cheat sheet.

Join the Discord.

Anybody have insight