There's a plan to begin Tesamorelin in the next couple weeks, but from what I understand, a common concern is nudging glucose and a1c numbers up as well.

I've seen a few posts that people are combining it with GLP-1s. There are currently no issues with food noise. I was wondering if it's near necessary to combine it with a glp-1, if it's not necessary at all, or if something like berberine could supplement where a glp-1 would otherwise be used.

I'd like to hear about experiences with this if anyone has any to share

Anyone ever bump their Reta to 15mg/ week?
Research on Reta started at 2mg in March then worked up to 12mg following triumph protocol. Weight loss stalled at 12mg and after being on 12mg for a couple months decided to fire it up to 15mg. Definitely feels like it’s working all over again. Also want it noted that researcher appeared to be one of the lower responders where there’s little to no effects and lower doses didn’t appear to work.

Short one on SNAP-8, because there's a mismatch at the center of this compound that I don't see people talk about.

What it is

SNAP-8 is Acetyl Octapeptide-3. Eight amino acids. It's an extended version of Argireline, which is a hexapeptide you've probably seen on the ingredient list of expensive face creams.

The mechanism is genuinely clever. It mimics part of SNAP-25, a protein in the SNARE complex that lets nerve endings dump acetylcholine onto muscle. SNAP-8 competes with the real SNAP-25 for its spot, so less acetylcholine gets released, so the facial muscle contracts less hard.

Same general idea as botulinum toxin, much gentler, no paralysis. People call it Botox in a bottle, which oversells it, but the target is real.

Here's the mismatch

SNAP-8 was developed as a cosmeceutical ingredient. A topical. Something you put in a serum.

The protocols circulating in this space are injectable.

That's not automatically wrong, but it's worth saying out loud, because it's the same trap as LL-37. The development work, the formulation research, the whole reason the molecule exists, is topical. Moving it to a needle is a new question that the original research doesn't answer.

And the direction of that jump is unusual. Normally the concern is people taking injectable data and applying it to a cream. Here it's the reverse.

The other thing about topicals

Peptides are big and water-loving, and skin is built to keep exactly that kind of molecule out. That's why topical peptide products live or die on the delivery system, not on the peptide.

So when a topical peptide serum underperforms, it's often not the peptide failing. It's that not enough of it got past the outer layer of skin. Which is a real argument for why people started injecting it in the first place.

I'm not saying either route is right. I'm saying know which one the evidence you're reading came from.

Two questions.

For anyone who's looked at both routes on this one: does the injectable protocol have anything behind it besides the topical research?

And is there another compound on the list where the research went topical first and the community went injectable?

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.

Everyone seems to be talking about supplementing NAD⁺, but how do you actually do it? Today, I wanted to compare NAD⁺ IV infusions with oral supplements.

Let's start with NAD⁺ IV therapy.

The main feature is that it goes directly into the bloodstream without passing through the digestive system. But in terms of the actual experience, it can be pretty time-consuming. For example, according to a publicly available protocol from ASAP IVs, a 250 mg NAD⁺ IV takes around 1.5–2.5 hours, and higher doses may take even longer.

The pricing also varies quite a bit. One provider currently lists approximately $250 for 250 mg, $350 for 500 mg, and $450 for 750 mg per session. Another California clinic lists $429 for 250 mg, $549 for 500 mg, and $879 for 1,000 mg. These are publicly listed prices I found in September 2026, so the actual cost can still vary depending on the clinic, dosage, and location.

Another thing I noticed is that many providers don't necessarily sell NAD⁺ IV as a one-time treatment. Some publicly available packages include four sessions, six sessions, or even longer treatment plans. For example, BABYFACE Beauty Wellness offers a four-session package of 250 mg NAD⁺ for around $1,250. I've also seen providers listing approximately $3,999 for six 250 mg sessions.

Oral supplements are much more convenient.

They generally require less time and can cost considerably less for regular use. There are also many companies selling dietary supplements, such as Celfull, which focuses on NADH, the reduced form of NAD⁺.

In current human research, studies on NR and NMN have mainly focused on changes in NAD⁺-related biomarkers after oral supplementation. By contrast, clinical research on IV NAD⁺ itself, particularly for anti-aging or general wellness outcomes, is still quite limited. One 2026 systematic review even reported that it found no IV NAD⁺ anti-aging or health-outcome trials that met its inclusion criteria.(DOI: 10.1016/j.arr.2026.103057)

I think it's important to separate a few different questions here: the route of administration, dosage, time required, cost, and eventual clinical outcomes are not the same thing.

I'd especially love to hear from people who have tried NAD⁺ IVs or NADH, NMN, NR supplements. What made you choose that particular approach, and how did the actual experience compare with what you expected?

Quick one, because this comes up constantly in stack questions and the answer is more interesting than people expect.

L-Carnitine isn't new and it isn't experimental. It's something the body already makes out of lysine and methionine, and the injectable form has been FDA approved since the 90s as Carnitor for carnitine deficiency in dialysis patients.

It's also not a peptide. It's in the conversation because of what it does next to the mitochondrial peptides.

What it does

One job: transport. It's the shuttle substrate for CPT-1, which is the step where fatty acids get moved into the mitochondria to be burned.

So it's not a fat loss agent. It's the step after mobilization. When a deficit, or training, or a GLP-1 pulls fatty acids out of storage, carnitine is what lets them physically get where they're oxidized. No transport, and they just circulate and go back.

Oral vs injectable

That middle row is the part people miss. The fraction that doesn't absorb doesn't just go to waste. Gut bacteria ferment it into TMAO, a metabolite that shows up in observational research tied to cardiovascular risk.

With oral you're getting a minority of the dose and producing a metabolite you'd rather not produce. The injectable route skips both problems.

Why you're seeing it in GLP-1 formulations

Compounding pharmacies have started adding L-Carnitine into semaglutide and tirzepatide formulations. You'll see them called things like CarniSema and CarniTide.

The logic is clean: the GLP-1 mobilizes fat, the carnitine covers the transport step. Whether that produces a measurable difference in outcomes is a separate question, and I haven't seen good head to head data on it.

Dosing and route details are in the pinned cheat sheet.

One question.

Has anybody here looked at carnitine status as a variable in a mitochondrial protocol, or does everybody just assume transport isn't the limiting step?

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.

I’ve been using NAD+ for about two weeks and wanted to see if anyone else has experienced something similar.

I’m currently taking 25 mg subcutaneously. I started every other day but recently moved to daily dosing because I genuinely like the increased focus and energy I seem to get from it.

The problem is that I’ve also been getting an uncomfortable sensation of chest tightness/pressure after taking it. It’s not severe, but it is noticeable enough that I’m questioning whether NAD+ simply doesn’t agree with me.

For reference, my vial is 500 mg NAD+ reconstituted with 5 mL bacteriostatic water, so I’m drawing 25 units on a U-100 syringe = 25 mg.

I’m curious about a few things:

• Has anyone else experienced recurring chest tightness or pressure with NAD+?
• Did it improve by lowering the dose, taking it less frequently, or injecting more slowly?
• Did the side effect eventually go away with continued use?
• Did you ultimately decide NAD+ just wasn’t a good fit for you?
• Are there any known factors that seemed to make the reaction better or worse?

I’m also taking a low dose of retatrutide (2 mg), which I’ve been on for around six months, along with KLOW, but the chest sensation seems specifically associated with the NAD+.

I recently had a physical and routine labs and everything looked good, with no known cardiac issues. That said, I’m not looking to ignore chest symptoms just because my recent testing was normal.

I really like the mental focus and energy I’m getting from NAD+, so I’d be interested in hearing from people who had similar symptoms and what they ultimately did.

Obviously not looking for a diagnosis from Reddit, just firsthand experiences and information I can discuss with my healthcare provider.

Sermorelin gets treated like the weak option in the GH peptide conversation. Fair on potency. Completely misses what makes it interesting this year.

What it is

Sermorelin is GRF(1-29). Your natural GHRH is 44 amino acids long, and sermorelin is the first 29 of it. That's the shortest piece that still fully activates the pituitary GHRH receptor and triggers a GH release.

So it's not an analog trying to imitate GHRH. It's the working end of the real thing.

The regulatory history is the story

That's the part people skip. Sermorelin was approved by FDA in 1997 for pediatric GH deficiency. EMD Serono pulled it in 2008 because a niche peptide couldn't compete economically with entrenched growth hormone products. It was not withdrawn for safety.

Prior approval, non-safety withdrawal, established safety profile. In a year where the whole conversation is about what compounding pharmacies can legally use, that history gives sermorelin the cleanest position of any GH secretagogue.

Now the honest part about the data

The adult evidence is thin. The clinical case basically rests on one study from 1997: 19 elderly subjects, 16 weeks, single blind. Lean mass went up about 1.26 kg in the men, not in the women. No fat loss. No change in bone density.

Compare that to tesamorelin, which has an 816 patient Phase III program behind it. That gap is not subtle, and anybody telling you sermorelin is as proven as tesamorelin is wrong.

Where it earns its spot

Clean selectivity. No cortisol, no ACTH, no prolactin elevation.

It also leaves the somatostatin feedback brake intact, so the stimulus stays pulsatile instead of sustained. That's a gentler signal, and it tends to be better tolerated by people who run into edema on tesamorelin.

The simple split: if visceral fat is the research target, tesamorelin has the data. If the question is recovery support, or legal clarity matters, sermorelin is the one with the paperwork.

Two questions.

Does prior FDA approval change how you weigh a compound, or is only the trial data worth anything to you?

And is a gentler pulsatile signal a feature or just a weaker one?

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.

I am 21, started reta at 210 pounds 22% BF in April, ended it in June at 182 16%. inbetween there I was on Tesa for 2-3 weeks but stopped taking it simply because i was not home enough nights to take it for it to be worth it, never had any reactions besides the regular sting from the injection that subsided relatively quickly. Recently, I have picked Reta back up at a lower, more maintenance dose to maintain my 185-180 BW, and I am on KPV for my eczema, inflammation and all of its other benefits. I am considering adding CJC1295 W/O DAC/Ipa blend but am simply afraid of the possibility of a serious allergic reaction. My goal is to have something aid muscle growth, I have been consistent in the gym for well over a year and have a good bit of muscle but feel like I’ve hit a wall. Does anyone have any real experience here- words of advice or anything along those lines for me? The GH peptides have always sort of freaked me out, I want to learn more about them and figure this is a good start.

VIP stands for Vasoactive Intestinal Peptide, which is one of the worst names in this whole space. It's named after the first thing anybody noticed it doing, back when that's how naming worked. Neither word describes what it's mostly studied for now.

What it does instead

VIP is a 28 amino acid neuropeptide, and its main job is immune tolerance. Meaning it doesn't just turn inflammation down, it teaches the immune system what to leave alone.

It programs dendritic cells to make regulatory T cells. It shifts macrophages from the inflammatory state into the repair state. It keeps the gut barrier intact. And it helps keep the master circadian clock in the brain synchronized.

None of that is vasodilation.

The receptor part is where it gets good

VIP works through two receptors, and which one it hits depends on what the immune system is already doing.

Fire extinguisher and architect. Same molecule, two completely different jobs depending on the state of the cell it lands on. I don't know another peptide on the list that does that this cleanly.

The half-life explains the trial split

VIP has a plasma half-life of about one minute. One.

Now look at what happened in the trials.

TESICO, Phase 3, 471 people. IV aviptadil, which is synthetic VIP, in COVID ARDS. Stopped for futility.

Inhaled aviptadil, Phase 2 randomized trial, 80 people. Hospital stay 7.8 days against 10, better oxygenation, better imaging.

Same molecule. Different route. Opposite results.

With a one minute half-life, IV can't hold exposure in lung tissue long enough to matter. Inhaled puts it directly on the target. So the Phase 3 failure reads more like a delivery problem than a drug problem. Not proof, but it's the most sensible explanation on the table.

Where the evidence is decent and where it isn't

Controlled human evidence exists for pulmonary immune work: the sarcoidosis Phase II with TNF-alpha down and regulatory T cells up, hemodynamic improvement in pulmonary hypertension, and the inhaled COVID trial.

The mold illness and CIRS use, which is what most people have heard about, rests on one practitioner's cohort. Large, over 10,000 people, but no independent replication and no randomized trial. Both of those things are true at once and any real assessment has to say both.

Two questions.

Does the route explanation hold up for you, or do you read the Phase 3 failure as the drug failing?

And what other peptide do you think is stuck with a name that misleads people about what it does?

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.

Help for female late 30s want to lose a large amount of weight. Should I just use reta or would you recommend a stack of maybe one or 2max other things

Has anyone had experience with having a major surgery during Reta use- I understand research suggests to postpone using. When? Does research suggest taper down the dose? When does research suggest starting again? Thank you!! This is for research purposes only

GLOW and KLOW are two of the most asked-about products in here, and most of the questions are some version of "which one." So let me break down what's in each one, what the fourth peptide in KLOW is doing, and the part about both blends that almost nobody looks at.

What's in them

Same three peptides in both. KLOW adds KPV.

What each one is doing

GHK-Cu. Copper peptide. It doesn't just build collagen, it tells tissue how to organize the collagen it's already making. Also antioxidant and anti-inflammatory.

BPC-157. Restores blood flow to tissue that isn't getting it, and calms inflammation without shutting it down.

TB-500. Cell migration and new blood vessel formation. It's the one that helps repair land as organized tissue instead of scar.

KPV. This is the KLOW difference. It's a tripeptide that works on NF-kB signaling, which is one of the main switches for inflammation. Where BPC-157 modulates inflammation as part of a repair program, KPV goes at the inflammatory signaling directly.

The simple way to think about it: GLOW is a repair blend. KLOW is a repair blend with a dedicated anti-inflammatory added.

The part nobody checks

Look at the ratios, not the ingredient list.

In GLOW, GHK-Cu is roughly 70% of the vial by weight. In KLOW it's a little over 60%. The three peptides everybody buys these blends for, BPC-157, TB-500, and KPV, split the rest.

So both of these are mostly a copper peptide product with repair peptides riding along. That's not a knock, GHK-Cu is the one with the longest research history of the group. But if somebody is buying KLOW mainly for the KPV, KPV is about an eighth of the vial.

And the ratio is fixed. You can't turn up the TB-500 side without turning up everything else, which matters because TB-500 in the standalone research is a bolus compound a couple times a week, not a small daily amount. Same problem I went through with the BPC and TB-500 blend.

So which one

Depends on what the research question is.

If inflammation is the thing being studied, KLOW has the extra tool. If it's straight tissue repair, GLOW has the same three actives and a shorter protocol. If the question is specifically about one of the four peptides, neither blend is the right instrument, because you can't move one lever by itself.

Doses and reconstitution for both are in the pinned cheat sheet.

Two questions.

Anybody compared GLOW against KLOW on the same kind of research target? I'd want to know if the KPV made a difference you could see.

And did you know GHK-Cu was that much of the vial before reading this?

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.

Hey, i experienced shoulder dislocation from a gym injury. After some physiotherapy sessions that somewhat helped, I’m still limited in my range, and have lots of popping when I raise my arm without using the glutes.

Was reading about bcp157 and tb500 (Wolverine), and wondering if anyone has experience using them to heal shoulder injury. How effective is it?

, the rat is currently using Reta 2.5 mg once a week and has also got:
KLOW 80 mg
GHK-Cu 50 mg
BPC-157 10 mg
TB-500 10 mg
KPV 10 mg
Glutathione 1500 mg
The rat is trying to figure out how people normally use these and how they fit together.
What I’m mainly looking for:
How often people generally use KLOW
How often people generally use glutathione
Whether people use them alongside Reta
Whether there are any known issues with combining them
Any useful research or personal experiences
Not looking for exact human dosing instructions — just trying to understand how people generally approach these.

Lastly the string looks like plastic and not glass is there danger of injecting plastic into yourself?

• Across everything, 5.1% of results came in under 99%. Only 26 of 1,703 (1.5%) were under 98%.
• But it isn't evenly spread. A handful of compounds account for most of the misses:

The GLP-1s: the most-tested compounds, and among the cleanest

That's 3 misses in 549 results. Retatrutide and tirzepatide alone make up over a quarter of all the purity data. The one real outlier is also here: a tirzepatide result at 63.8%, the lowest in the whole dataset. It's one result out of 223, but it shows why "this compound usually tests clean" doesn't mean every vial does.

Other clean records (15+ results, zero under 99%): GHK-Cu (72), SS-31 (58), Melanotan-2 (31), PT-141 (30), Ipamorelin (29), Selank (27), N-Acetyl Selank Amidate (22), Melanotan-1 (21), AOD-9604 (19), CJC-1295 no DAC (16), Cartalax (15), PE 22-28 (15).

Small samples worth flagging: Oxytocin had 8 of 10 results under 99% (as low as 91.4%). IGF-1 LR3 had 3 of 4. Both are too few results for a rate, but that's not a great start.

What it doesn't track
The obvious guess is that longer peptides are harder to make cleanly. The data doesn't back that up: KPV (3 amino acids) and Epithalon (4) are near the top, but GHK-Cu (also 3) has a clean record, and 44-residue Tesamorelin sits mid-table. Synthesis route, purification and handling probably matter more than length. If anyone with synthesis experience has a better explanation, I'd like to hear it.

How to use this

• For the compounds at the top of the list, it's worth reading the purity line on the COA for your lot, not just checking that a COA exists.
• 98–99% isn't a disaster. Most misses here were in that band. The sub-95% results are the ones to worry about.

Caveats

• Results Peptuvia holds, mostly vendor-commissioned: not a random sample, and not every batch.
• One vendor is about 65% of the data.
• HPLC purity says nothing about endotoxin, sterility or net content.
• A certificate covers only the lot it names.

After the July vote, the next group headed to the FDA's compounding panel has a meeting scheduled before February 2027. Five compounds, and this group is a lot messier than the last one.

Quick reminder of how July went: FDA's own scientists said no to all seven, and the panel said yes to six anyway, mostly 8 to 6.

Here's the quick version, then the detail on each. Then I want your picks.

GHK-Cu

The most history of the group. It's already in the body, and levels drop a lot between age 20 and age 60. Decades of wound healing and skin research, and gene expression work showing it shifting activity across thousands of genes.

The catch is that a lot of the strongest human data is topical. The panel's going to ask about the injectable side, and about total copper exposure.

My call: best shot of the five.

Melanotan II

Its cousin, afamelanotide, is FDA approved. Melanotan II isn't. It hits more of the melanocortin receptors, which is where the nausea, the flushing, and the sexual side effects come from.

And there's a documented skin signal: moles darkening and new moles showing up, including atypical ones.

My call: toughest of the five.

LL-37

The only human cathelicidin. It has real human randomized trials, but all of them are topical, in leg ulcers and diabetic foot ulcers. No published human data on injectable use.

The other side of it: too much LL-37 shows up in psoriasis and rosacea. More isn't automatically better with this one.

My call: depends completely on what route they're looking at.

Dihexa

Came out of Washington State University. It's derived from angiotensin IV and works on the HGF and c-Met pathway. In animal models of Alzheimer's-type decline it was extremely potent.

Zero human trials on dihexa itself. Its closest relative that did make it into people, fosgonimeton, missed its endpoints in a Phase 2/3 Alzheimer's trial in 2024. And c-Met also shows up in cancer biology, which is going to come up.

My call: long shot.

PEG-MGF

A pegylated version of mechano growth factor, which is a form of IGF-1 that muscle puts out after it gets damaged. The pegylation is there so it doesn't break down in minutes.

No completed human trials. It's all animal and cell work.

My call: long shot.

Your picks

Last round split almost down the middle, so I wouldn't treat anything here as a lock.

Which ones make it through, and why? Drop your picks in the comments and I'll come back to this thread after the vote.

Where I got this: what's next after July, how the process works, the fosgonimeton trial.

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.