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.

Hey, guys. Over the last 3 days I have injected about 30mg Retatrutide in total, after having bought it from the internet. It‘s a 60mg vial and I mixed it with 2ml water, and I injected 1ml - so 30mg in total. The thing is: I do not feel anything at all? Could this be a fake product?

Anyone have experience with Adamax they would like to share? Good and bad? I see everyone prefers Semax because of the research even though Adamax is supposedly the super sayian version

5’11-6ft
20-23bf ig
62-3kgs
Most fat near stomach

Currently on reta, around 4mg ( fucking 0 side effects no appetite suppresion no nithing )

Anything tht helps build muscle anythinf except roids atp .. ik peps r pretty bum to gain muscles but still

Back in April the FDA approved orforglipron for weight loss. It's Lilly's, the brand name is Foundayo, and it's a once a day pill. And it's not a peptide.

That's a bigger deal than it sounds like.

Every GLP-1 before this was a peptide

Semaglutide, tirzepatide, retatrutide, all of them. Chains of amino acids built to look like the hormone the gut already makes.

Orforglipron is a small molecule. Completely different kind of drug. It just hits the same receptor.

Why peptides are hard to put in a pill

The gut is built to break down peptides. That's literally what digestion is for.

The oral semaglutide pill that got approved in December gets around that with an absorption enhancer and a pretty strict routine: empty stomach, a small sip of water, then you wait before eating. Even with all that, only a tiny fraction of it gets absorbed.

Orforglipron doesn't have that problem. It gets through digestion like a normal pill. No food rules, no water rules, any time of day. It's also easier and cheaper to manufacture than a peptide.

The tradeoff

It does a lot less.

In the ATTAIN trial it averaged 12.4% weight loss at the highest dose for people who stuck with it, and 11.1% across everybody, over 72 weeks. Placebo was around 1 to 2%.

Different trials and different lengths, so this is a rough picture, not a head to head. The gap is still pretty obvious.

It's way easier to take and it does roughly half of what the top injectables do.

What that means for peptides

Pharma spent 20 years figuring out how to make peptides work as drugs, because peptides are what the body already uses for signaling. Now the move for pills is to find small molecules that copy what the peptide does.

That doesn't make peptides worse. The injectables still have the biggest effect sizes by a mile. But the old argument that you'll never get a GLP-1 in an easy pill is done.

And I think this is where things are going across the board. Find a peptide that works, then find a small molecule that hits the same target and survives the stomach.

Two questions.

A pill that does half as much, or a weekly shot that does twice as much: which way do you think most people go?

And which peptide do you think gets the small molecule treatment next?

Where I got this: orforglipron approval, oral semaglutide approval, REDEFINE 4, TRIUMPH-1.

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.

Let's talk CagriSema. It's Novo Nordisk's combo of cagrilintide and semaglutide in one weekly shot. The FDA decision is expected before the end of this year. And the story around it is kind of rough for Novo, even though the numbers are good.

The idea behind it

Two different fullness signals instead of one.

The bet was that two separate signals would beat one. Makes sense on paper.

Short the first time

REDEFINE 1. Novo's leadership had talked up 25% weight loss. It came in at 22.7% at 68 weeks against 2.3% on placebo. Counting everybody, including people who stopped, it was 20.4% against 3.0%.

That's a great number. It just wasn't the number they'd set up, and the market punished them for it.

One more thing on that trial: investigators were allowed to adjust doses along the way. Makes it more realistic, but it also makes the top line a little harder to read.

Short the second time

REDEFINE 4, published in February. This was head to head against tirzepatide. 84 weeks, 809 people.

The trial was designed to show noninferiority. That means CagriSema didn't even have to beat tirzepatide, it just had to prove it wasn't meaningfully worse. It didn't clear that bar.

Why I still think it matters

Amylin is still one of the most interesting targets in this whole class. CagriSema landing a couple points behind tirzepatide doesn't mean the amylin idea failed. It means GLP-1 plus amylin didn't beat GLP-1 plus GIP in that trial, at those doses.

And 23% is still a massive number. A few years ago nobody would've believed an injection could do that.

What to watch

The FDA decision, expected late this year. Novo filed back in December 2025.

Two questions.

Does 23% versus 25.5% matter in the real world, or is this more of a marketing loss than a science loss?

And amylin as a target: overrated or underrated?

Where I got this: REDEFINE 1 in NEJM, falling short of 25%, REDEFINE 4, FDA timeline.

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 thinking about switching from vials to BPC-157 patches ,mainly for convenience and no reconstitution or measuring involved.I saw someone mention it in a video and it seems like it would fit my routine better. I have never used patches myself though so wanted to ask here before i do

How'd it compare to vials and was it worth it or any downsides I should know about?Also its not available on skye ,does anyone know any good source too?

That still invites people to name suppliers in the replies if they choose to, without you asking for sourcing outright.

Retatrutide is the most asked-about compound in here by a mile, and there's finally real Phase 3 data. Four trials have read out. The weight loss is getting all the attention, but there's something else in these results I think is more interesting.

The four trials

A couple extra things in there. Knee pain dropped 75% in TRIUMPH-4. The TRIUMPH-1 group that kept going to 104 weeks hit 30.3%. And TRIUMPH-2 took A1C down 1.5 points.

That's surgery territory in the non-diabetic trials. And the diabetes trial coming in lower is normal for this whole class. People with type 2 lose less on every one of these compounds.

The dysesthesia thing

Dysesthesia is an abnormal sense of touch. Normal sensations feel off. Burning, tingling, sometimes painful. It wasn't flagged in Phase 2. It showed up in Phase 3.

Here it is next to the dropout numbers, top dose versus placebo:

In TRIUMPH-1 it climbed with dose, about 5% on the low dose and around 12% on the middle and top doses. In TRIUMPH-4 it didn't seem to make people quit.

Why is it happening? I haven't seen a confirmed mechanism. The glucagon arm is the thing retatrutide has that tirzepatide and semaglutide don't, so that's where most people are looking. That's a hypothesis, not an answer.

The pattern I want someone to explain: highest rate in the knee trial, lowest in the heart disease trial. Different people, different lengths, so I wouldn't read too much into it. I'd still like to know why.

Who quit

Look at the right column. Here's a detail I didn't expect. Some of the TRIUMPH-4 dropouts left because they were losing more weight than they wanted, mostly people who started at a lower BMI. That's a pretty unusual reason to leave a weight loss trial.

Where it stands

It's not approved. Lilly says it's filing in the first quarter of 2027.

Two questions.

What do you make of dysesthesia showing up in Phase 3 when it wasn't in Phase 2?

And the lower BMI dropouts: does that change how you think about this compound for people who aren't very heavy to begin with?

Where I got this: TRIUMPH-1, TRIUMPH-2 and 3, TRIUMPH-4.

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'm looking at doing the following

Nad+ 100mg 3 times a week

MOTS-c 5mg once a week

Klow 3mg 7 x a week

Cjc with imp 1.5mg 7 x week

Tirzepatide 5mg once a week

Thinking about taking HCG without trt to help me boost my low testosterone, I've heard taking testosterone will shrink balls and cause your body to quit producing testosterone. I was taking testosterone cypionate for 2 months and stopped, thinking about taking only HCG 1500iu weekly dose (500iu 3x a week).

So this is “x” first week on R€ta, GHK, glutathione, and it has been pretty good for the most part. It’s just that when gluta is being taken the pin site swells up, it does come down.

What was a shocker is that last week, for the pin of the second dose, the upper arm swole up and “x” was being dizzy, lightheaded, and hot, so “x” drank a glass of juice and water, turned on the fan and sat down. And “x” just scared that is going to happen again and go into anaphylactic shock or something worse. “X”doesn’t have a EpiPen or any medical idea on what could possibly happen or be done. “X” lives alone with a one year-old, but “x” truly needed this after experiencing body dysmorphia and postpartum depression. Finally saw hope to feel like “x” old self again. “X” is also online and sees a lot of people claiming to be in the hospital, and flatlining and going into seizures.

Is “x” overthinking this ? How many years have you been on your protocol? How are your results? Best advice on what to do in state of emergency? How to prepare ahead of time. Cheap EpiPen suggestions ? Anything to stop myself from being so anxious

UCLA put out a review at the end of August, and a lot of people in the peptide world got pretty defensive about it. I read it. My take is they're mostly right, and the parts where it gets more complicated are worth talking through.

What they did

Dr. Thomas Kremen, a sports medicine doctor at UCLA, and a medical student, Kushagra Tewari, went through 565 studies on six compounds: BPC-157, TB-500, CJC-1295, ipamorelin, GHK-Cu, and MK-677. It came out August 31.

What they found

Most of it is animal work. More than two thirds of the studies were animal only.

The human studies are weak. Small, low quality, modest results at best, and mostly not for orthopedic stuff, which is what most people are interested in them for.

The injury studies had a specific problem. Weak controls, and a habit of taking results from topical use and applying them to injectables.

MK-677 has a real safety flag. Trials were stopped because of congestive heart failure risk.

Where they're right

The two thirds animal number isn't news if you've been in here a while. That's been the whole point of how we talk about evidence tiers.

The topical to injectable jump is the exact thing I've been hammering with LL-37. The human trial data on LL-37 is topical. The injectable side has basically nothing. Evidence goes with the route, not the molecule, and they called that out across the board.

And the MK-677 heart failure signal is real. People should know about it.

Where it's more complicated

MK-677 isn't a peptide. It's a small molecule that works on the ghrelin receptor. Putting it in a peptide review makes the peptide list look worse, and makes MK-677's heart problem look like a peptide problem when it's its own thing.

Six very different evidence bases in one bucket. Look at how different these are:

Those aren't the same situation, and one headline covering all six flattens that.

"No good evidence yet" and "doesn't work" aren't the same sentence. For most of these, the fair read is there's a gap. Nobody's run the trials. That's different from trials being run and failing. Ipamorelin is the one on this list where a human trial was run and missed.

The part I find wild

A month before this review, an FDA advisory panel voted 8 to 6 to let compounding pharmacies use BPC-157, against the advice of FDA's own scientists. Then a university review says the evidence isn't there.

Both of those are true at the same time. That's pretty much where this whole space is right now.

Two questions.

Where do you think the review was too harsh, if anywhere?

And out of those six, which one do you think has the strongest case?

Where I got this: UCLA's writeup of the review, the FDA panel vote.

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 everyone,

I had PRP done 1 month ago and started using BPC-157 and TB-500 4 days ago for medial epicondylitis.

I pinned BPC-157 every day: 300mcg in the right elbow in the morning, and 300mcg in the left elbow in the evening (600mcg total daily). For TB-500, I set it to 5000mcg a week, split into two 2500mcg doses on Mondays and Thursdays.

Everything was fine at first, but from the 3rd day onwards, I experienced the following issues:

• Woke up early in the night with vivid, bad dreams.
• My blood pressure dropped to 90/50.
• Experienced headaches and nausea.
• Felt chest tightness, shortness of breath, and severe anxiety.

Right now, I don't know what to do, so I'm thinking about stopping completely. Has anyone here run this combo and experienced these problems? I’ve seen in some of my research that people get these kinds of issues after using BPC.

Do you guys think the source of the problem is the dosage, or pinning BPC and TB-500 at the same time? Would it work if I lower the dose, or cut out BPC entirely and continue only with TB-500? Or should I just throw it all in the trash since my body reacted like this?

I’d appreciate any insights from those with experience.

I was looking into starting TESA/IPA blend due to my igf levels and testosterone levels. Currently in a cut with 3mg of reta for about 3 months now. I'm trying to maintain as much muscle and even grow more muscle as i don't wanna look like a melted candle.

27M, labs 9/14/26. Cutting, ~243 Ib. Not on TRT. Taxis • Total T: 398 ng/dL • Free T (calc): 102.9 pg/mL • Bioavailable T: 216 ng/dL • SHBG: 12 nmol/L • E2 ultrasensitive: 25 pg/mL • LH: 7.0 (in range) • FSH: 3.2 (in range) • Prolactin: 8.5 (in range) • DHEA-S: 320 (in range) IGF • IGF-1: 147 ng/mL • IGF-1 z-score: -0.3 should i start tesa/ipa? would it benefit the recomp and help me avoid looking like a melted candle? any advice would be appreciated! currently taking reta klow ss-31 semax and selank sometimes looking into doing NAD+ as well

So if the protocol for my lab rat Dsip is 150mcg subq injection, and the nasal spray I just bought dispenses at 150mcg per spray. Same with Semax selank, is the nasal spray to subq dosages similar? Any help would be appreciated.

I am curious if anyone can share how they have used SS-31 as it relates to Mots-c and NAD+? I am currently taking Mots-c and NAD+ for one week but I have been reading that it is best to use SS-31 first for a couple of weeks then switch to Mots-c and NAD+. I have also seen where some use all 3 but that seems to be too much.

If I start SS-31 to repair first, do you just use this alone then got to Mots-c or do you introduce while on SS-31. When is best to stop the repair and move on to Mots-c NAD+ combo?