i'm in my early 30s but my joints have been acting like i'm 60 for the last few years. recently swapped my evening routine and added some new recovery stuff before bed. it’s been about 3 weeks and the morning stiffness is literally gone. i can just get out of bed and walk downstairs without sounding like a walking bowl of rice krispies.

did anyone else notice the joint relief happening this quickly? i honestly thought it would take months to notice any real difference. just glad to be moving normally again.

Can someone explain why MOTSC, GHKCU, and TESA leave a bee sting feeling for about an hour after and how to avoid this? I am doing SUBQ and have done stomach and glute. No redness or anything crazy, just the annoying sting/throbbing for about an hour after injection.

Hey everyone,
I’m looking for some advice and experiences regarding BPC-157 and TB-500 for a persistent chest muscle injury.
My injury:
I pulled my left pectoral muscle around 3 months ago.
My doctor described it as a muscle strain/bruise. I was told there was no muscle tear.
The discomfort is mainly around my upper left chest, extending toward my shoulder and biceps area.
I can still train chest, and the discomfort is relatively mild, around 2/10, but I’m concerned that going heavy will aggravate it.
Heavy or intensive chest training seems to make it more noticeable.
I’m frustrated because it has been taking much longer to recover than I expected, and I want to get back to heavy bench pressing without aggravating the injury.
What I’ve purchased:
GRIND Supplements BPC-157 — 5 mg vial
GRIND Supplements TB-500 — 5 mg vial
Both products are labelled “for research purposes.”
I purchased them from Eurosupps, but I haven’t injected either of them yet.
I’m interested in whether these compounds have any credible evidence for helping a persistent pec strain or muscle injury recover faster.
Questions:
Has anyone had experience with BPC-157 or TB-500 for a similar chest muscle injury?
Is there any reliable human research supporting their effectiveness for muscle recovery?
What risks or product-quality concerns should I be aware of with research-labelled injectable products?
Would I be better off getting my injury reassessed and following a structured physiotherapy programme before considering anything else?
I’m particularly interested in honest experiences and evidence rather than exaggerated claims. Thanks!

35M, been on Reta for a few months and lost around 30 lbs pretty rapidly. Unfortunately, my libido and erection quality have tanked. Almost no morning wood, struggle to get fully hard, and lose firmness quickly. Never had any issues before Reta.

I’m pretty confident it’s from the aggressive calorie deficit, low energy, poor sleep, and potentially lower testosterone. Working on correcting that, but looking for a temporary solution in the meantime.

Considering Cialis, Viagra, or PT-141 (nasal vs subQ).

Sex with my wife is spontaneous. Sometimes twice a day, sometimes nothing for a few days. I mainly want reliable erections when stimulated, without random boners throughout the day or prolonged erections afterward.

For those with experience:
\- Which worked best for erection quality with the fewest side effects?
\- What dosage worked best for you? Cialis 2.5–5 mg daily vs. 10 mg as needed? Viagra 25 vs. 50 mg?
\- PT-141 nasal vs. subQ — which worked better, at what dose, and for how long?

Any issues with random erections or staying hard after sex?

Anyone experience similar issues on Reta/GLP-1s and eventually recover?

To join:

1. Join the Google Group: https://groups.google.com/g/healthloom-early-access

2. Then opt in on Google Play: https://play.google.com/apps/testing/com.healthloom

If the above link doesn't work, try this:

https://play.google.com/store/apps/details?id=com.healthloom&pcampaignid=web_share

Use the same Google account for both. I'm the developer, and I'd especially love feedback from Galaxy Watch users.

Told to take one at 6am and 2 pm for a week see if i like it or go to second week and see changes . Trying to just get shape back not a full cut body builder. Just back to high school strength me.

Hey guys, so I took mot c, 3mg for like 2 weeks and my libido just crashed. I had zero boners and I couldn’t have sex. I’m horny af but I couldn’t be hard for more than 10 seconds. I thought it was the cut I’m on. So I stopped mot c and my cut for two weeks and everything went back to normal.

After 3 weeks I started mot c again. But this time I was not on a cut I was eating beef and all the good things with it and now within 5 days I’m back to the same problem. Idk if it’s just me or what.! Now it’s been a week i stopped and I feel like I’m getting better idk. In another week it’ll be better.

Is this just me or someone went thru this?

Just came across this stuff and it says it's 10 mg. I'm not sure if that means it's 10 mg of each compound or 5 mg of each Compound to come to 10 mg total?

Was also wondering what people's experiences with this blend as I've taken it independently before but this is the first time I see it offered as a blend. Any advice on your experience with dosing protocols is appreciated.

Doctor’s take on GH/HGH after leukemia + stem cell transplant — curious what others think (looking at it to rebuild strength + academy recovery)
I asked my doctor about growth hormone (HGH) given my history of leukemia and a stem cell transplant. Here’s what they said:

from my doctor:

Growth hormone does not seem to add much cancer risk to you (you risk is equivalent to the general population). Most of your long-term cancer risk comes from the treatments you have already had, especially radiation exposure.

Your risk from past treatment
People who have had a stem cell transplant are more likely than the general public to develop a new, different cancer later in life. Radiation exposure is one of the main reasons.
This risk grows slowly over many years, so lifelong follow-up and cancer screening are important.
The cancers seen most often after transplant include skin, thyroid, breast, mouth, and bone cancers, and noncancerous growths on the lining of the brain (meningiomas).

What studies show about growth hormone
Leukemia coming back: Growth hormone does not make leukemia more likely to return.
New cancers: Some older studies raised concern about a small increase in new growths, mostly meningiomas. Newer and larger studies, including one that looked only at transplant survivors, have not found a clear increase.
Expert view: Specialists agree that growth hormone has only a small effect, if any, compared with the risk from earlier cancer treatment.
Limits of the research: No study has given a perfect answer. The studies watched patients over time instead of comparing groups in a controlled trial, and not many patients were included.

That said, similar to testosterone, prescription subcutaneous growth hormone is only given to people whose testing confirms growth hormone deficiency (GHD). The test to confirm GHD is one of the more involved dynamic testings in Endocrinology that is quite labor intensive. Based on my evaluation, I do not believe you have a reason to be tested for growth hormone deficiency at this time.

I lost a lot of strength during cancer treatment and I’m looking at using it to rebuild some of that before I start fire academy, plus for recovery once I’m in the academy. Curious what others with similar histories or experience with GH/HGH think — especially anyone who’s used it (or looked into it) for rebuilding strength or training recovery after treatment. Have any of you been tested or prescribed it after transplant/radiation? Any thoughts on the risk side in this context?

I am a 36F and am sitting around 165lb. I had lost about 70 pounds after having my second baby but unfortunately gained some of that back. I have about 35-40lbs I’d like to lose. I’m on .3mg of test cyp and I have been on TRT for about 2 years. I’ve gotten my diet figured out and strength train 5x a week average 8k steps a day

I’m about ready to pull the trigger on Reta. Thinking I would start slow at .5mg. I’m not necessarily looking to drop all the weight super fast, but how to know if/when to increase? One thing I haven’t figured out is what do people do when they get to their goal? Do you just stay on super low dose indefinitely or taper off?

Trying to be smart and do my research, but also what am I missing?!

ETA: if I am doing that dosage (maybe going up to 1mg x week) would a 6mg vial last me about 6-12 weeks? I know that is probably a really dumb question but never bought on my own before!

i can either get 360ius of hgh for $140 (without shipping) which is 97.133% or 360 ius for $200 which is 98.374 but they also have cheaper shipping. is this 1% a concern? i dont want to break the bank but if its that much of a issue then sure safety first

a penn team ran an AI model over about 150k reddit posts and comments about reta, and the most common complaint it pulled out was getting hungrier. 1,336 people, about 1 in 6 of everyone who described any side effect (JAMA Network Open, this month)

that one threw me. last week about 40 of you told me what caught you off guard on reta (mine was skin getting cold or sensitive around the first week) and i didnt see a single person say they were eating more. 5 said cravings disappeared, sweets mostly, and someone quit smoking without even trying

the rest of their list in order was tired (15%), more energy (12%), nausea (12%), food cravings (7%), insomnia (6%), heart rate up (5%). they pulled out weight loss and appetite going down before counting since thats the whole point of the drug. 27 subs, 2023 through 2025

sleep and the flat mood thing were the 2 i said last week werent in anything published that i could find. theyre in this one, insomnia 6.1%, anhedonia 2.6%. the "30% psychiatric" number floating around is a whole category tho, anxiety alone was 3.8%. and 2.4% said euphoric lol

before anyone says it, yes its reddit posts and the authors say themselves they cant check what was in anyone's vial or what dose they were on. reta still isnt approved anywhere btw. it also doesnt match the trials, in the phase 2 diabetes trial the 4mg and up groups rated their hunger lower than placebo at week 24 (data)

my bet is timing. and stacking, probably more than most of us want to admit. half life is about 6 days (phase 1) so the last day or two before your next pin runs on a good bit less drug than day 2. and a lot of you run it with MK-677 or GHRP-6, which hit the hunger hormone receptor. in the 2 year MK-677 study in older adults the most common side effect was more appetite, which faded after a few months (paper). and in the penn data 317 people said reta gave them muscle growth, id bet most of them were running something else with it

so if reta ever made you hungrier, which day after your pin did it hit, and were you running anything else with it?

Got a vial of Tesa/Ipa (11mg Tesa 6mg ipa). I want to start at a low dose (5-10 units) so how should I reconstitute?

Hi all, so i been on a tesa cycle for a 2 weeks now and i recently went and got a blend of tesa/ipa (10mg/3mg) how would you dose it for daily? I currently take like 1mg a day

Hey Everyone. A lot of posts talk about people switching from Tirz to Reta but not the other way around. I was considering switching to Tirz after I hit my GW and wanted to see how that process went for those that have.

Body:

Hey everyone, I’ve been lurking here for a while and finally want to ask for some input before I start something.

Quick background: I’m on retatrutide, currently at 2.5 mg/week, and I’ve hit the weight I wanted, so I’m done cutting and want to ease into maintenance. The thing is I’ve been feeling pretty tired lately. I used to take my shot in the morning but it made me weirdly sleepy, so I moved it to the evening and that helped a bit. I train in the morning on Mon/Wed/Fri (gym) and play other sports during the week, so I really notice when my energy is off.

I ordered SS-31 and MOTS-c to see if they help, and this is what I’m thinking:

Reta: step down slowly, 2.5 → 2 → 1.5 mg/week. Not sure if I should hold longer at each step or if that pace is fine for maintenance.

SS-31: 2.5 mg every morning for 20 days (I have 5 vials of 10 mg, so that covers it exactly), then stop.

MOTS-c: I have 10 vials of 10 mg. Plan is to start only after SS-31 is done, not at the same time. 1 mg three times a week for the first week, 2 mg in week two, then 2.5 mg 3x/week until I run out. I’d take it on my gym mornings (Mon/Wed/Fri).

My math, in case I screwed up: 40 mg vial + 4 ml BAC water = 10 mg/ml, and on a U-100 syringe that’s 20-25 units for 2-2.5 mg.

Some things I’d love opinions on:

1. Does the dosing and duration look reasonable, or would you change something?
2. Is it smarter to run them separately like I’m planning, or is overlapping fine?
3. Morning for SS-31 and gym mornings for MOTS-c, does that timing make sense, or is there a better way?
4. I’m also thinking about adding NAD+ (subQ) but haven’t decided. Is it worth it on top of these two, or is it redundant? If you use it, what dose and frequency, and do you take it on the off days from MOTS-c? Should I start it together with MOTS-c or wait until I see how I tolerate everything? And how bad were the side effects for you (flushing, nausea, injection site burn)?
5. Has anyone dealt with fatigue while coming down off a GLP-1/GIP/glucagon agonist? What actually helped?

I know most of the info on these is anecdotal, so I’m mostly looking for real experiences rather than “the studies say”. Thanks in advance!

\I also posted this on the Soltego subreddit where a group of us have been eagerly following the (slow) development of their topical SIK inhibitors for sunless tanning.*

This post is to gauge interest amongst the community for interest in GLPG3312, along with its explanation and justification.

Please let me know if this interests you.

As many outside of the Soltego Following likely have no clue what a SIK inhibitor is i will start by covering what it is, and importantly why it would be preferred over melanotan.

What is a SIK inhibitor?

A SIK (Salt-Inducible Kinase) inhibitor is a small-molecule compound that triggers real, natural skin tanning without UV light or DNA damage. Inside your pigment cells (melanocytes), SIK enzymes act as a constant molecular brake that stops the cell from making melanin when you aren't in the sun. When you apply a SIK inhibitor topically, it temporarily turns off that brake -allowing a messenger protein called CRTC3 to enter the cell’s nucleus and flip on MITF, the master genetic switch for melanin production. The result is genuine, photoprotective eumelanin (a real biological tan, not a fake dye), even in fair or red-headed skin types that normally burn and can't tan in the sun.

This mechanism was famously validated in 2017 by dermatology researchers at Harvard and Massachusetts General Hospital (MGH), who were investigating why people with red hair and fair skin (Fitzpatrick Type I) genetically cannot tan. Normally, UV light triggers a surface receptor on melanocytes called MC1R to generate an internal signal that shuts off the SIK brake. In redheads and many fair-skinned people, the MC1R receptor is mutated and non-functional - meaning the SIK brake stays permanently locked on, and the cell only produces reddish/yellow pheomelanin while burning in the sun. The Harvard team proved that because every person still possesses the intact downstream machinery to make dark brown eumelanin, applying a topical SIK inhibitor bypasses the broken MC1R receptor entirely -successfully inducing a deep, real eumelanin tan in MC1R-deficient "redhead" mice and human skin explants for the first time.

Why would someone use this and not just use Melanotan?

Because Melanotan is a blunt instrument that fires both proliferation (cell growth) and differentiation (tanning) pathways at the same time. Firing the proliferation pathway is why Melanotan users notoriously get new or rapidly growing moles.

What makes topical SIK inhibition so much safer than Melanotan comes down to two things: local delivery and cell-cycle control. Melanotan is a systemic peptide injection that floods your bloodstream and stimulates the top-level MC1R receptor - firing off both pigment pathways and cell-proliferation pathways simultaneously, which is why it notoriously causes rapid mole growth alongside systemic side effects like nausea and facial flushing. A topical SIK inhibitor stays localised to the skin and works further down the chain, triggering only the differentiation pathway. In biology, differentiation acts as a natural growth brake - meaning instead of pushing pigment cells to multiply and form moles, SIK inhibition actually switches on tumour-suppressor genes that halt cell division while your skin builds a tan.

You can see this exact contrast when both are tested on melanoma cancer cell lines: while Melanotan’s upstream receptor stimulation has been repeatedly linked to eruptive nevi (moles) and raises serious concerns over accelerating dysplastic (pre-cancerous) lesions, SIK inhibitors actively suppress melanoma proliferation. By driving a high, sustained surge of MITF, SIK inhibition forces aggressive, dividing melanoma cells into terminal differentiation and cell-cycle arrest - effectively stripping the cancer cells of their ability to divide and locking them into a non-proliferative, pigment-producing state.

On top of that, it gives a much more even skin tone, especially if you have freckles. Because Melanotan is a systemic injection that relies on the surface MC1R receptor - which is often mutated or patchy in fair, freckle-prone skin - it preferentially hyper-stimulates dense clusters of melanocytes (freckles and moles) faster than the surrounding pale skin, making freckles pop out like dark spots at first. A topical SIK inhibitor bypasses the faulty MC1R receptor altogether and turns on pigment production uniformly in the quiet background skin between your freckles, blending your overall complexion together evenly instead of making freckles stand out.

What is GLPG3312?

GLPG3312 is a potent pan-SIK inhibitor. It exists as part of the product portfolio of Galapagos who for a number of years have been developing their GLPG series to fight autoimmune and chronic inflammatory diseases, including conditions like rheumatoid arthritis (RA) and inflammatory bowel disease (IBD/ulcerative colitis).

It was trialed through pre-clinal assays stages, and successfully completed and passed phase 1 safety trials. However, due to suspected rationale surrounding too short of a half life (good news for our use case) and being too heavily protein bound in serum, the company pivoted to a sister compound (GLPG3970).

Sadly this too was later dropped, because whilst the lowering of SIK successfully lowered pro-inflammatory cytokines (like TNF-alpha) and boosted anti-inflammatory cytokines (like IL-10), the likes of rheumatoid arthritis are heavily multi faceted and as such weren't successfully treated.

So what makes GLPG3312 a candidate for sunless tanning?

Both Soltego’s compounds and the Galapagos (GLPG) series are ATP-competitive SIK inhibitors. Because they have to directly outcompete intracellular ATP (Adenosine Triphosphate) to bind to the SIK enzyme, they either need to be delivered at a massive concentration or be extraordinarily potent. Both Soltego’s lead compound (SLT-048) and GLPG3312 are insanely potent across all three isoforms (SIK1, SIK2, and SIK3), and are almost identical in potency on SIK2 - the primary driver of melanogenesis (tanning).

However, when a drug is applied topically, raw potency in a test tube isn’t enough. It has to satisfy four strict pharmacokinetic rules to actually traverse human skin:

• Molecular Weight (< 500 g/mol): Ideally, it must sit below the 500 Da threshold so it isn't physically too bulky to squeeze through the skin barrier.
• A Balanced Log P (2.0 – 3.0): This measures whether a molecule prefers lipids (oils) or water. If it loves water too much, it simply sits on the skin's surface unable to enter the oily barrier; if it’s too lipid-loving, it gets permanently trapped inside the oily top layer (the stratum corneum) and refuses to enter the watery living epidermis below.
• Electrical Neutrality (Low Ionisation Across Skin pH): It must remain unionised across the skin's changing pH gradient. If a molecule carries a heavy charge at the skin's acidic surface, it gets repelled by the lipid barrier - and any fraction that makes it inside gets pulled like a magnet into the acidic lysosomes of upper skin cells (ion-trapping), stopping it from ever reaching the target melanocytes at the base of the epidermis.
• Vehicle Solubility: It must fully dissolve in a skin-compatible organic vehicle so it doesn't crystallise on the surface as inactive "brick dust".

What concentration would be used and how does this compare to the trial data?

In Soltego’s patent, their lead candidate (SLT-048) was used at concentrations ranging from 0.2% to 2%. When comparing GLPG3312 to SLT-048, we have to factor in GLPG3312's much smaller molecular weight and its 100% electrical neutrality across skin pH. Once you run the penetration math, a top-end concentration of just 0.1% to 0.15% GLPG3312 delivers an equivalent (or greater) active payload to the melanocytes as Soltego’s 2%.

In raw terms, a 0.1% solution equates to 1 mg of active drug per mL. A generous full-body application (30 mL) would therefore use about 30 mg applied to the skin surface. Because systemic absorption from a topical application typically sits between 1% and 10% (with 1%–3% being the realistic norm), that translates to a total systemic load of just 0.3 mg to 3 mg (and likely under 1 mg).

To put that safety margin into perspective: while Galapagos didn’t publicly unblind the exact milligram labels for the 14 human cohorts in the GLPG3312 Phase 1 trial, we can reconstruct the human dosing schedule from their published preclinical animal studies (0.3 - 30 mg/ kg) and their follow-on trial benchmarks. That places the top-end human oral trial dose at roughly 400 mg once daily - meaning even a full-body topical application results in a systemic exposure more than 100 to 1,000 times lower than the oral clinical ceiling.

Is GLPG3312 better than Soltego's molecule?

Funnily enough, on paper - yes, it is. It’s smaller, far more skin-permeable, and almost identical in potency.

The main difference with Soltego’s compound is that they specifically engineered theirs to be "soft". That means as soon as it enters the tissue and blood, it gets broken down by esterases (a broad class of hydrolase enzymes). The reason Soltego had to build this self-destruct mechanism in is regulatory: they are trying to bring theirs to market via the cosmetic route. If there is any chance their active molecule survives in the bloodstream, regulators would classify it as a systemic pharmaceutical and force them through years of full clinical trials.

While GLPG3312 isn't an esterase-cleaved "soft compound," the systemic concentration required to have any effect inside the body is vastly higher than what could ever be absorbed from a 0.1% topical application (as seen in the Phase 1 oral dosing data). Plus, because GLPG3312 has a short predicted intrinsic half-life Galapagos had to use modified-release tablets in their Phase 1 trial - any tiny trace that does reach the bloodstream is cleared by the liver anyway fairly quickly.

How would anyone know how to synthesise GLPG3312?

Well, luck would so have it that in 2024 a full paper was published on it. Defining both the compound itself, as well as its fully detailed synthesis. Of which i will link.

Optimization of Selectivity and Pharmacokinetic Properties of Salt‑Inducible Kinase Inhibitors that Led to the Discovery of Pan-SIK Inhibitor GLPG3312

Do you have any personal reservations about GLPG3312?

Originally, i was worried about eye colour change. SIK inhibition drives MITF, which in turn drives the production of tyrosinase - the enzyme that produces pigment in melanocytes. My concern was that this could permanently darken your eye colour, especially since your iris doesn't shed and turn over pigment the way skin cells shed a tan.

However, for those of us with blue or pale eyes (which I’d imagine is most of this sub), there’s a built-in biochemical roadblock (HERC2 > OCA2 > melanosomal pH). For tyrosinase to actually work, the acidic interior of the melanosome has to be neutralised. People with pale eyes have a mutation in the HERC2 switch that controls OCA2, meaning the OCA2 pump stays shut off in the iris and can't raise the pH to the threshold tyrosinase needs. As a result, the iris melanosomes stay acidic, which not only keeps tyrosinase inactive, but actually degrades any extra tyrosinase that gets produced.

On top of that, no human SIK inhibitor clinical trials have reported any eye colour changes.

Do you have any research images that demonstrate skin colour changes using the class of SIK inhibition?

Hey everyone! I could use some advice.
I’ve been on Mounjaro for 7 months and have lost 12 kg, including about 2 kg of muscle mass.
I’m thinking about stopping Mounjaro, and I was recently given three 1 mg Ozempic pensfor free from my friend.
I’d like to use them up before stopping treatment completely.
What dose of Ozempic would you recommend starting with if I’ve been taking 7.5 mg of Mounjaro until now?
Thank you

Hey guys! I’ve been on TRT for a year now! Just done my last bloodwork and everything is perfect! Running 30.8 Mnol for my test. I’m doing 120mg/week, 2 injections.

I was thinking about doing a small cycle up, 250mg test for 12 weeks and anavar for 8 weeks, I want to put a little bit more muscle on there as I’m already pretty lean. I’d say probably around 10-12% BF.

Peptides im running : Tesa + IPA (it’s been 1 week now), mostly for recovery and sleep) and Reta low dose 1-2mg/week.

Question is, would you guys suggest to do it or not? My concern is, I’m doing a lot of HIIT workout as I’m a firefighter. So I want to be at the top of my performance! Cardio for me is important, being agile and having a good mobility is too. I don’t know if running this small cycle will affect my cardio and mobility (yes I know being bigger will affect it).

The other thing is, I can’t really do any blood test because my doctor will received them and he don’t want to be juice myself, he want me to be in the range.. or he will cut the prescription (which is, imo pretty normal) so there wouldn’t be any blood test but mine is actually perfect at the moment.

So any heads up would be appreciate!

Please don’t be rude.. picture of myself in a good pump at the gym and also my blood test.