Losing weight is now too easy. Keeping muscle is next.

Step 01 — The appetite off-switch (yes, it started with lizard venom)

The GLP-1 class is the reason weight loss stopped being a willpower contest. Fun origin story the clinics never lead with: the first GLP-1 drug, exenatide, was derived from a hormone found in Gila monster venom. A lizard. Modern medicine's biggest hit is a refined descendant of reptile spit, and honestly we respect it.

Ranked by trial evidence, not vibes: retatrutide sits at the top — its phase 2 results showed the largest average weight loss ever published for a drug, but it's still in trials and not approved, so anything sold under that name online is not the trial drug. Then tirzepatide (that's the molecule inside Mounjaro and Zepbound — same drug, two brand names) with monster phase 3 data and real approval. Then semaglutide (Ozempic / Wegovy), the one that started the gold rush — still excellent, just outgunned in head-to-head data.

Not into weekly injections at all? Orforglipron is the daily-pill version — phase 3 trials done and approval filings in motion, but as of this writing it's not on pharmacy shelves yet.

These are prescription medicines with weekly (or daily) regimens set by their labels and prescribers — not by us, and definitely not by a Telegram vendor. The legitimate versions come from Eli Lilly and Novo Nordisk via an actual pharmacy. That's the whole sourcing conversation.

• Retatrutide — the full profile
• Tirzepatide (Mounjaro / Zepbound)
• Semaglutide (Ozempic / Wegovy)

Step 02 — The boring protein maths everyone agrees on

The one thing dietitians, sports scientists and gym bros all actually agree on: when you're losing weight, protein is what stands between you and losing muscle along with the fat. The commonly cited sports-nutrition range is roughly 1.6–2.2 g of protein per kg of bodyweight, and the popular simple version — 1–2 g per kg of your goal weight — gets you to basically the same place.

The maths really is idiot-friendly: aiming to weigh 70 kg? The commonly cited range puts you somewhere around 70–140 g of protein a day. That's it. No powder cult membership required — though the reason this matters doubles when a GLP-1 has murdered your appetite and you're accidentally eating like a bird.

Step 03 — Give your muscles a reason to exist

Muscle is use-it-or-lose-it, and never more so than in a calorie deficit. If you drop weight without resistance training, your body happily jettisons muscle along with fat — and you land at your goal weight weaker, softer and with a slower metabolism. 'Skinny but somehow worse' is a real and popular outcome of the GLP-1 era.

Lifting things (or resistance work of any flavour) is the signal that tells your body the muscle is still needed. This isn't peptide science, it's just biology, and it's the least optional part of the whole picture — for now.

The next wave: drugs that guard the muscle while the fat burns

Here's why 'for now' is doing heavy lifting in that last sentence. Your body has a built-in brake on muscle called myostatin — it exists to stop you carrying more muscle than you 'need.' Animals born with broken myostatin genes are absurdly, cartoonishly muscular. Big pharma looked at that biology, then looked at millions of people losing muscle on GLP-1s, and did the obvious thing.

Three antibodies are now in human trials to block that brake during weight loss: apitegromab (Scholar Rock — its phase 2 trial paired with tirzepatide reported similar weight loss with far less of it coming from lean mass), bimagrumab (now owned by Eli Lilly — its trials with and without semaglutide have shown large weight loss coming overwhelmingly from fat, with lean mass protected or even gained), and trevogrumab (Regeneron — phase 2 with semaglutide, encouraging interim data).

If these pan out, GLP-1 + myostatin inhibitor becomes the first pharmaceutical stack where fat loss and muscle retention arrive in the same syringe schedule: the appetite suppressant handles the deficit, the myostatin blocker stops your body eating its own muscle to pay for it. That's why we've profiled all three — this is the most consequential stack-in-waiting in the entire field.

• Apitegromab — full profile
• Bimagrumab — full profile
• Trevogrumab — full profile

Now the deflation, because that's the job

• 'Inevitable' is not a grade. The muscle-preservation results are phase 2 data — genuinely impressive phase 2 data, but the graveyard of drugs that aced phase 2 and died in phase 3 is large and well-tended.
• Preserved lean mass on a DEXA scan is not automatically preserved strength or function. That question is still open.
• None of the three is approved, anywhere, for anything — and long-term safety of chronically blocking a fundamental growth pathway is unestablished.
• The grey-market warning is even blunter than usual: these are monoclonal antibodies, made in living-cell bioreactors with cold-chain handling. A peptide-synthesis vendor cannot make one. Any 'bimagrumab' vial on a research-chem site is a scam by definition, not just by probability.
• Myostatin inhibitors sit on the WADA prohibited list. If you compete in tested sport, this entire category is a ban waiting to happen.

Questions to ask a qualified professional

• Is a GLP-1 medicine appropriate for me, and which approved one fits my situation?
• How should I protect muscle during weight loss with what's proven today — protein targets, resistance training, monitoring?
• How much of my weight loss is fat vs lean mass, and how would we measure that?
• When muscle-preservation drugs reach approval, what would make me a sensible or terrible candidate?

We're peptide nerds, not your doctor. This is education about where the field is heading, not a protocol — the medicines are prescribed by clinicians, the trial drugs are unobtainable, and the maths on protein is nutrition-textbook stuff. Talk to a qualified professional before doing anything spicy.