Pemvidutide
ALT-801
Pemvidutide (ALT-801) is a metabolic & fat loss research compound. GLP-1/glucagon dual agonist — glucagon arm drives energy expenditure and hepatic fat loss on top of GLP-1 appetite control.
Pemvidutide quick facts
| Reported research dose | 1.2mg-2.4mg |
| Route | Subq |
| Frequency | 1x Weekly |
| Half-life | ~Weekly dosing |
| Forms | Injectable |
| Evidence level | Phase 2 human (~15.6% at 2.4mg) |
Strong body-comp and liver data. Same dual logic as survo/mazdutide.
How Pemvidutide works
GLP-1/glucagon dual agonist — glucagon arm drives energy expenditure and hepatic fat loss on top of GLP-1 appetite control.
Proposed benefits
Researched for fat oxidation, appetite and energy regulation, insulin sensitivity and endurance capacity.
Where to get Pemvidutide
See vetted vendors for Pemvidutide →Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for Pemvidutide
Graded by what exists behind each claim.
✅ Clinically validated
- In phase 2. Altimmune's GLP-1/glucagon dual agonist. The MOMENTUM obesity trial reported around 15.6% weight loss at 48 weeks, with the company highlighting that roughly 75% of the loss was fat mass rather than lean — unusually high preservation for this class.
- Phase 2 in MASH reported significant liver fat reduction. Lean-mass preservation is a claim to watch rather than accept — body-composition sub-studies are small and methodologically variable.
📊 Correlative data
- No marketed use. Trial tolerability is class-typical, with the glucagon-driven heart rate increase noted as with the other duals.
🧪 Theoretical / extrapolated
- A GLP-1/glucagon dual agonist engineered with a 1:1 receptor ratio — a deliberately higher glucagon weighting than most competitors, using a lipid modification for duration.
- The ratio is the whole design thesis. More glucagon means more energy expenditure and more hepatic fat oxidation, which is the mechanistic case for both the lean-mass and liver findings. It also means more of glucagon's downsides, and where the optimal ratio sits is genuinely unsettled.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Pemvidutide actually does
The first thing to fix is which drug this is. Pemvidutide is sold on this site as a weight-loss compound, and the entire peer-reviewed record for it is liver: three randomized trials, all in fatty liver disease, two of them with a biopsy or an MRI endpoint Harrison 2024 Browne 2025 Noureddin 2025. The obesity phase 2 that everybody quotes — the 15.6% figure on the card — has no primary publication in the indexed literature. It exists as a company presentation. That does not make it false; it makes it a different tier of evidence from the three liver trials, and no page anywhere draws the distinction.
The mechanism: GLP-1 plus glucagon, and the glucagon arm is the whole point. A GLP-1 receptor agonist reduces intake. A glucagon receptor agonist increases expenditure and, specifically, drives hepatic fat oxidation — the liver burns its own stored triglyceride. Those are two different levers on the same scale, and combining them is why a dual can outperform a single at a matched GLP-1 exposure.
The ratio, and what is actually published about it. This site’s card states a 1:1 GLP-1-to-glucagon ratio and calls it the design thesis, which is a fair summary of the developer’s public position. It is worth being exact about where that number comes from: none of the three published trials prints a receptor potency ratio Harrison 2024 Browne 2025 Noureddin 2025. For a molecule whose entire differentiation is its glucagon weighting, the defining number is not in the peer-reviewed record. That is not unique to this compound — it is true of every multi-agonist in this cohort — but it is most conspicuous here, because here the ratio is the marketing.
The evidence that the glucagon arm is real does not come from a ratio. It comes from the liver. At 12 weeks, relative liver-fat reduction was 46.6% at 1.2 mg, 68.5% at 1.8 mg and 57.1% at 2.4 mg, against 4.4% on placebo, p < 0.001 Harrison 2024. A GLP-1 alone does not do that in 12 weeks at 6% body-weight loss. Something is oxidizing hepatic fat faster than the weight is coming off, and glucagon receptor agonism is the available explanation.
Now look at those three numbers again, because they are not monotonic. 46.6, then 68.5, then 57.1. The middle dose beat the top dose. The same paper reports that weight loss, alanine aminotransferase and corrected cT1 all reached their maximum at 1.8 mg rather than at 2.4 mg Harrison 2024. Four separate readouts peaked at the middle dose. That is either small-group noise in a 94-person trial with four arms, or it is a genuine inverted-U — and there is a mechanistic story for the second: past some threshold the glucagon arm’s effect on hepatic glucose output and on appetite-independent metabolic stress may start to cost more than the extra fat oxidation buys. The developers appear to have taken it seriously: the pivotal 48-week MASH trial dropped 2.4 mg entirely and ran 1.2 and 1.8 mg Noureddin 2025. The site’s dose card still tops out at 2.4 mg, which is the dose the sponsor stopped using.
Cell, rodent, human — and where it stops
Step one, in cells and in animals: not published under this name. No discovery paper, no receptor-activation assay and no rodent study for pemvidutide appears in the indexed literature. That is a genuine hole. Every other compound in this cohort with phase 2 or phase 3 data also has a discovery paper describing what it does to a receptor; this one starts at humans.
Step two, humans, 12 weeks, liver fat by MRI. 94 participants with BMI ≥ 28.0 kg/m2 and liver fat content ≥ 10%, randomized to pemvidutide 1.2, 1.8 or 2.4 mg or placebo weekly for 12 weeks (NCT05006885). Relative liver-fat reductions 46.6%, 68.5% and 57.1% versus 4.4% on placebo, p < 0.001. At 1.8 mg, 94.4% of participants achieved a ≥ 30% liver-fat reduction and 55.6% reached normalization at ≤ 5% liver fat Harrison 2024.
Step three, the same people carried to 24 weeks. 64 completers continued their original doses (NCT05292911). Baseline mean BMI 36.7 kg/m2, liver fat 22.2%, 26.6% with type 2 diabetes. At 24 weeks the relative liver-fat reductions were 56.3%, 75.2% and 76.4% against 14.0% on placebo, p < 0.001; at 1.8 mg, 84.6% achieved a ≥ 50% reduction and 53.8% normalized. Body weight fell 6.2% over the 24 weeks, p < 0.001 Browne 2025. Two things worth noticing: the placebo arm’s liver fat fell 14% by itself, which is what trial participation does and is why uncontrolled liver-fat anecdotes are worthless; and the non-monotonicity resolved by 24 weeks, with 1.8 and 2.4 mg landing together.
Step four, the pivotal trial — and this is where the page earns its keep. IMPACT: 48-week, double-blind, phase 2b, biopsy-confirmed MASH with F2/F3 fibrosis, 83 sites across the USA and Australia, 212 randomized (NCT05989711). The published 24-week results carry two primary endpoints, and the drug met one and missed the other.
Met. MASH resolution without worsening of fibrosis: 20.9% on placebo (18 patients), 58.5% at 1.2 mg (24 patients; difference 38%, 95% CI 21–56; p < 0.0001) and 52.9% at 1.8 mg (45 patients; difference 32%, 95% CI 19–46; p < 0.0001) Noureddin 2025.
Missed. Fibrosis improvement without worsening of MASH: 27.9% on placebo (24 patients), 31.7% at 1.2 mg (p = 0.59) and 35.3% at 1.8 mg (p = 0.27) Noureddin 2025. Neither dose separated from placebo.
That pair of results is the most informative thing about this drug, and it is the thing nobody quotes. Read together they say: pemvidutide clears the inflammation and the fat — the steatohepatitis — decisively and at both doses, and over 24 weeks it does not measurably reverse the scar. Those are different biology. Fat clears in weeks; collagen turns over in months to years. So the honest reading is not ‘the drug failed’ — it is that a 24-week readout is short for a fibrosis endpoint and that the fibrosis question is still open at 48 weeks.
The obstacles, named one at a time. (1) Everything above is liver, and this compound is bought for weight. The largest published weight number is 6.2% at 24 weeks Browne 2025, in people selected for liver fat rather than for obesity. The 15.6% figure on the card comes from an obesity trial with no primary publication. (2) The lean-mass claim is unpublished. ‘Roughly 75% of the loss was fat mass’ is a company statement; no indexed pemvidutide paper reports body composition. (3) No cardiovascular outcome data and no phase 3 readout. (4) No head-to-head against a GLP-1, a GIP/GLP-1 dual or the triple agonist whose liver numbers are larger — retatrutide cut liver fat 81.4% at 8 mg by 24 weeks Sanyal 2024, against pemvidutide’s 75.2% at 1.8 mg over the same interval, in different populations and different trials, which is exactly why the comparison needs running rather than asserting.
Pemvidutide pharmacokinetics — how much of it actually gets in
The catalog says ‘~Weekly dosing’. That is a schedule, and no published pemvidutide half-life exists to replace it. None of the three trials reports a terminal half-life, a Cmax or an AUC Harrison 2024 Browne 2025 Noureddin 2025. So this section is a bound, built from what the molecule has to be doing.
What holds it in the body. A once-weekly peptide in this class survives by reversible albumin binding through a lipid side chain: bound drug is too large for glomerular filtration and is shielded from circulating peptidases, and the free fraction is topped up continuously from that depot Muller 2022. The dosing interval is the evidence — a peptide without that modification cannot be given weekly at all.
What degrades it. Once free of albumin, proteolysis by plasma and tissue peptidases, plus renal handling of the unbound fraction. Not a cytochrome substrate, which is why this class carries no CYP-interaction list; the one such study performed anywhere in this cohort found a sibling compound changed rosuvastatin exposure by 6% and digoxin exposure by 16%, both inside the range that gets called no interaction Li 2026.
The number, borrowed and labeled as borrowed. The only measured half-life in this cohort belongs to ecnoglutide: 124 to 138 hours at steady state, 5.2 to 5.8 days Guo 2023. Any weekly acylated incretin sits near there, which puts steady state at roughly 4 to 5 weekly doses — about a month. That single number reframes the trial data: the 12-week readout Harrison 2024 captured roughly 8 weeks at steady state, not 12, and the non-monotonic dose response sits inside that shorter window. By 24 weeks Browne 2025 the same doses had 20 weeks at steady state and the anomaly had resolved. That is not proof, but it is the cheapest available explanation and it can be checked by anyone who plots the two papers together.
The oral barrier. Absolute. Gastric acid, pancreatic proteases, brush-border peptidases, then hepatic first-pass extraction for anything that crosses. No oral pemvidutide exists and none is described.
The injectable comparator. Every human dose in every published trial was subcutaneous, once weekly, at 1.2, 1.8 or 2.4 mg. Note that the pivotal MASH trial ran only 1.2 and 1.8 mg Noureddin 2025: the top of the site’s dose range is a dose the sponsor stopped taking forward.
What would have to be true, and how you would know it was not
Four predictions. The second one cuts against the compound, and the third is the one that would settle the argument this drug is actually in.
1. ALT should fall, early, and out of proportion to the weight lost. Alanine aminotransferase improved maximally at 1.8 mg in the 12-week trial Harrison 2024, and the 24-week extension took liver fat down 75.2% while body weight fell only 6.2% Browne 2025. That ratio is the glucagon arm’s fingerprint. Draw a CMP at baseline, 6 weeks and 12 weeks and watch ALT. The prediction that distinguishes this drug from a plain GLP-1 is that ALT falls faster than the scale does. If ALT tracks weight one-for-one, the glucagon arm is not contributing what the design claims.
2. Resting heart rate should rise, and this is the cost side of the glucagon arm. Heart-rate elevation is a measured, meta-analyzed consequence of incretin agonism Yang 2023, and adding glucagon adds to it. Seated resting pulse, every morning before caffeine, for a week before starting and weekly after. This is the prediction that argues against the product: the same receptor that produces the liver result produces the tachycardia, and no formulation change separates them.
3. Fasting glucose and HbA1c, watched for the wrong direction. Glucagon raises hepatic glucose output; GLP-1 suppresses it. A deliberately glucagon-heavy ratio is exactly the design in which that balance could tip. 26.6% of the 24-week cohort had type 2 diabetes Browne 2025, so the question has been asked in a small way and never isolated. Draw HbA1c and fasting insulin at baseline, 12 and 24 weeks. Weight falling with fasting glucose rising is a ratio problem, and it is visible on a standard panel.
4. Lean mass will not be spared, and the 75% claim needs a scan. Across weight-loss pharmacotherapy more than 25% of total weight lost comes from fat-free mass Stefanakis 2024. The company’s 75%-fat-mass figure would be a genuine outlier if replicated, and no indexed pemvidutide paper reports body composition at all. Measure grip strength at baseline, 12 and 24 weeks, and a DXA if you can get one. Grip falling with weight is the failure this compound is specifically marketed as avoiding, which makes it the one worth measuring here.
What nobody has tested yet
Four things nobody has tested, and the first one is not exotic at all.
1. Nobody has published what this molecule does to a receptor. There is no discovery paper, no cAMP EC50, no binding constant and no potency ratio in the indexed literature for pemvidutide. The 1:1 ratio that is the entire commercial thesis has never appeared in a peer-reviewed publication. A single receptor-activation panel would move this compound from ‘claimed ratio’ to ‘measured ratio’ and would let it be compared with mazdutide, survodutide and retatrutide on the axis that actually differentiates them.
2. Whether the fibrosis endpoint moves at 48 weeks. The published IMPACT readout is 24 weeks, and fibrosis did not separate from placebo at either dose Noureddin 2025. The trial runs to 48. Collagen turnover is slower than fat turnover, so a null at 24 weeks and a positive at 48 is a live possibility rather than special pleading — and it is the single result that decides whether this is a liver drug or a liver-fat drug.
3. Whether the inverted-U at 12 weeks is real. Liver fat, weight, ALT and cT1 all peaked at 1.8 mg rather than 2.4 mg in the same trial Harrison 2024, and the sponsor subsequently dropped 2.4 mg Noureddin 2025. Nobody has run 1.8 versus 2.4 mg to steady state with liver fat as the primary endpoint, which is the experiment that would separate ‘noise in a 94-person study’ from ‘a genuine ceiling on glucagon agonism’. It is one of the more interesting unrun experiments in this class, because a real ceiling would apply to every glucagon-containing molecule and not just this one.
4. Whether the liver effect survives weight-matching. No trial has compared pemvidutide against a diet arm producing the same weight loss. Until that exists, the split between ‘glucagon-driven hepatic fat oxidation’ and ‘what happens to any liver when the person loses 6% of their weight’ is an assumption. The 24-week data makes the assumption look reasonable — 75.2% liver fat against 6.2% weight Browne 2025 is a very steep ratio — but reasonable is not measured.
Pemvidutide — its own safety story, not its class's
The class block on this page is written for GLP-1 receptor agonists. This molecule has a second receptor, and the second receptor carries most of what is specific here.
1. What the trials actually reported, stated plainly. In the 48-week MASH trial, adverse events occurred in 78–81% of treatment groups against 67% on placebo, predominantly mild to moderate, and discontinuations for adverse events were none at 1.2 mg, one (1.2%) at 1.8 mg and two (2.3%) on placebo Noureddin 2025. More people stopped placebo than stopped the top dose. That is an unusually clean tolerability signal for this class and it deserves saying as loudly as the risks.
2. Heart rate is the glucagon-specific risk. Incretin agonism raises heart rate as a measured class effect Yang 2023, and a deliberately glucagon-weighted molecule has more of the receptor that drives it. This is not a titration artifact that fades; the retatrutide phase 2 showed the rise building over months before declining Sanyal 2024. A resting pulse is free and nobody takes one.
3. Hepatic glucose output, which is the risk that runs opposite to expectation. People take this for a fatty liver and for weight. Glucagon receptor agonism raises hepatic glucose production, and the GLP-1 arm is what keeps that from showing up as hyperglycemia. In someone on insulin or a sulfonylurea, the interaction is bidirectional and the ratio governing it has never been published.
4. Gallbladder disease, sized properly. Across 76 randomized trials and 103,371 patients, GLP-1 receptor agonist use carried a relative risk of gallbladder or biliary disease of 1.37 (95% CI 1.23–1.52), rising to 2.29 (1.64–3.18) in weight-loss trials and increasing with dose and duration He 2022. Rapid hepatic fat mobilization is exactly the physiology that concentrates bile. Right upper quadrant pain after meals is the symptom.
5. The honest limit of the safety record. The published safety database for pemvidutide is roughly 370 people across three trials, the longest of which reports 24 weeks Harrison 2024 Browne 2025 Noureddin 2025. There is no cardiovascular outcome trial, no pregnancy data, no long-term registry and no post-marketing surveillance, because there is no market. Anything said about years of use is extrapolation from a 24-week record.
Sources read for this page
- Harrison SA, et al. Effect of pemvidutide, a GLP-1/glucagon dual receptor agonist, on MASLD: A randomized, double-blind, placebo-controlled study. Journal of Hepatology 2024 · PMID 39002641
- Browne SK, et al. Safety and efficacy of 24 weeks of pemvidutide in metabolic dysfunction-associated steatotic liver disease: A randomized, controlled clinical trial. JHEP Reports 2025 · PMID 41113119
- Noureddin M, et al. Safety and efficacy of weekly pemvidutide versus placebo for metabolic dysfunction-associated steatohepatitis (IMPACT): 24-week results from a multicentre, randomised, double-blind, phase 2b study. Lancet 2025 · PMID 41237796
- Sanyal AJ, et al. Triple hormone receptor agonist retatrutide for metabolic dysfunction-associated steatotic liver disease: a randomized phase 2a trial. Nature Medicine 2024 · PMID 38858523
- Guo W, et al. Discovery of ecnoglutide - a novel, long-acting, cAMP-biased glucagon-like peptide-1 (GLP-1) analog. Molecular Metabolism 2023 · PMID 37364710
- Li F, et al. Effect of a Novel GLP-1 Analogue Ecnoglutide on the Pharmacokinetics of Rosuvastatin and Digoxin in Healthy Participants. Diabetes, Obesity and Metabolism 2026 · PMID 42310888
- Yang Y, et al. Impact of a dual glucose-dependent insulinotropic peptide/glucagon-like peptide-1 receptor agonist tirzepatide on heart rate among patients with type 2 diabetes: A systematic review and pairwise and network meta-analysis. Diabetes, Obesity and Metabolism 2023 · PMID 37860884
- He L, et al. Association of Glucagon-Like Peptide-1 Receptor Agonist Use With Risk of Gallbladder and Biliary Diseases: A Systematic Review and Meta-analysis of Randomized Clinical Trials. JAMA Internal Medicine 2022 · PMID 35344001
- Stefanakis K, et al. The impact of weight loss on fat-free mass, muscle, bone and hematopoiesis health: Implications for emerging pharmacotherapies aiming at fat reduction and lean mass preservation. Metabolism 2024 · PMID 39481534
- Muller TD, et al. Anti-obesity drug discovery: advances and challenges. Nature Reviews Drug Discovery 2022 · PMID 34815532
Pemvidutide — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- These slow gastric emptying and act on hypothalamic and brainstem appetite centers. Almost everything that goes wrong follows from the gastric emptying, not from anything exotic: nausea, early fullness, reflux, constipation, and — when someone titrates faster than their gut adapts — vomiting.
- The composition risk is the one nobody warns about. Appetite suppression does not discriminate. It suppresses the appetite for protein too, and in a deficit without adequate protein and a resistance stimulus a meaningful share of the loss is lean mass. That lowers the maintenance intake you eventually eat back into, which is the mechanism behind most of the rebound stories.
- Slowed emptying also delays absorption of anything else taken by mouth — a pharmacokinetic consequence rather than a drug interaction, but it matters for anything time-critical.
What has actually been reported
- GI effects are extremely common and mostly settle over weeks. Gallbladder problems are a recognized signal, and rapid weight loss of any cause raises gallstone risk — the drug is not doing something unusual, it is doing rapid weight loss well.
- Pancreatitis is reported and rare. The presentation to know is severe upper abdominal pain radiating to the back, usually with vomiting.
- A thyroid C-cell tumor signal exists in rodents and has not been demonstrated in humans; it is why the labeled contraindication for medullary thyroid carcinoma and MEN2 exists.
How to reduce the risk
Same mechanism as the prediction.
- Follow the titration schedule even if you feel fine. It exists for gut adaptation, not for legal cover. Almost everyone who quits in the first month escalated faster than their stomach could keep up.
- Hit your protein target first at every meal, before anything else on the plate. This is the single highest-leverage habit on the drug — 1.6–2.2 g/kg, and eat it while you still have the appetite to.
- Lift while you are on it. The compound handles intake; resistance training is the only thing handling what you keep.
- Aim for 0.5–1% of bodyweight per week, deliberately. The drug removes the hunger signal that would normally stop you going too hard, so the rate has to be a decision rather than a by-product.
- Fiber and electrolytes from day one, not from week four when constipation has already made up your mind about the drug.
- If nausea is winning, step back one dose rather than quitting the class. Almost nobody needs to be at the top of the range.
What it does to your bloodwork
A fact about the assay.
- HbA1c and fasting glucose should improve — that is the drug working, and it is the cleanest confirmation you have.
- Rapid loss moves lipids, liver enzymes and uric acid transiently. A wobble at 8 weeks into aggressive loss is usually the loss, not a new problem — but it is a reason to have the baseline.
- Worth a thyroid panel and a lipid panel before starting, simply so a later result has something to be compared against.
Don't run this if
- Personal or family history of medullary thyroid carcinoma, or MEN2.
- Previous pancreatitis.
- Active gastroparesis — you would be adding a drug whose main action is the thing already wrong.
The honest unknown
- What happens to body composition over repeated multi-year cycles of loss and regain on and off these drugs. Weight is well studied; the muscle-to-fat ratio of what comes back is not.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Pemvidutide — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Pemvidutide moves on your bloodwork
Expected direction, not a measured one.
- HbA1c (Hemoglobin A1c) — ↓ expected to fall
Falling HbA1c is the compound working. Expect it.
What to do: Baseline and 12 weeks. It moves slowly by design — a 4-week retest tells you very little. - Fasting Insulin — ↓ expected to fall
Insulin sensitivity improves as weight falls and the incretin effect restores first-phase insulin release.
What to do: Useful alongside HbA1c; the two together read the trend properly. - Lipid Panel (Cholesterol, HDL, LDL, Triglycerides) — ↓ expected to fall
Triglycerides in particular fall with weight loss and improved insulin sensitivity.
What to do: Re-check at 12 weeks rather than chasing early numbers. - Lipase — ↑ expected to rise
Lipase and amylase can rise without pancreatitis on this class. An isolated mild elevation in someone with no symptoms is common.
What to do: Severe, persistent abdominal pain radiating to the back is the thing that matters, not the number. Symptoms decide, not a mild enzyme rise. - Comprehensive Metabolic Panel (CMP) — ◆ worth watching
Rapid weight loss and reduced intake shift electrolytes and kidney markers; dehydration from nausea or vomiting shows up here first.
What to do: Worth a baseline. If you have been vomiting, this is the panel that catches the consequence. - Ferritin — ↓ expected to fall
Not the drug — the eating. Sharply reduced intake drops iron, B12 and protein intake with it, and this is the most commonly missed consequence of a good response.
What to do: Check ferritin and B12 at 12 weeks. Muscle loss and hair shedding on a GLP-1 is very often a nutrition problem wearing a drug's name.
The pattern with this class is that the frightening-looking numbers (lipase) are usually fine and the boring ones (ferritin, B12) are where the real damage happens.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Needle gauge and injection site
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Pemvidutide in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Pemvidutide
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| HbA1c (Hemoglobin A1c) | Where you started, so you can prove the change was real |
| Fasting Insulin | Moves years before HbA1c does — the earliest signal you get |
| Lipid Panel (Cholesterol, HDL, LDL, Triglycerides) | Rapid fat loss shifts triglycerides fast, in both directions |
| Comprehensive Metabolic Panel (CMP) | Liver, kidney and electrolytes while intake is restricted |
The Metabolic Health & Prediabetes panel covers these in one order — 8 markers, $81.45 with the discount applied.
Check results you already have → · All 103 markers A–Z
Pemvidutide — frequently asked questions
What is Pemvidutide?
Pemvidutide (ALT-801) is a metabolic & fat loss research compound. GLP-1/glucagon dual agonist — glucagon arm drives energy expenditure and hepatic fat loss on top of GLP-1 appetite control.
Is the full Pemvidutide protocol on this page?
The reported research dose is on this page, along with how Pemvidutide works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of Pemvidutide?
Pemvidutide has an approximate half-life of ~Weekly dosing, which is part of what determines how often it's dosed.
What's the evidence behind Pemvidutide?
Current evidence level: Phase 2 human (~15.6% at 2.4mg). Pemvidutide is offered for research purposes only and is not an approved medicine.
What Pemvidutide is used for
Pemvidutide appears under 2 goals in the goal router.
Related Metabolic & Fat Loss compounds
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.