Mibavademab dosage and evidence
Written by Aaron CuhaReviewed Sep 2026
The short answer
Mibavademab cut weight only in people whose leptin was already low, below 8 ng/mL. It did nothing in people with higher leptin. It is a rare drug that showed who it is for.
Evidence grade for Mibavademab: Limited. The rule: people have taken it in a published study, but fewer than 100 of them. The sum on this page: 2 completed trials, 1 person given it. A grade counts how much has been done to people, not whether it works.
- People given it
- 1
- Human studies
- 2
- Found nothing
- 1
Dose
No human dose established
Amounts that were given in studies sit in Human evidence on this page. None of them is a personal dose.
2 completed trials, 1 person given it
No first-hand reports gathered yet. That is a gap in what we have collected, not a finding that nothing has been reported.
Goal pages: Fat loss and metabolism, Gut health
In plain English
In plain English, from Aaron
This is how I would explain it to a friend. The evidence, with the numbers, is further down the page.
Mibavademab is an antibody shot that switches on the leptin receptor. Leptin is the hormone fat uses to tell the brain how much fat you carry. It is not a peptide. It is not approved anywhere.
What people take it for
- Weight loss in people with low leptin.
- Lipodystrophy, a rare disease where the body cannot store fat properly.
- Extra weight loss on top of tirzepatide.
What studies in people showed
In an early study against a dummy shot, it was well tolerated. Over 12 weeks, it cut weight only in people whose leptin was under 8 ng/mL. In people with higher leptin, which is most people with obesity, it did nothing. That came from a smaller group inside a small study, so it needs checking. One patient treated outside a trial had better blood fats and less liver fat. A 392 person study with tirzepatide ended in April 2026 and has not reported. A lipodystrophy study was stopped early.
What people report
Reports, not study results
The good
- It was well tolerated in the early study, and nobody made antibodies against it.
The bad
- It did nothing for weight in people with normal or high leptin.
- A lipodystrophy study was stopped early, and the reason is not public.
Where these come from: From the studies on this page. We have not collected user reports on this one yet.
My bottom line
My opinion: I like that it showed who it works for. Most people with obesity are not that person. If you want to know where you stand, a leptin blood test is the start.
An opinion, not a finding. I am a coach, not a doctor.
What it has been measured to do
Measured in people
Goals Mibavademab has been tested for in people, biggest studies first. We count only what the studies on this page say, so the real numbers may be higher.
- Losing weight1 people · 2 studies · 1 found nothing
- Feeling less hungry1 people · 1 study · 1 found nothing
- Blood sugar and insulin1 people · 1 study · 1 found nothing
- Liver fat and liver health1 people · 1 study · 1 found nothing
32 of the 36 indexed goals have no study of any kind behind Mibavademab
No study in people, animals or cells on this page reports a result for these. That does not prove Mibavademab does nothing for them. It does mean anything you have heard about Mibavademab and one of these did not come from a study cited here.
Show full evidence
What is Mibavademab?
Mibavademab cut weight only in people whose leptin was already low, below 8 ng/mL. It did nothing in people with higher leptin. It is a rare drug that showed who it is for.
Leptin is the hormone fat tissue uses to tell the brain how much fat there is. A few rare people make none, and giving it back changes their lives. In ordinary obesity, leptin is high and the brain has stopped listening. That is why leptin failed as a weight loss drug decades ago.
This antibody switches on the leptin receptor directly, with or without leptin around. The early human study is the interesting part, and it is about who, not how much. Over 12 weeks, it cut body weight in people with low leptin in the blood, under 8 ng/mL. It had no effect on weight in people whose leptin was higher. One patient given it outside a trial had better triglycerides and less liver fat.
That is a drug telling you who it works for, which almost nothing in this field does. It also explains why it is being tested with tirzepatide. Fast weight loss lowers leptin. That may create the low leptin state where this antibody does something.
In mice bred without leptin, it brought weight, eating and blood sugar back to normal.
How does Mibavademab work?
It is a fully human antibody that switches on the human leptin receptor, called LEPR, with or without leptin present. That sets it apart from metreleptin, which is lab made leptin. Metreleptin is useless where the receptor has stopped responding, or where the body has made antibodies that neutralise leptin. In mice bred without leptin, this antibody brought body weight, food intake, blood sugar and insulin response back to normal. In an animal model of lipodystrophy, a disease where the body cannot store fat properly, it eased overeating, high blood sugar, insulin resistance, bad blood fats and fatty liver.
What have studies in people found about Mibavademab?
An early human study, compared with a dummy shot, with a clear result that depended on who got it. There is also a separate report on blood levels, one patient treated outside a trial, and a mid-stage trial that was stopped early.
- Early two part study in people, compared with a dummy shot. Well tolerated, with acceptable safety.
- Body weight fell over 12 weeks in people with leptin under 8 ng/mL.
- No effect on body weight in people with higher leptin, which is most people with obesity.
- One patient treated outside a trial, with a rare partial lipodystrophy and antibodies that blocked metreleptin, had better triglycerides and less liver fat.
- A combination study with tirzepatide is registered. The thinking is that weight loss lowers leptin into the range where the drug works.
- One lipodystrophy mid-stage trial is listed as stopped early (TERMINATED).
What this does not tell you: The low leptin weight loss result comes from a smaller group picked out within an early study. That is the weakest place to find an effect in one kind of person, and the most likely place for a fluke. It needs repeating in a study built around that 8 ng/mL cutoff. The one patient treated outside a trial cannot support any general claim. And the group where this worked is small. Most people with obesity have high leptin, which is exactly where the antibody did nothing.
The state of the research
Leptin is the warning story of weight loss drugs. Its discovery in 1994 looked like the answer. Then giving it to people with ordinary obesity did almost nothing, because their leptin was already high and the brain had stopped responding. Everything since has had to work around that.
What makes this antibody interesting is that it did not repeat the mistake. The early study found the line instead of averaging across it. Below 8 ng/mL of leptin it worked, and above that it did not. Most drug programmes would report a modest overall effect and hide both halves. Reporting the cutoff is more useful and also more limiting, because it points to a small group of people.
The tirzepatide combination is the interesting next step. Fast weight loss may drop leptin into the range where this antibody acts. If so, a drug that fails in obesity might work in people who have already lost weight. That is a different question from the one leptin failed at.
The evidence, in charts
Fig. 1a · how many people
1people, across 1 study in people cited here
| Study | People | Share |
|---|---|---|
| Science Translational Medicine 2023 | 1 | 100% |
The whole total is one study of 1. Counts are the number of people each study on this page says it signed up. That includes studies that only watched people and gave nobody the compound. 3 more studies in people give no headcount and are not counted here. Studies still signing people up are left out, and only studies cited on this page are counted.
Fig. 1b · evidence mix
All 4 sources here are studies in people.
- Study in people · done in people4100%
Counted from the list of sources on this page. It counts only what we cite, so there may be more studies out there. A review counts once, however many studies it sums up.
Fig. 2 · evidence over time
The studies cover 3 different years, 2023 to 2026, counted from the list of sources on this page.
Fig. 3 · legal status at a glance
US
Not approved
UK
Not approved
AU
Not approved
CA
Not approved
Not approved in any of the four countries shown. This is what the law says, not a verdict on the science. See Legal status below for the full text and any notes.
Fig. 4 · how much does what
Nobody has tested different amounts in people
This chart would show how the effect changes as the amount goes up. For this compound, nobody has measured that in people. So we leave it empty. We will not borrow an animal chart and pretend it works the same in people.
Fig. 5 · what the molecule is
- Kind of compound
- Biologic
- Molecule weight
- Fully human monoclonal antibody, roughly 150 kDa. Not a peptide.
- Half-life
- Stated in words, not a numbersee the exact wording below
- Chain length
- None on file
Half-life as stated on file: Not asserted. Pharmacokinetics were characterised in a first-in-human study; no half-life figure was resolved in the sources loaded. Monoclonal antibodies of this class generally clear over weeks.
No amino acid sequence is on file for Mibavademab, so none is drawn rather than guessed from a name.
The studies we cite
- Study in people2023Preclinical, randomized phase 1, and compassionate use evaluation of REGN4461, a leptin receptor agonist antibody for leptin deficiency
The antibody only worked in people who were already short of leptin. In an early study in people, compared with a dummy shot, it was well tolerated. In the authors' words, it reduced body weight over twelve weeks in people with low leptin in the blood, and had no effect on weight in people whose leptin was higher. One patient given it outside a trial had better triglycerides and less liver fat. In mice bred without leptin, it brought weight, eating and blood sugar back to normal.
A fully human antibody activating the leptin receptor with or without leptin. In obese leptin knockout mice it normalised body weight, food intake, blood glucose and insulin sensitivity. In a randomised double-blind placebo-controlled two-part phase 1 it was well tolerated. Verbatim: treatment of individuals with overweight or obesity decreased body weight over 12 weeks in those with low circulating leptin concentrations, under 8 ng/mL, but had no effect on body weight in individuals with higher baseline leptin. Compassionate use in one patient with atypical partial lipodystrophy and neutralising antibodies to metreleptin was associated with improvements in triglycerides and hepatic steatosis.
- Study in people2024Pharmacokinetics and pharmacodynamics of mibavademab (a leptin receptor agonist): results from a first-in-human phase I study
The blood-level report from the first human study carries a real result of its own. 56 people completed the single-dose part and 55 the repeat-dose part. Blood levels did not rise in step with the dose, because the drug is mopped up by its own target. In the repeat-dose part, the people whose leptin was under 8 nanograms per millilitre lost more weight on average than those whose leptin was higher. Nobody developed antibodies against the drug. Regeneron employees ran and wrote it up.
The dedicated pharmacokinetic and pharmacodynamic report from the first-in-human programme.
- Study in people2026A study of mibavademab in combination with tirzepatide in adults with obesity
The combination trial has finished and has published nothing. Eli Lilly enrolled 392 adults with obesity to compare tirzepatide plus mibavademab against tirzepatide alone, and it completed in April 2026. No results are posted. It matters because losing weight fast drives leptin down, and low leptin is the only state in which this antibody has done anything in people.
The combination programme. Relevant because rapid weight loss lowers leptin, which is the state in which this antibody had an effect in phase 1.
- Study in people2024A study of REGN4461 in patients with lipodystrophy
The trial in the disease this drug was aimed at was stopped early. Regeneron enrolled 20 adults with an inherited partial lipodystrophy and terminated it in April 2024. The registry does carry posted results. A terminated trial belongs in the record, because a drug programme that halts in its target disease tells you something a list of ongoing studies never will.
Registry status TERMINATED. Reported because a terminated trial is part of the record.
Common questions
Has Mibavademab been tested in people?
Yes. 1 person given it across 2 completed trials cited here, 1 of which found nothing. Mibavademab cut weight only in people whose leptin was already low, below 8 ng/mL. It did nothing in people with higher leptin. It is a rare drug that showed who it is for.
What is the Mibavademab dosage?
No human dose established. Amounts that were given in studies sit in Human evidence on this page. None of them is a personal dose. 2 completed trials, 1 person given it
Is Mibavademab FDA-approved?
Investigational. Not approved. One mid-stage study is marked TERMINATED (stopped early).
Does mibavademab cause weight loss?
Only in people whose leptin is already low, under 8 ng/mL. In people with higher leptin, which describes most people with obesity, it had no effect on body weight over 12 weeks. That comes from a smaller group inside an early study, so it needs confirming in a study built around that cutoff.
How is it different from metreleptin?
Metreleptin is leptin itself. So it fails where the receptor has stopped responding, or where a patient's body has made antibodies against leptin. This antibody switches on the receptor directly, with or without leptin present. That is why the one patient treated outside a trial was someone who had antibodies to metreleptin.
Why combine it with tirzepatide?
Because fast weight loss lowers leptin, and low leptin is when this antibody had an effect. If that holds, it would work in people after weight loss rather than in people with untreated obesity. That study is registered and has not reported.
What does the terminated trial mean?
One lipodystrophy mid-stage trial is listed as stopped early (TERMINATED) on ClinicalTrials.gov. The reason is not in the public record, and this page does not guess. The rest of the programme continues.