Mibavademab vs Metreleptin
Written by Aaron CuhaReviewed Sep 2026
The short answer
Both act on leptin signalling, and both turned out to help a specific group rather than people in general. Mibavademab cut weight only in people whose leptin was already below 8 ng per mL. It did nothing in people with higher levels.
- Mibavademab people
- 1
- Mibavademab nulls
- 1
- Metreleptin people
- 0
- Metreleptin nulls
- 0
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
Dose
No human dose established
No published study on this page has given this compound to people and reported a result.
1 human study where nobody was given it
First-hand reports are counted on each profile and never added together. This page sets two published records side by side. It does not pick a winner.
Column A
MibavademabMibavademab (REGN4461), leptin receptor agonist antibody
It 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.
Column B
MetreleptinMetreleptin (Myalept), recombinant human leptin analogue
Life-changing in people who make almost no leptin, and useless for ordinary obesity. The clearest case on this site of a hormone that only works when you are short of it.
Side by side, on the facts we can check
| What we compare | Mibavademab | Metreleptin |
|---|---|---|
| Category | Metabolic | Hormone |
| FDA status | Investigational. Not approved. One mid-stage study is marked TERMINATED (stopped early). | FDA-approved as Myalept for problems caused by too little leptin in generalised lipodystrophy, a rare condition where the body has almost no fat. It carries a boxed warning, the FDA's strongest, for two risks. The body can make antibodies that block the drug, and it can raise the risk of T-cell lymphoma, a blood cancer. It is only supplied through a restricted program. Not approved for obesity or partial lipodystrophy. |
| Half-life | 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. | Roughly three to four hours after subcutaneous injection, which is why it is dosed daily. |
| Molecular weight | Fully human monoclonal antibody, roughly 150 kDa. Not a peptide. | 16.2 kDa. A 147-amino-acid recombinant protein. |
| How it works | 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. | Metreleptin is a lab-made copy of human leptin, with one extra amino acid (methionine) added. Fat cells release leptin in line with how much fat you carry. It acts on the brain's hunger center (the hypothalamus). It turns down the nerve cells that drive hunger (NPY and AgRP) and turns up the ones that curb it (POMC). It also tells the systems for reproduction, thyroid and immunity that there is enough food. With no leptin, all those signals read as starving, no matter how much energy the body has stored. That is why replacing it does so much. In ordinary obesity, leptin is already high and the brain has stopped responding, so adding more changes little. |
| Studies in people | 4 | 1 |
| Evidence | Limited: 2 completed trials, 1 person given it | Preliminary: 1 human study where nobody was given it |
| Legal status, US | Investigational, not approved | FDA-approved, prescription only |
Frequently asked questions
What is the difference between Mibavademab and Metreleptin?
Mibavademab: It 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. Metreleptin: Life-changing in people who make almost no leptin, and useless for ordinary obesity. The clearest case on this site of a hormone that only works when you are short of it.
Which has stronger research evidence, Mibavademab or Metreleptin?
Each compound gets a band worked out from facts we counted, with the math shown. Mibavademab is Limited (2 completed trials, 1 person given it). Metreleptin is Preliminary (1 human study where nobody was given it). That counts how much has been done in people. It does not rate whether either one works, and neither one is called the winner.
Are Mibavademab and Metreleptin FDA-approved?
Mibavademab: Investigational. Not approved. One mid-stage study is marked TERMINATED (stopped early).. Metreleptin: FDA-approved as Myalept for problems caused by too little leptin in generalised lipodystrophy, a rare condition where the body has almost no fat. It carries a boxed warning, the FDA's strongest, for two risks. The body can make antibodies that block the drug, and it can raise the risk of T-cell lymphoma, a blood cancer. It is only supplied through a restricted program. Not approved for obesity or partial lipodystrophy..
Reviewed Sep 2026. This page puts two published records side by side. It is for learning, and it is not medical advice. When this site shows a dose, it is the dose a trial or a clinic actually used, or what people say they did, with the source attached. None of it tells you what to take.