AOD-9604 dosage research: what was administered, to what, by which route.

Before the details

This page reports AOD-9604 dosage only the way studies report it: a number, a species, and a route. It is not a how-to. There is no approved human dose, because the molecule is not approved, and the one human program that set doses did not produce a weight-loss benefit.

In plain terms: scientists gave AOD-9604 to mice, rabbits, and (in tablet form) to obese adults at a range of amounts. The human trials covered daily oral doses from a quarter of a milligram up to 54 milligrams. The peptide leaves the bloodstream fast — about a three-minute half-life after an IV injection in an animal model — because the body chews it up from one end. None of that translates into a recommendation. Read every figure below as "studied at X in [species] by [route]," not as a protocol.

Doses studied, by species and route

Reported as research context, never as guidance:

• Obese (ob/ob) mice, oral: foundational preclinical dosing with synthetic hGH 177-191 in the ob/ob obesity model ^[8].
• Obese mice and beta-3 AR knockout mice, intraperitoneal: 14-day chronic IP administration ^[4].
• Humans, intravenous (Phase I): single doses across roughly 25-400 mcg/kg in early Metabolic Pharmaceuticals studies.
• Humans, oral (Phase II): daily oral doses ranging from 0.25 mg up to 54 mg across studies; a 24-week trial used 0.25 mg, 0.5 mg, and 1 mg/day ^[5].
• Rabbit knee OA, intra-articular: 0.25 mg per knee, weekly for 4-7 weeks, with or without 6 mg hyaluronic acid ^[14].

The human oral program is the centre of gravity here — and it is the program that ended without an efficacy win ^[9].

Half-life and routes studied

Half-life is short. Approximately 3 minutes after intravenous injection in a pig pharmacokinetic model; the intact peptide is rapidly cleared, degrading by sequential removal of amino acids from the N-terminus in a cascade fashion ^[7]. The disulfide bridge gives reasonable stability in lyophilised form, but in plasma the peptide is rapidly degraded from the N-terminus by aminopeptidases.

Routes studied: oral (the primary route in the human obesity program), intravenous (Phase I human PK and pig PK), intra-articular injection (the rabbit osteoarthritis model), and intraperitoneal or continuous infusion (preclinical mouse studies). Subcutaneous human pharmacokinetics have not been published in the peer-reviewed literature — a gap worth noting given how often community use assumes a subcutaneous route.

What the dosage record does not contain

It does not contain a validated human dose for any indication. It does not contain long-term human dosing data beyond about 24 weeks. It does not contain published subcutaneous human pharmacokinetics. And it does not contain evidence that any dose produces meaningful human fat loss — the pivotal trial that tested the obesity hypothesis at defined oral doses did not beat placebo ^[10]. Anyone reading dose figures here should read them as the historical record of what was studied, not as a template for use.