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Harm-reduction information only β€” not medical advice. In crisis or experiencing adverse effects, contact a healthcare professional or your local emergency services immediately.

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Peptides Weight Loss Preclinical (animal) data

Adipotide

FTP peptide

58 min
Half-life
1–5 mg
Typical dose

Experimental peptide that targets the blood supply of white fat; research-stage, notable risks.

Key takeaways

  • Experimental peptide that destroys the blood vessels feeding white fat β€” no human trials exist.
  • Obese monkeys lost weight and improved insulin sensitivity, but developed reversible kidney injury.
  • Development was discontinued; it isn't approved and has no active clinical program.
  • Plotter half-life (roughly 1 hour) and bioavailability are estimates, not measurements.
🚧 Expanded guide coming soon. This compound has PK data and a source β€” a full overview, mechanism, and dosing guide is pending editorial review.

Reported dosing protocols

Protocols reported in research literature and clinic/community use β€” informational context, not a dosing recommendation.

Use case Dose Route Frequency
Human use None established β€” β€”

Pharmacokinetic summary

Model tier
Simple (tΒ½ + F, Tmax estimated)
Half-life
58 min
Bioavailability
50%
Typical dose
1–5 mg

Frequently asked questions

Has adipotide ever been tested in humans?

No. Published data stops at rodents and rhesus monkeys. The primate study showed weight loss alongside dose-dependent kidney injury, and no human trial ever followed. Any human use today sits entirely outside clinical or regulatory oversight.

Why was adipotide abandoned?

The kidney toxicity seen in monkeys (renal tubular injury that reversed after stopping) set the risk bar too high for a weight-loss drug. Obesity compounds need wide safety margins, and a drug that injures kidneys doesn't clear that bar.

Is adipotide like other weight-loss peptides?

No. GLP-1 drugs reduce appetite; adipotide was designed to physically kill fat-tissue blood vessels. It's a fundamentally riskier mechanism with a completely different evidence base; unlike GLP-1 drugs, it has zero human data.

References

Related compounds

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