Adipose Vasculature DisruptorPhase 1 Halted (Renal Toxicity)Research Chemical (no human approval)
Adipotide is a synthetic targeting peptide consisting of a homing motif (CKGGRAKDC, which binds prohibitin on white adipose tissue vasculature) fused to a pro-apoptotic domain (D(KLAKLAK)2). Designed to selectively destroy the blood vessels supplying white fat depots, causing rapid fat loss in obese primates without significantly affecting other organs in preclinical studies. Phase 1 trials in obese humans were initiated but limited by dose-dependent renal toxicity. Not FDA-approved; remains an experimental research chemical with significant safety concerns.
Quick Start
Route
Subcutaneous
Start low
0.43 mg/kg/day SubQ
Frequency
Daily during 28-day cycle
Timing
Independent
Starting dose. 0.43 mg/kg/day — Phase 1 starting
Daily for 28 days per published clinical schedule. NOT a chronic-use peptide. Renal monitoring (creatinine, BUN, urine protein) recommended throughout cycle and post-cycle.
❋
Start here. Every protocol below is ordered lowest-first. Begin at the smallest effective dose, hold about a week to assess tolerance, and step up only if needed.
Tiered Protocols · lowest first
Conservative start
ANIMAL-ONLY / RENAL RISK — Live PubMed record 22072637 reports reversible renal proximal-tubule changes in obese monkeys. No verified human dosing source is attached to this card.
ANIMAL-ONLY / RENAL RISK — Live PubMed record 22072637 reports reversible renal proximal-tubule changes in obese monkeys. No verified human dosing source is attached to this card.
0.25-0.5 mg · SubQ · Daily
animal study · Barnhart et al. 2011 (Sci Transl Med 3:108ra112)
Causes targeted cell death in the blood vessels feeding fat cells, literally starving adipose tissue of blood. The study cited here is animal research. It shows the mechanism, not a human dose, and this amount is community practice rather than a trial result.
0.25-0.5 mg
Daily
Reconstitution CalculatorU-100
050100u
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How it works
Adipotide combines two functional domains:
Targeting Domain (CKGGRAKDC)
Binds prohibitin, a protein highly expressed on white adipose tissue vasculature endothelial cells. This provides selectivity for white fat depots over other tissues.
Pro-Apoptotic Domain (D(KLAKLAK)2)
A synthetic peptide that disrupts mitochondrial membranes upon internalization, triggering apoptosis in cells where it accumulates.
Net Effect
Selective destruction of white adipose vasculature → ischemic apoptosis of underlying adipocytes → rapid fat loss. In obese primate studies, treatment produced 11% weight loss over 4 weeks with preserved lean mass.
Toxicity Mechanism
Phase 1 trials in obese men (Barnhart et al. 2014) showed dose-dependent nephrotoxicity (elevated creatinine, proteinuria) - thought to reflect renal accumulation and/or off-target prohibitin binding in the kidney. This limited dose escalation and ultimately the program's clinical viability.
Week 2-4: peak fat loss in primate models; renal signal may emerge.
Later
Weeks 4–12
Post-cycle: 4-week observation with renal labs.
03
Evidence
HumanPresent
AnimalStrong
In-vitroPresent
Each reference below was re-fetched from its PubMed record, and the quoted sentence was
confirmed to appear in that abstract and to support the claim it sits under. Follow any of
them to read the source.
Mechanism: the CKGGRAKDC targeting peptide binds vascular prohibitin in white adipose tissue.
We show that the CKGGRAKDC peptide associates with prohibitin, a multifunctional membrane protein, and establish prohibitin as a vascular marker of adipose tissue.
Evidence scope. Animal (mouse), preclinical discovery study; describes only the targeting-peptide binding mechanism, not whole-compound efficacy.
Mechanism/effect: adipotide induced apoptosis in white-adipose blood vessels and reduced weight in obese monkeys.
Treatment with adipotide induced targeted apoptosis within blood vessels of white adipose tissue and resulted in rapid weight loss and improved insulin resistance in obese monkeys.
At experimentally determined optimal doses, monkeys from three different species displayed predictable and reversible changes in renal proximal tubule function.
Evidence scope. Animal (non-human primate/monkey), preclinical; not human data.
Claims we could not support
No abstract we checked supports these for this molecule at this route. That is not the
same as saying they are false — it marks where the evidence is missing.
Exact dose/route: 0.43 mg/kg/day SubQ for 28 days. The primate abstract does not state this dose or the subcutaneous route; it cannot verify the displayed regimen.