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Adipotide (FTPP)9 residuesCKGGRAKDCEach bubble = one amino acid. Size = residue mass. Color = chemical class.Also known as: FTPP, Fat-Targeted Proapoptotic Peptide, Prohibitin-TP01
Obese rhesus monkeys lost 38% of their total body fat in 28 days. Adipotide (FTPP, Prohibitin-TP01) is a chimeric peptidomimetic that starves fat cells by destroying the blood vessels feeding them. The mechanism worked so well it couldn't be separated from kidney damage. MD Anderson's Phase 1 human trial was terminated for nephrotoxicity at doses 70 times below the effective primate dose. Arrowhead Research shut down all clinical development in 2019. A small number of forum users still attempt very low doses with kidney monitoring, but the community consensus calls this "impressive science, too dangerous to use."
Obese monkeys lost 7 to 15% of their body weight in four weeks. That's the headline from Barnhart and colleagues' 2011 primate study [1], published in Science Translational Medicine. MRI and DEXA confirmed a 38% drop in total body fat and 27% reduction in abdominal fat. Insulin resistance improved alongside the fat loss. Adipotide (also called FTPP or Prohibitin-TP01) is a synthetic peptidomimetic with two connected domains. The homing peptide (CKGGRAKDC) locks onto prohibitin on the surface of blood vessel cells lining white adipose tissue. The proapoptotic domain, D(KLAKLAK)2, then destroys those endothelial cells from the inside by collapsing their mitochondrial membranes. Without blood supply, downstream fat cells die from oxygen starvation. The mechanism is genuinely different from anything else in weight loss pharmacology. GLP-1 agonists suppress appetite. Adipotide physically dismantles the vasculature feeding fat depots. Then the kidneys became the problem. Every treated primate showed dose-dependent renal lesions. When MD Anderson ran a Phase 1 human trial in 2012, nephrotoxicity appeared at 0.03 mg/kg/day, roughly 70-fold lower than the primate effective dose. The trial was terminated. All clinical development ended permanently in 2019; no new trials are registered or planned. Adipotide sits in an almost unique pharmacological category: dramatic efficacy that cannot be separated from its own toxicity. It's available only as a research chemical with no pharmaceutical-grade product on the market.
Two functional domains joined by a glycine-glycine linker. That's the architecture of adipotide. The N-terminal homing domain (CKGGRAKDC) is a cyclic peptide identified through in vivo phage display screening. It binds prohibitin (PHB), a membrane protein on the luminal surface of endothelial cells lining white adipose tissue vasculature. Prohibitin sits in a trimolecular complex with annexin A2 and CD36, regulating fatty acid transport from blood into fat tissue. Once prohibitin binding occurs, the peptide enters the cell through receptor-mediated endocytosis. The C-terminal proapoptotic domain takes over from there. D(KLAKLAK)2 is a synthetic amphipathic peptide built entirely from D-amino acids, making it resistant to proteolytic degradation. Inside the cell, this domain localizes to the mitochondrial outer membrane. Its amphipathic structure inserts into that membrane and disrupts it. Membrane potential collapses. Cytochrome c releases. Caspases activate. The intrinsic apoptotic cascade kills the endothelial cell. Scale that process across the microvasculature of a fat depot and you get ischemic death of the adipocytes downstream. No blood supply means no oxygen, no nutrients, no survival. The kidney problem traces to the same domain. During renal filtration and excretion, D(KLAKLAK)2 causes collateral apoptosis in proximal tubular epithelial cells. The compound can't distinguish between target endothelial cells and kidney cells it passes through during clearance.
Adipotide produced dramatic fat loss in primate studies: 7–15% body weight, 38% total fat in 28 days. The mechanism (vascular ablation of adipose tissue) is well-characterized and genuinely novel. However, dose-dependent nephrotoxicity was observed in every treated animal, and the Phase 1 human trial was terminated due to kidney toxicity at doses 70x below the effective primate dose. No human efficacy data exists. All clinical development was discontinued in 2019. No new clinical trials are registered or planned as of 2026.
Barnhart et al. 2011, "A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys" (Sci Transl Med, PMID 22072637)
No completed human trial. Primate efficacy cannot be separated from primate nephrotoxicity: the effective dose range overlaps the toxic dose range. Human kidneys appear far more sensitive than primate kidneys.
Community interest is infamy-driven: most threads discuss the danger rather than personal use. A small number of users on MESO-Rx, ExcelMale, and eroids report trying 0.5–1 mg/day for short runs. Reports of fat loss exist but are sparse, uncontrolled, and overshadowed by the Bostin Loyd death. The overwhelming consensus is "impressive science, too dangerous to use."
Science and community agree that adipotide causes fat loss and damages kidneys. They diverge on whether any dose is usable: science says no (the trial was terminated), while a tiny minority of community users attempt very low doses with monitoring. The community is not enthusiastic: this is not a BPC-157 or semaglutide situation. Most forum discussions are cautionary, not protocol-sharing.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 0.5mg | Daily |
| Moderate | 1mg | Daily |
| Aggressive | 2mg | Daily |
Start with the math. A 5 mg vial reconstituted with 2 mL bacteriostatic water gives you 2.5 mg/mL. At 0.5 mg per dose, that's 0.2 mL per injection, or 20 units on an insulin syringe. One 5 mg vial covers 10 days at that dose. A full 28-day cycle at 0.5 mg/day needs roughly three 5 mg vials (14 mg total). Store lyophilized powder at -20C. This compound degrades faster than simpler peptides at warmer temperatures. Once reconstituted, refrigerate at 2 to 8C and use within 14 days. The thing most people miss: the effective primate dose (0.43 mg/kg/day) translates to about 30 mg/day for a 70 kg human. Community doses of 0.5 to 1 mg/day are 30 to 60 times lower. You're almost certainly below the therapeutic threshold, and that's intentional. You'll hit kidney toxicity before you hit efficacy if you try to close that gap. Get a full renal panel before you start. Creatinine, BUN, urinalysis, GFR. Repeat at day 7 and day 14. If creatinine moves more than 20% from baseline, you're done. Stop NSAIDs at least a week before starting. Drink 3-plus liters of water daily; your kidneys concentrate this peptide during excretion.
All published research used 28-day (4-week) treatment cycles. Extended use beyond 28 days has not been studied and is strongly discouraged given the cumulative nephrotoxic risk. Prolonged washout periods of at least 8 weeks are recommended to allow full renal recovery. Kidney function should be assessed before, during, and after any treatment cycle.
The 4-week-on / 8-week-off cycle isn't based on receptor desensitization or antibody formation: it's purely a safety constraint. All published primate research used 28-day treatment windows, and kidney lesions were cumulative over that period. The 8-week off period exists to allow renal tubular repair, which was documented as occurring during washout in primate studies. No one knows if 8 weeks is enough for human kidneys. The cycle length is a ceiling, not a target: shorter cycles (14–21 days) carry less cumulative renal risk.
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Expected: Modest fat reduction possible based on primate data extrapolation: but no human efficacy data exists. Many users at this dose may see no measurable change. The primary goal is to avoid kidney damage, not to maximize fat loss.
Monitor: Renal panel at baseline, day 7, day 14, day 28, and at weeks 2, 4, and 6 post-cycle. Urinalysis at each check. GFR at baseline and post-cycle.
Aim the stream against the glass wall, not directly onto the powder. Swirl gently. This gives a concentration of 2.5 mg/mL.
For a 0.5 mg dose, draw 20 units on an insulin syringe (0.2 mL). For a 1.0 mg dose, draw 40 units (0.4 mL). For a 10 mg vial with 2 mL BAC water, those numbers become 10 units and 20 units respectively.
Clean the injection site with an alcohol swab and let it dry.
Rotate sites with each dose. Pinch a fold of skin and insert at a 45-degree angle.
Stay well hydrated throughout the day (3-plus liters minimum).
Use within 14 days. Do not freeze reconstituted solution.
Follow with an 8-week minimum washout period.
Monitor kidney function at baseline, day 7, day 14, day 28, and weeks 2, 4, and 6 post-cycle. Stop immediately if creatinine rises more than 20% above your baseline.
Additive nephrotoxic risk: well-documented interaction. NSAIDs reduce renal blood flow, compounding adipotide's renal tubular damage.
Do not combineSynergistic kidney toxicity. Aminoglycosides are independently nephrotoxic via tubular mechanisms.
Do not combineMay compound renal hemodynamic effects and worsen kidney function during adipotide use.
Increased risk of lactic acidosis if renal function is compromised by adipotide.
Pricing updated 2026-04-09
Kidney damage is the defining risk of adipotide, and it cannot be separated from the drug's mechanism of action. Every primate treated in the 2011 Barnhart study [1] showed dose-dependent renal lesions. The proapoptotic domain D(KLAKLAK)2 causes collateral apoptosis in renal proximal tubular epithelial cells during kidney filtration. This is not an idiosyncratic reaction; it is a predictable pharmacological effect. The human data made the situation worse. MD Anderson's Phase 1 trial enrolled cancer patients with obesity at 0.03 mg/kg/day, roughly 70 times below the effective primate dose. The trial was still terminated for nephrotoxicity. Human kidneys appear far more sensitive to this mechanism than primate kidneys. No human efficacy data exists because the dose could never reach the therapeutic range. Renal injury shows up as raised serum creatinine, rising BUN, proteinuria, and hematuria. In primates, these changes were characterized as reversible during washout. Whether that holds for humans is unknown because the trial was stopped too early to study recovery. A creatinine rise of more than 20 to 25% from your baseline should trigger immediate discontinuation. Bostin Loyd, a bodybuilder widely discussed in forum threads, died while reportedly using approximately 5 mg/day. That's well above any dose tested in clinical research. At that level, off-target apoptosis in renal tubular cells during clearance overwhelms kidney function. Beyond nephrotoxicity, reported side effects include transient dehydration (the kidneys work harder to clear the compound), mild proteinuria at subclinical levels, and injection site reactions. These are minor next to the renal risk, but proteinuria specifically should trigger immediate discontinuation. Contraindicated in anyone with pre-existing kidney disease, impaired renal function, or concurrent use of other nephrotoxic agents including NSAIDs, aminoglycosides, iodinated contrast dyes, cyclosporine, or tacrolimus. Pregnancy and breastfeeding are absolute contraindications. No pediatric safety data exists. If you experience dark or foamy urine, flank pain, back pain, or edema during use, stop immediately. Get labs within 24 hours. Hydration matters enormously; dehydration concentrates the compound in the kidneys during excretion and increases toxicity.
Verify Adipotide (FTPP) dosing and safety with a second opinion
No pharmaceutical-grade product exists. Adipotide is a complex chimeric peptidomimetic with a D-amino acid domain: harder to synthesize correctly than simple linear peptides. It was never manufactured at clinical scale. All available product is research-grade from peptide synthesis vendors with varying quality control. Misfolded or truncated product could have unpredictable toxicity profiles.
| Test | When | Target |
|---|---|---|
| Serum creatinine | Baseline, day 7, day 14, day 28, then weeks 2, 4, 6 post-cycle | Must stay within 20% of YOUR baseline. A rise above 25% = stop immediately. |
| BUN (Blood Urea Nitrogen) | Same schedule as creatinine | 7–20 mg/dL (normal). Trending upward from baseline is a red flag. |
| Urinalysis with albumin/creatinine ratio | Baseline, day 7, day 14, day 28 | Albumin/creatinine ratio <30 mg/g. Any proteinuria or hematuria = stop. |
| Estimated GFR (eGFR) | Baseline and 4–6 weeks post-cycle | >90 mL/min/1.73m² (normal). Any decline warrants extended monitoring. |
Primary marker for renal tubular damage: the dose-limiting toxicity of adipotide
Reflects kidney filtration function. Rising BUN with stable creatinine can indicate early tubular dysfunction.
Detects proteinuria and hematuria: both are early markers of renal injury. More sensitive than serum creatinine for catching tubular damage early.
Overall kidney function assessment. Comparing pre- and post-cycle GFR tells you whether lasting damage occurred.
Initial treatment phase. Based on primate data, measurable changes in body composition may begin. Renal markers (creatinine, BUN) should be monitored closely from the outset. Early signs of kidney stress may appear even at low doses.
Fat reduction becomes detectable via imaging in animal models. Primate studies showed progressive weight loss during this window. Renal tubular changes may begin to appear on urinalysis. Continued monitoring is essential.
Significant fat loss is observed in animal models. In obese monkeys, this period corresponded to the steepest weight loss trajectory. Kidney injury markers may become elevated; dose reduction or discontinuation should be considered if creatinine rises above baseline.
End of the standard 28-day treatment cycle. Primate data showed 7-15% total body weight loss and up to 38% reduction in body fat by this point. Treatment should be discontinued at day 28. Renal function monitoring should continue for at least 4-6 weeks after cessation.
Washout and recovery phase. Some weight regain is expected as adipose vasculature regenerates over time. Renal lesions observed in primate studies were reported as reversible during washout. Do not restart treatment until all renal markers have normalized.
Days 1 through 7, first week, establishing tolerance: Based on primate data, vascular changes in adipose tissue may begin at the cellular level. Don't expect anything visible. Renal tubular stress can start even at low doses. Most community users report nothing noticeable this week. Some mention mild injection site irritation and a slight uptick in urination. The real purpose of week one is your day 7 kidney labs. Days 8 through 14, second week, the monitoring window: Fat reduction became detectable via imaging during this period in primates. Your kidney markers may start shifting, and this is the checkpoint that matters most. Users who report any effect typically notice subtle changes in how fat tissue feels (softer, less firm) around days 10 to 14. Scale weight barely moves. Watch for creatinine elevation and mild proteinuria. Days 15 through 28, second half, risk accumulation: Primate studies showed the steepest weight loss curve here, with 7 to 15% total body weight gone by day 28. Kidney lesions also progressed. Both the wanted effects and the unwanted ones are cumulative. Community users who complete 28 days at low doses report modest abdominal fat reduction, far less dramatic than primate data because the dose is far lower. Watch for proteinuria, creatinine drift, fatigue, and edema. Weeks 5 through 12, post-cycle washout: Primate kidney lesions were reported as reversible during this phase. Adipose vasculature regenerates over time, so some fat regain is expected. Community users report weight returning over 4 to 8 weeks. Kidney markers typically normalize within 2 to 4 weeks if they were mildly raised. Full renal recovery is not guaranteed in humans. Do not restart until every renal marker has returned to your baseline.
Based on primate data, measurable vascular changes in adipose tissue may begin. No visible body composition changes yet. Renal tubular stress may begin even at low doses.
Most users report nothing noticeable in week 1. Some report mild injection site irritation. A few report slight increase in urination.
In primates, fat reduction became detectable via imaging during this window. Renal markers may start shifting: this is the critical monitoring checkpoint.
Users who report any effect typically start noticing subtle changes in how fat "feels" (softer, less firm) around day 10–14. Weight scale changes are minimal.
Primate studies showed the steepest weight loss trajectory in this window (7–15% total body weight by day 28). Kidney lesions also progressed. The compound's effects, both wanted and unwanted, are cumulative.
The few users who complete 28 days at low doses report modest fat reduction, primarily in abdominal area. Results are far less dramatic than the primate data would suggest, consistent with doses being far below the effective primate dose.
Primate kidney lesions were reported as reversible during washout. Adipose vasculature regenerates over time, so some fat regain is expected. The timeline for vascular regeneration in humans is unknown.
Users report some weight/fat regain over 4–8 weeks post-cycle. Kidney markers typically normalize within 2–4 weeks if they were mildly elevated. Full renal recovery is not guaranteed in humans.
Source: Estimated from peptide pharmacokinetics; no published human PK data available. Short peptide with D-amino acid stabilization may extend half-life modestly.
Loading the interactive decay curve.
Adipotide has no FDA approval. It has no approval from any regulatory agency worldwide. MD Anderson's Phase 1 trial (2012) was terminated for nephrotoxicity, and Arrowhead Research permanently discontinued all clinical development in 2019. No new Investigational New Drug applications or clinical trials are registered or planned. The compound is available only as a research chemical through peptide synthesis vendors. No pharmaceutical-grade or GMP-manufactured product exists. The D-amino acid proapoptotic domain D(KLAKLAK)2 is difficult to synthesize correctly; misfolded or truncated product could have unpredictable toxicity. Adipotide is not scheduled as a controlled substance in the United States. Its WADA status for athletes is unconfirmed, but any compound used for body composition changes would likely fall under prohibited methods. Purchasing for "research purposes" occupies a legal gray area that varies by jurisdiction. This content is for educational and research reference purposes only. It does not constitute medical advice. Consult a physician before considering any investigational compound, particularly one with a terminated clinical program and documented organ toxicity.
Peptide Schedule Research TeamReviewed Apr 20265 Citations
