Adipotide (Injectable) dosing

What it is

Adipotide is a lab-made peptide designed to kill fat cells by cutting off their blood supply. Its full chemical name is CKGGRAKDC-GG-D(KLAKLAK)2, and it is also called FTPP (Fat Targeted Proapoptotic Peptide) or Prohibitin-TP01.

It is built from two joined parts. The first is a homing sequence that seeks out proteins found on the blood vessels inside white adipose tissue — ordinary body fat. Those proteins are prohibitin and annexin A2. The second is a pro-apoptotic sequence. Apoptosis is programmed cell death, the orderly self-destruct process cells use; a pro-apoptotic sequence switches it on. So the first half finds the blood vessels in fat, and the second half tells those vessel cells to die. Without their blood supply, the fat cells starve and die too, and the body clears the dead tissue away.

This is unlike every other fat loss compound. It does not suppress appetite, does not raise your metabolic rate, and does not change how your body burns fuel. Because it acts out in the body rather than on the brain, it stands in sharp contrast to drugs that work centrally on hunger. Results are also reported to happen regardless of whether a person changes their diet or exercise.

It started life as a cancer drug. The plan was to starve tumours by destroying the blood vessels feeding them. Researchers at MD Anderson Cancer Center noticed that treated animals lost dramatic amounts of body fat and switched focus to obesity. The first mouse study was published in 2004, a monkey study followed in 2011, and a Phase 1 human trial began in 2012 but was stopped before completion with no results ever published. As of 2026 there is zero published human efficacy or safety data. Everything known comes from mice, monkeys, and a handful of scattered user reports.

It comes as a dry powder in a sealed vial. You add bacteriostatic water — sterile water with a preservative — then inject just under the skin, a subcutaneous injection, with the abdomen recommended.

Read the side effects and monitoring notes before going near this one. The kidney effects are not incidental; they are the reason clinical development appears to have been abandoned.

Adipotide (CKGGRAKDC-GG-D(KLAKLAK)2; also FTPP, Fat Targeted Proapoptotic Peptide, or Prohibitin-TP01) is a chimeric peptide that ablates white adipose tissue vasculature, killing adipocytes by ischaemia rather than mobilising their lipid.

Structure: a cyclic homing sequence, CKGGRAKDC, targeting the prohibitin (PHB)–annexin A2 (ANXA2) complex on adipose endothelium, conjugated to the pro-apoptotic sequence D(KLAKLAK)2. Apoptotic tissue is subsequently cleared. There is no appetite-suppressant, thermogenic, or fuel-partitioning component to the mechanism; the peripheral, non-CNS site of action is the explicit mechanistic contrast with central appetite-modulating agents, and is the reason the compound is of interest as a class rather than as another incretin variant. Effects are also described as independent of diet or exercise modification.

Development history: originally an anti-angiogenic oncology construct intended to starve tumour vasculature. MD Anderson investigators observed marked adiposity loss in treated animals and pivoted to obesity. Kolonin et al. (2004) is the discovery paper, Barnhart et al. (2011) the primate study, and Phase 1 trial NCT01262664 was initiated in 2012, terminated before completion, and never published. Arrowhead Research Corporation, which held commercial rights, appears to have discontinued development as of 2019. As of 2026 there is no published human efficacy or safety data.

The dose-limiting toxicity is renal. Primate data show dose-dependent renal tubular injury with creatinine elevation above 0.25 mg/kg, glucosuria, proteinuria, tubular degeneration and necrosis, and dehydration at the highest doses, most changes reversing within 28 days of cessation. Pre-existing renal impairment is a hard contraindication.

Research interest beyond obesity persists because prohibitin is also expressed on some tumour vasculature, and Staquicini et al. (2011) confirmed the annexin A2–prohibitin receptor system on human white adipose tissue vasculature in cancer patients.

How it works

Adipotide has two working parts stuck together, and each does a separate job.

The first part, CKGGRAKDC, is the address label. It was found by injecting billions of random peptide sequences into mice and picking out the ones that piled up in the blood vessels of white fat. It sticks to two proteins, prohibitin and annexin A2, that sit on the surface of the cells lining fat tissue blood vessels. Those two proteins are much more common on fat tissue vessels than on vessels elsewhere in the body, and that difference is what gives Adipotide its aim. The same pair also works with a protein called CD36 to pull fatty acids out of the blood and into fat cells, so the target is the very machinery fat uses to grow.

The second part, D(KLAKLAK)2, is the demolition charge. Once Adipotide has stuck to its target and been pulled inside the vessel-lining cell, this half breaks up the cell's mitochondria — its power plants. That triggers the cell's built-in self-destruct programme and the cell dies. The vessel collapses, and the fat cells downstream lose their oxygen and nutrients and die as well.

Why this matters: every other fat loss tool either reduces how much you eat, raises how much you burn, or shifts how you use fuel. All of those only shrink fat cells. The cells stay alive and refill when you eat more than you burn, which is a big part of why weight comes back. Adipotide kills the cells outright, so in theory the loss could be more lasting. Whether that holds true in people is unknown, because no human results have been published.

The aiming is not perfect. Prohibitin and annexin A2 are concentrated on fat vessels but are not exclusive to them. The kidneys are packed with blood vessels, and in monkeys the most consistent harm was dose-dependent damage to the kidney tubules. That collateral damage is the central safety trade-off.

One oddity: in a 2010 mouse study, treated animals ate less even though their leptin — the hormone that signals fullness — was falling. Falling leptin normally drives hunger up. The researchers concluded that destroying fat tissue vessels releases some unknown signal that suppresses appetite, and nobody has identified it. A 2012 comment by Criscione asked whether the monkeys' weight loss actually came from the vessel destruction or simply from eating less. Both may be happening at once.

Adipotide is bifunctional: a targeting domain fused to a killing domain.

Targeting domain (CKGGRAKDC). A cyclic sequence identified by in vivo phage display against white adipose tissue vasculature. It binds a surface complex of prohibitin (PHB) and annexin A2 (ANXA2) on adipose endothelium, where both proteins are expressed at far higher density than on endothelium elsewhere; that differential expression is the basis of selectivity. The complex is functional rather than a passive marker: Salameh et al. (2016) showed PHB/ANXA2 acts with CD36 to mediate fatty acid transport from plasma into adipocytes, with fatty acid exposure triggering assembly of the ANXA2–PHB–CD36 surface complex. Disrupting the interaction markedly reduces adipocyte lipid uptake capacity, so the construct hits both the vasculature and the lipid import machinery.

Killing domain (D(KLAKLAK)2). A cationic amphipathic pro-apoptotic sequence. Following receptor binding and internalisation it disrupts mitochondrial membranes, driving cytochrome c release and caspase cascade activation. Endothelial apoptosis collapses the microvessel; downstream adipocytes undergo secondary apoptosis from ischaemia.

Class distinction. Caloric restriction, incretin agonists, thermogenics, and hormonal repartitioning all reduce adipocyte volume while leaving the cell viable and able to refill. Adipotide deletes the cell. The theoretical corollary is reduced regain potential; this has never been tested in humans.

Selectivity limits. PHB and ANXA2 are preferential, not exclusive, to adipose vasculature. The kidney's large endothelial surface area makes it the principal off-target organ, and dose-dependent renal tubular injury was the most consistent adverse finding in primates. In the Barnhart 2011 data, creatinine rose without proportional BUN elevation, consistent with selective proximal tubule dysfunction rather than global renal failure. This trade-off is the likely reason clinical development was abandoned.

Unresolved mechanism. Kim, Woods and Seeley (2010) found reduced food intake in treated mice despite falling leptin, concluding that adipose vascular ablation elicits an uncharacterised adipose-derived anorexigenic signal acting independently of leptin. Criscione (2012) challenged the vascular mechanism outright, proposing that weight loss in monkeys may have derived from reduced food consumption; treated animals did eat less, and the two mechanisms are not mutually exclusive.

What it does

Fat: it destroys the blood vessels supplying white fat tissue, so the fat cells lose their blood supply and die. The body then clears the dead tissue. This is targeted destruction of fat cells, not appetite suppression and not simple shrinkage — the cells are gone rather than emptied, which in theory could make the loss harder to reverse.

How much, in animals: obese mice in the 2004 study lost about 30% of their body weight in 4 weeks. Obese rhesus monkeys treated for 28 days in 2011 lost 7.4 to 14.7% of body weight, with total body fat falling 38.7% against 14.8% in controls, and waist measurement falling 6.5 to 14.3% in 9 of 10 treated animals.

Visceral fat: it preferentially affects white fat tissue, including visceral fat — the fat packed around your internal organs. Visceral fat is linked to cardiovascular disease, diabetes, and metabolic risk, so reducing it can bring bigger health gains than losing general body weight.

Blood sugar and insulin: in the monkey study, insulin sensitivity improved alongside the fat loss. Insulin area under the curve fell 36.2% against controls, and the insulinogenic index — a measure of how much insulin the pancreas releases in response to glucose — fell 48.5% in treated animals while rising 33.8% in controls. A 2012 mouse study found glucose tolerance improved within just 2 to 3 days, faster than weight loss alone can explain. Improved insulin support in people with Type 2 diabetes has also been claimed.

Only in the obese: lean monkeys given therapeutic doses did not lose weight. Only obese animals lost fat, which suggests the mechanism needs the expanded, abnormal blood vessel network of obese fat tissue to work on.

Appetite: it does not bind to any hunger or fullness receptor and does not work through GIP, GLP-1, or glucagon. That said, animals did eat less through some unknown route, so appetite may still be affected indirectly.

Cancer research: prohibitin, the protein it targets, is also present in the blood vessels of some tumours, which keeps the construct interesting to cancer researchers.

Adipose. Apoptotic ablation of white adipose tissue vasculature with secondary ischaemic adipocyte death and clearance of apoptotic tissue — cell deletion rather than lipid mobilisation. Preclinical magnitude: approximately 30% body weight loss over 4 weeks in diet-induced obese mice (Kolonin et al., 2004); 7.4 to 14.7% body weight loss, BMI down 3.7 to 17.3%, abdominal circumference down 6.5 to 14.3% in 9 of 10 animals, and total body fat down 38.7% versus 14.8% in controls over 28 days in obese rhesus macaques (Barnhart et al., 2011). White adipose tissue volume fell 17.5% by end of treatment and continued to 27.0% by end of the recovery period.

Visceral compartment. Preferential effect on white adipose tissue including perivisceral fat; visceral adiposity carries disproportionate cardiovascular, diabetic, and metabolic risk, so its reduction outweighs equivalent general weight loss.

Glycaemic. Insulin AUC down 36.2% versus controls and insulinogenic index down 48.5% versus a 33.8% increase in controls in the primate study. Kim et al. (2012) demonstrated glucose tolerance improvement within 2 to 3 days, preceding meaningful weight loss, with falling serum insulin and triglycerides, attributed to reversal of high-fat-diet-induced adipose mitochondrial dysfunction and altered branched-chain amino acid metabolism. Improved insulin support in Type 2 diabetics has also been reported.

Obesity-conditional action. Lean monkeys at therapeutic doses showed no weight loss, consistent with the expanded, metabolically abnormal vasculature of obese adipose tissue carrying higher PHB/ANXA2 target density.

Appetite. No binding at hunger or satiety receptors and no activity at GIP, GLP-1, or glucagon pathways, yet reduced food intake was observed in both mouse and primate work via an uncharacterised adipose-derived signal. Criscione (2012) argued this may account for part or all of the observed weight loss.

Oncology relevance. Prohibitin expression in some tumour vasculature; Daquinag et al. (2016) showed a related pro-apoptotic construct (D-WAT) depleted tumour stromal and perivascular cells, reducing tumour vascularity and growth in mouse carcinoma models.

Class position. Peripheral, non-CNS action, presented as a mechanistic contrast to central appetite-modulating agents, with effects described as independent of diet and exercise modification.

Benefits

Evidence grades: what the labels mean

Human trials Supported by randomised or placebo-controlled human trials.
Limited human data Some human evidence, such as pilot studies, case reports or observational data, but no controlled trials.
Animal or lab only Shown in animal or cell studies only; not yet tested in people.
Anecdotal No published studies; based on user reports or theory.

Each grade reflects the strongest published support for that specific claim, not for the compound as a whole.

Kills fat cells rather than shrinking them — the cells undergo programmed death and are cleared, so in theory they cannot refill. This has never been tested in humans.Animal or lab only
Large fat loss in animals: about 30% of body weight in obese mice over 4 weeks, and 7.4 to 14.7% of body weight in obese monkeys over 28 days.Animal or lab only
Total body fat fell 38.7% in treated monkeys against 14.8% in controls, with waist measurement down 6.5 to 14.3% in 9 of 10 animals.Animal or lab only
Targeted visceral fat reduction — it preferentially affects white fat tissue, including the visceral fat packed around your organs.Animal or lab only
Visceral fat is linked to cardiovascular disease, diabetes, and metabolic risk, so reducing it can bring bigger health gains than losing general body weight.Anecdotal
Better insulin and glucose numbers in animals: insulin area under the curve down 36.2% and insulinogenic index down 48.5% in treated monkeys, and glucose tolerance improving within 2 to 3 days in mice. Improved insulin support in people with Type 2 diabetes has also been claimed.Anecdotal
Appears to act only where there is excess fat — lean monkeys on therapeutic doses did not lose weight.Animal or lab only
No appetite-suppressing mechanism of its own, so it does not rely on the gut side effects that come with GLP-1 drugs.Anecdotal
It works out in the body rather than through the brain, a genuine mechanistic contrast to drugs that suppress appetite centrally.Animal or lab only
Of interest to cancer researchers, because prohibitin — the protein it targets — is also present in the blood vessels of some tumours.Animal or lab only
Results are described as occurring regardless of whether diet or exercise change.Anecdotal

Adipocyte deletion rather than volume reduction — apoptosis and clearance, with a theoretical reduction in regain potential that remains untested in humans.Animal or lab only
Preclinical magnitude: approximately 30% body weight loss in obese mice over 4 weeks; 7.4 to 14.7% body weight loss and BMI down 3.7 to 17.3% in obese rhesus macaques over 28 days.Animal or lab only
Total body fat down 38.7% versus 14.8% in controls; abdominal circumference down 6.5 to 14.3% in 9 of 10 treated animals; WAT volume down 17.5% at end of treatment and 27.0% at end of recovery.Animal or lab only
Targeted visceral fat reduction via preferential action on white adipose tissue vasculature; visceral adiposity reduction carries disproportionate cardiometabolic benefit relative to equivalent general weight loss.Anecdotal
Insulin sensitivity gains: insulin AUC down 36.2% and insulinogenic index down 48.5% versus a 33.8% increase in controls.Animal or lab only
Weight-independent glycaemic effect — glucose tolerance improved within 2 to 3 days in mice, attributed to reversal of adipose mitochondrial dysfunction. Improved insulin support in Type 2 diabetics has also been reported.Anecdotal
Obesity-conditional action: no weight loss in lean primates at therapeutic doses, consistent with target density scaling with adipose vascular expansion.Animal or lab only
No incretin, GIP, or glucagon receptor activity and no direct orexigenic or anorexigenic receptor binding — an option outside the incretin class for those intolerant of its gastrointestinal profile.Anecdotal
Peripheral, non-CNS action — a mechanistic contrast to central appetite-modulating agents.Animal or lab only
Research relevance in oncology: prohibitin is expressed in some tumour vasculature, and related pro-apoptotic constructs suppressed tumour growth in mouse models.Animal or lab only
Effect described as independent of diet and exercise modification.Anecdotal

What to expect

Start from the honest position: there is no published human data to set expectations against. No human trial results have ever been released. Everything below is taken from monkey studies and a very thin set of user reports.

What the monkey data suggests. In Barnhart 2011, obese rhesus monkeys dosed daily for 28 days showed measurable weight and body composition change within the treatment window, confirmed by MRI and DEXA. Total body fat was down 38.7% by the end of the study period, which was 28 days of treatment plus 28 days of recovery. Abdominal white fat volume fell 17.5% by the end of treatment and kept falling to 27.0% by the end of recovery, as if damaged blood vessels carried on failing after the peptide was stopped. Mild to moderate kidney effects appeared during treatment and largely resolved within 28 days of stopping.

What users report. Very few people have used this and even fewer have written anything up. The scattered reports that exist mention severe injection site pain and lumps, extreme thirst, cloudy or discoloured urine, nausea, insomnia, and fatigue or weakness. There is no settled protocol in circulation the way there is for BPC-157 or the GLP-1 drugs.

The most widely known case is bodybuilder Bostin Loyd, who used it at doses reportedly well above what the primate studies suggested, with some accounts citing 5 mg per day. He was hospitalised in 2020 with stage 5 kidney failure, which he publicly attributed to FTPP. He refused dialysis and tried to manage the condition with other compounds. He died in February 2022 at age 29; the cause of death was found to be a dissecting aneurysm of the ascending aorta, a hereditary condition his father also had, not the kidney failure. Two things follow: doses well above the studied range can cause severe and possibly permanent kidney damage, and pinning any outcome on one compound in someone using many at once is close to impossible.

The silence itself is information. This has been available from research suppliers for years, yet almost nobody is using it and reporting back, while compounds with far less data generate thousands of reports. Expect to be running an experiment on yourself with no human safety data to guide you.

No published human efficacy or safety data exists; expectations derive entirely from primate work and extremely sparse anecdote.

Primate trajectory (Barnhart et al., 2011). Obese rhesus macaques dosed daily for 28 days showed MRI- and DEXA-confirmed reductions in white adipose tissue within the treatment period. Total body fat fell 38.7% by the end of the study period (28 days treatment plus 28 days recovery). Abdominal WAT volume fell 17.5% by end of treatment and continued to 27.0% by end of recovery, consistent with ongoing failure of damaged vasculature after cessation. Mild to moderate renal effects emerged during dosing and largely resolved within 28 days of stopping.

User-level data. Almost nonexistent. The reports that exist cite severe injection site pain and nodules, extreme thirst and signs of dehydration, cloudy or discoloured urine, nausea, insomnia, fatigue and weakness, and hypoglycaemia-like symptoms. No established practical protocol circulates; the figures that do circulate are rough extrapolations from primate data, frequently 0.5 to 1.0 mg/kg per day against an identified optimal primate dose of 0.43 mg/kg and a renal toxicity threshold above 0.25 mg/kg.

The most severe documented outcome is the Bostin Loyd case: use at doses reportedly far above the primate therapeutic range, with some accounts citing 5 mg per day, followed by hospitalisation with stage 5 renal failure in 2020, which he publicly attributed to FTPP. He declined dialysis and attempted management with peptides, EPO, glutathione, and stem cells. He died in February 2022 aged 29 of a dissecting aneurysm of the ascending aorta, a hereditary condition also present in his father, not of renal failure. The case supports two conclusions: supratherapeutic dosing can produce severe and potentially irreversible nephrotoxicity, and attribution in polypharmacy is unreliable.

The near-total absence of experience reports for a compound available through research suppliers for years, in a user population that routinely trials thinly evidenced peptides, is itself a signal about how the risk-reward calculation lands.

Reconstitution and dosing

Nothing here rests on human dose-finding data, because none has been published.

What the research used. The original mouse study gave the compound into the abdominal cavity of diet-induced obese mice for 4 weeks. The primate study tested 0.10 to 0.75 mg/kg as daily subcutaneous injections; the best therapeutic dose was 0.43 mg/kg, kidney toxicity appeared above 0.25 mg/kg, the dose-finding phase ran 63 days, and the efficacy phase used 28 days of treatment then 28 days of recovery. The human Phase 1 trial started at 0.03 mg/kg daily for 28 days and was terminated with no results published.

The important context in one line: the dose that works in monkeys, 0.43 mg/kg, is already above the 0.25 mg/kg where kidney effects start. On current data there is no way to separate the fat loss from the kidney risk at doses that actually work.

A conservative protocol that circulates is 0.5 mg/kg of body weight per day, once daily, subcutaneous, for a maximum of 4 weeks, with at least 4 weeks off between cycles. By body weight that works out at roughly 34 mg daily at 150 lbs (68 kg), 41 mg at 180 lbs (82 kg), 45 mg at 200 lbs (91 kg), and 50 mg at 220 lbs (100 kg).

Those weight-based figures are vastly larger than the milligram-per-day schedule in the protocol table below, which uses a 10 mg vial mixed with 2.5 mL (250 units) of bacteriostatic water — "units" means the marks on an insulin syringe, where 100 units is 1 mL. That table runs 0.33 mg once a day on days 1–7, 0.55 mg once a day on days 9–14, and 1 mg once a day on days 15–28, over a 28-day cycle followed by 12 to 28 days off. The two approaches disagree by a very wide margin. Treat the far higher weight-based numbers with extreme caution and recognise that no published human data supports either.

Inject under the skin, abdomen recommended. Any time of day or night; you do not need to be fasted.

Hydration is not optional. Stay extremely well hydrated throughout. The primate study noted dehydration at higher doses, and the kidneys are under stress from this compound by design; poor hydration could amplify that.

Monitoring. Get baseline kidney bloodwork before starting — BUN, creatinine, GFR, and a urinalysis — and repeat it weekly during use. Any rise in creatinine, any protein or glucose appearing in urine, or any fall in GFR is a signal to stop immediately.

No published human dose-finding data exists for any subcutaneous protocol.

Research doses. Kolonin et al. (2004) dosed intraperitoneally in diet-induced obese mice for 4 weeks. Barnhart et al. (2011) tested 0.10 to 0.75 mg/kg as daily subcutaneous injections, identifying 0.43 mg/kg as the optimal therapeutic dose with renal toxicity above 0.25 mg/kg; the dose-finding phase ran 63 days and the efficacy phase 28 days of treatment plus 28 days of recovery. Phase 1 NCT01262664 opened at 0.03 mg/kg daily for 28 days before termination without published results.

The therapeutic window is inverted: the optimal primate dose sits above the threshold at which renal effects appear. On current data, efficacy cannot be separated from nephrotoxicity.

Conservative extrapolated protocol: 0.5 mg/kg body weight per day, once daily, subcutaneous, 4 weeks maximum, at least 4 weeks off between cycles. Body-weight tiers at that dose: approximately 34 mg daily at 68 kg, 41 mg at 82 kg, 45 mg at 91 kg, 50 mg at 100 kg. Figures circulating elsewhere run 0.5 to 1.0 mg/kg per day.

The earlier fixed-dose presentation carried in the protocol table is a different animal entirely: 10 mg in 2.5 mL (250 units) of bacteriostatic water, giving 4 mg/mL, escalating 0.33 mg on days 1–7, 0.55 mg on days 9–14, and 1 mg on days 15–28, once daily, across a 28-day cycle with a 12–28 day washout. Recomputed draws agree with the table's unit figures to within about 3% (0.33 mg computes to 8.25 units against 8; 0.55 mg to 13.75 against 14), and the schedule's day numbering skips day 8. The divergence between that schedule and the weight-based extrapolation is enormous and unresolved by any human data; the higher figures warrant the greater scepticism.

Route and timing: subcutaneous, abdominal region recommended, any time of day, fasting not required. Daily rather than weekly dosing against a documented dose-dependent renal effect is why the washout is not optional.

Hydration: maintain aggressively. Dehydration was documented at higher primate doses and the renal tubules are under mechanistic stress; hypovolaemia would be expected to amplify tubular injury.

Monitoring: baseline BUN, creatinine, GFR, and urinalysis before starting, repeated weekly during use. Creatinine elevation, proteinuria or glucosuria, or falling GFR is a stop signal. Note that high-dose creatine raises serum creatinine and can mask the primary monitoring marker.

Standard, 10 mg vial

Mix with 2.5 mL (250 units) of bacteriostatic water.

4 mg/mL · 40 mcg per unit

Cycle: 28-day cycle followed by a 12–28 day washout · Frequency: Daily for the duration of the cycle; subcutaneous, abdominal region recommended; any time of day or night; fasting not required

When	Dose	Draw	How often
Days 1–7	330 mcg	8.25 units	1×/day
Days 9–14 (numbering skips day 8)	550 mcg	13.75 units	1×/day
Days 15–28	1 mg	25 units	1×/day

Alternative protocols

Alternative protocols reflect older community practice and are kept for reference.

Alternative, 10 mg vial

Mix with 2.5 mL (250 units) of bacteriostatic water.

4 mg/mL · 40 mcg per unit

Cycle: 28-day cycle followed by a 12–28 day washout · Frequency: Daily for the duration of the cycle; subcutaneous, abdominal region recommended; any time of day or night; fasting not required

When	Dose	Draw	How often
Days 1–7	330 mcg	8.25 units	1×/day
Days 9–14 (numbering skips day 8)	550 mcg	13.75 units	1×/day
Days 15–28	1 mg	25 units	1×/day

Protocol

Peptide in vial (mg)

Bacteriostatic water (mL)

Target dose

Syringe size

Draw to

8.25units

on a 1 mL insulin syringe

0102030405060708090100

10 mg in 2.5 mL is 4 mg/mL, or 40 mcg per unit. Draw 8.25 units (0.083 mL) for 330 mcg.

Volume per dose

0.083 mL

Concentration

4 mg/mL

Doses per vial

Who should avoid it

Anyone with kidney disease or any history of kidney problems. This is the hard no — the kidneys are the organ most affected.
Anyone with impaired kidney function or an abnormal GFR (a blood test measure of how well the kidneys filter).
Anyone with active cancer. The compound was originally designed for cancer applications and its effects on the blood vessels feeding tumours are complex and unpredictable.
Anyone with cardiovascular disease or a vascular condition, since the compound acts on blood vessels.
Anyone with diabetes that has vascular complications, in particular diabetic kidney disease (diabetic nephropathy).
Anyone pregnant or breastfeeding. There is no safety data of any kind.
Extreme caution with high blood pressure (extra strain on blood vessels), a history of blood clots, any metabolic disorder, and any medication that affects kidney function.
Avoid anything else that stresses the kidneys: NSAIDs such as ibuprofen, certain antibiotics (aminoglycosides, vancomycin), contrast dyes used in scans, high-dose paracetamol/acetaminophen, and certain chemotherapy drugs. Take care with ACE inhibitors and ARBs, which change blood flow through the kidneys.
Avoid high-dose creatine. It raises creatinine in blood tests and can hide the early warning signs of kidney damage.
Take care if you are on blood sugar-lowering medication such as insulin, or on lipid-modifying drugs such as statins. Because Adipotide affects fat tissue metabolism and possibly insulin sensitivity, there could in theory be interactions — no controlled data exist.
If you are on any prescription medicine that affects kidney function, do not use this compound.
Talk to a doctor before starting, and get baseline kidney bloodwork first.

Any renal disease or history of renal impairment, or abnormal GFR — the hard exclusion given confirmed dose-dependent nephrotoxicity in primates.
Active malignancy: the construct was developed for anti-vascular cancer applications and effects on tumour vasculature are complex and unpredictable.
Cardiovascular or vascular disease, given the anti-angiogenic, endothelium-directed mechanism.
Diabetes with vascular complications, diabetic nephropathy in particular.
Pregnancy or breastfeeding — no safety data of any kind.
Extreme caution: hypertension (additional vascular stress), history of thrombosis, any metabolic disorder, any medication affecting renal function.
No formal interaction studies exist. Avoid concurrent nephrotoxic agents: NSAIDs, aminoglycosides, vancomycin, certain chemotherapeutics, iodinated contrast agents, high-dose acetaminophen. Caution with ACE inhibitors and ARBs, which alter renal haemodynamics.
Avoid high-dose creatine — it elevates serum creatinine and can mask the primary monitoring signal.
Caution with glucose-lowering agents (insulin, hypoglycaemics) and lipid-modifying agents, given effects on adipose metabolism and possibly insulin sensitivity; no controlled data exist.
Baseline renal panel (BUN, creatinine, GFR, urinalysis) before starting and weekly repeat testing during use. Any creatinine elevation, proteinuria, glucosuria, or GFR decline is a stop signal.
Stop immediately and seek medical evaluation for blood or protein in urine, dark, cloudy or reduced urine output, severe lower back pain, peripheral oedema, or unexplained persistent fatigue or weakness. Most emergency physicians will not be familiar with Adipotide, so bring the compound name, mechanism, and dose used.

Side effects

Kidney injury to the filtering tubules. In the primate study this was dose-dependent and mostly reversible, with most changes resolving within 28 days of stopping.
Raised creatinine in the blood — a marker of kidney strain — seen at doses above 0.25 mg/kg in monkeys. Creatinine rose without a matching rise in BUN, which points to a specific part of the kidney tubule being affected rather than whole-kidney failure.
Glucose in the urine (mild to marked) and protein in the urine (mild to moderate), plus more kidney lining cells appearing in urine.
Lower blood phosphorus and potassium — an electrolyte imbalance, meaning the salts and minerals in your blood move out of their normal range.
Dehydration, seen at the highest doses in monkeys and described by users as extreme thirst. Staying very well hydrated matters.
Increased urine output, and cloudy or discoloured urine.
Injection site reactions — redness, swelling, itching, and in user reports severe injection site pain and lumps.
Loss of appetite, nausea, fatigue and weakness, dizziness, insomnia, and symptoms that feel like low blood sugar.
No abnormal fat build-up or liver changes were noted in the primate study, and the animals stayed bright, alert, and normally active during treatment.
The mouse studies reported no significant adverse effects, but mice are not a good guide to kidney risk in primates or people.
The worst documented outcome is a single case of stage 5 kidney failure after use at doses reportedly well above those studied in monkeys.

Dose-dependent renal tubular injury: histological tubular degeneration, necrosis, and regeneration. Most alterations reversed within 28 days of stopping treatment in the primate study.
Serum creatinine elevation at doses above 0.25 mg/kg, without a proportional rise in BUN — consistent with selective proximal tubule dysfunction rather than global renal failure.
Mild to marked glucosuria, mild to moderate proteinuria, and increased transitional and renal epithelial cells in urine.
Decreased serum phosphorus and potassium; electrolyte disturbance generally.
Dehydration at the highest dose levels; increased diuresis. Hydration status is a direct modifier of renal toxicity.
Injection site reactions (erythema, swelling, pruritus); user reports describe severe injection site pain and lumps.
Anorexia, nausea, fatigue and weakness, dizziness, insomnia, hypoglycaemia-like symptoms, cloudy or discoloured urine in anecdotal reports.
No abnormal lipid accumulation or hepatic changes were noted in the primate study; animals remained bright, alert, and normally active throughout treatment.
Mouse studies reported no significant adverse effects and are not predictive of primate or human toxicity for this compound.
Renal toxicity is the dose-limiting effect, not an incidental one. The primate optimal therapeutic dose of 0.43 mg/kg sits above the 0.25 mg/kg threshold at which renal effects appear, so efficacy and renal risk cannot be separated on current data. One documented case of stage 5 renal failure followed use at doses reportedly well above the studied range.

What the evidence shows

All the good data comes from animals. As of 2026 there is no published human efficacy or safety data at all.

The first study (Kolonin et al., 2004, Nature Medicine) found the fat-homing peptide sequence and joined it to a cell-killing sequence. Obese mice lost about 30% of their body weight over 4 weeks, and their metabolic markers improved. No adverse effects were reported in the mice.

Two later mouse studies added detail. Kim, Woods, and Seeley (2010) found treated mice ate less even though leptin — the hormone that signals fullness — was falling, which normally drives appetite up. The signal responsible has never been identified. Kim et al. (2012) found blood sugar handling improved within 2 to 3 days, faster than weight loss alone could explain.

The key study is Barnhart et al., 2011 (Science Translational Medicine), in monkeys: rhesus macaques (n=39), cynomolgus macaques (n=52), and baboons (n=2), dosed daily by injection under the skin. Doses ran from 0.10 to 0.75 mg/kg, and 0.43 mg/kg was judged the best dose. Ten obese rhesus monkeys then had 28 days of treatment plus a 4-week recovery. They lost 7.4 to 14.7% of their starting body weight, BMI fell 3.7 to 17.3%, waist measurement fell 6.5 to 14.3% in 9 of 10 animals, and total body fat fell 38.7% versus 14.8% in controls. Fat volume in the belly area fell 17.5% by the end of treatment and kept falling to 27.0% by the end of recovery. Insulin measures improved: insulin area under the curve fell 36.2% and the insulinogenic index fell 48.5%, against a 33.8% rise in controls. Lean monkeys given therapeutic doses did not lose weight. The main harm was dose-dependent kidney tubule injury, with creatinine rising above 0.25 mg/kg; most changes reversed within 28 days of stopping. The study was funded by Arrowhead Research Corporation, which held the commercial rights.

A published comment (Criscione, 2012) argued the monkey weight loss may have come partly or wholly from eating less rather than from vessel destruction. Supporting work showed prohibitin and annexin A2 form a complex that controls fat transport into fat tissue (Salameh et al., 2016), that related fat-targeting killing peptides slow tumour growth in mice (Daquinag et al., 2016), and that the target receptor system does exist on human fat tissue blood vessels (Staquicini et al., 2011).

A Phase 1 human trial (NCT01262664) was registered in 2010 and started in 2012 in patients with metastatic castrate-resistant prostate cancer and obesity, at a starting dose of 0.03 mg/kg daily for 28 days. It was terminated before completion and no results were ever published. Development appears to have been abandoned as of 2019.

Kolonin et al., 2004 (Nature Medicine) identified CKGGRAKDC by in vivo phage display, demonstrated prohibitin binding on white adipose tissue vasculature, and showed that the CKGGRAKDC-GG-D(KLAKLAK)2 construct produced approximately 30% body weight loss over 4 weeks in diet-induced obese mice with normalisation of metabolic markers and no detectable adverse effects. Limitations: murine diet-induced obesity model, differing metabolism from primates.

Kim, Woods, and Seeley, 2010 (Diabetes) showed reduced food intake despite falling circulating leptin, implying an uncharacterised adipose-derived anorexigenic signal acting independently of the leptin pathway. Kim et al., 2012 (Diabetes) demonstrated improved glucose tolerance within 2 to 3 days with decreased serum insulin and triglycerides, before meaningful weight loss, attributed to reversal of high-fat-diet-induced adipose mitochondrial dysfunction and altered branched-chain amino acid metabolism. Neither weight-independent effect is confirmed in primates or humans.

Barnhart et al., 2011 (Science Translational Medicine) is the pivotal dataset: rhesus macaques (n=39), cynomolgus macaques (n=52), baboons (n=2), daily subcutaneous administration. Dose-finding spanned 0.10 to 0.75 mg/kg with an optimal therapeutic dose of 0.43 mg/kg. In the efficacy arm, 10 obese rhesus received 28 days of treatment plus a 4-week recovery: weight loss 7.4 to 14.7% of pretreatment body weight, BMI down 3.7 to 17.3%, abdominal circumference down 6.5 to 14.3% in 9 of 10 animals, total body fat down 38.7% versus 14.8% in controls, abdominal white adipose tissue volume down 17.5% at end of treatment and 27.0% at end of recovery on MRI and DEXA. Insulin AUC fell 36.2%; insulinogenic index fell 48.5% versus a 33.8% increase in controls. Lean monkeys at therapeutic doses did not lose weight, consistent with preferential targeting of expanded, receptor-rich obese adipose vasculature. Dose-limiting toxicity was renal: creatinine elevation above 0.25 mg/kg, mild to marked glucosuria, mild to moderate proteinuria, increased transitional and renal epithelial cells in urine, decreased serum phosphorus and potassium, tubular degeneration, necrosis and regeneration histologically, dehydration at the highest doses, with most alterations reversing within 28 days of cessation. Creatinine rose without proportional BUN increase, indicating selective proximal tubule dysfunction. Limitations: small per-group sample sizes, 28-day exposure, no long-term safety data, sponsorship by Arrowhead Research Corporation, which held commercial rights.

Criscione, 2012 (Science Translational Medicine comment) challenged mechanistic attribution, proposing that reduced food consumption rather than targeted vascular ablation may account for part or all of the weight loss.

Supporting mechanism work: Salameh et al., 2016 (JCI Insight) established that prohibitin and annexin A2 form a functional endothelial surface complex regulating CD36-mediated fatty acid transport into adipose tissue. Daquinag et al., 2016 (Molecular Therapy) showed a related proapoptotic construct (D-WAT) depleting adipose stromal and perivascular cells reduced tumour vascularity and growth in mouse carcinoma models. Staquicini et al., 2011 (PNAS) confirmed the annexin A2-prohibitin receptor system on human white adipose tissue vasculature in cancer patients.

Phase 1 human trial NCT01262664 (MD Anderson Cancer Center), registered 2010 and initiated 2012 in metastatic castrate-resistant prostate cancer with obesity, starting dose 0.03 mg/kg daily for 28 days, was terminated before completion with no published results. Arrowhead appears to have discontinued clinical development as of 2019. As of 2026 there is zero published human efficacy or safety data.

User reports

From public forums

There is almost no user experience data for Adipotide. Very few people have used it, and the ones who have rarely write anything detailed.

The best known case is bodybuilder Bostin Loyd, who used it during contest preparation at doses reportedly well above what the monkey studies suggested — some sources cite 5 mg per day. In 2020 he was hospitalised with stage 5 kidney failure, which he publicly blamed on FTPP (Adipotide). He refused dialysis and tried to manage the condition with peptides, EPO, glutathione, and stem cells. He died in February 2022 at age 29, but the autopsy gave the cause of death as a dissecting aneurysm of the ascending aorta, an inherited condition his father also had. So the kidney failure was very likely caused by Adipotide, but it was not what killed him. Two lessons: doses well above the range studied in monkeys can cause severe and possibly permanent kidney damage, and pinning an outcome on one compound in someone using dozens at once is nearly impossible.

Forum searches across peptide and bodybuilding boards turn up almost no first-person logs. Most threads are someone asking if anyone has tried it, with no real answers. The few reports that exist mention injection site pain, cloudy urine, extreme thirst, nausea, insomnia, and fatigue. One user said they read about kidney damage and possible destruction of fat cells in the brain and avoided the compound entirely.

The silence is itself information. Adipotide has been available from research suppliers for years, yet almost nobody uses it or reports results, while compounds like BPC-157 and TB-500 generate thousands of reports. That level of avoidance among people who routinely try barely studied compounds says a lot about how the risk looks in practice.

Anecdotal data is close to nonexistent relative to any other compound in this space, and that absence is the primary signal.

The most widely discussed case is bodybuilder Bostin Loyd, who used Adipotide in contest preparation at doses reportedly well above the primate therapeutic range, with some sources citing 5 mg per day. He was hospitalised in 2020 with stage 5 renal failure, which he publicly attributed to FTPP, declined dialysis, and attempted management with peptides, EPO, glutathione, and stem cells. He died in February 2022 at age 29; autopsy attributed death to a dissecting aneurysm of the ascending aorta, a hereditary condition also present in his father, not renal failure. The case is confounded by extensive polypharmacy but is directionally consistent with the dose-dependent nephrotoxicity established in primates, and suggests reversibility cannot be assumed at supratherapeutic exposure.

Searches across Reddit (r/Peptides, r/steroids), ExcelMale, The Iron Den, Eroids, UK-Muscle and similar boards return effectively no first-person logs; threads are typically enquiries with no substantive replies. The sparse reports reference severe injection site pain and lumps, extreme thirst and dehydration signs, cloudy or discoloured urine, nausea, insomnia, fatigue and weakness, and hypoglycaemia-like symptoms. One user cited concerns about renal damage and destruction of brain fat cells as the reason for avoidance.

No established user protocol exists in the way it does for BPC-157, growth hormone secretagogues, or GLP-1 agonists. The figures that circulate on forums and vendor pages are rough extrapolations from the primate data, often quoting 0.5 to 1.0 mg/kg per day against a primate optimal dose of 0.43 mg/kg and a renal toxicity threshold above 0.25 mg/kg. Anyone using it is running an uncontrolled self-experiment with no human safety data.

User reports are individual experiences submitted by site visitors. They are not medical advice, are not verified for accuracy, and do not reflect Amino Reference's views. Read the evidence section above and talk to a clinician. Full disclaimer.

Stacking

No combination data exists
There is no published data on combining Adipotide with anything. Everything below is reasoning from mechanism only. Given the documented kidney effects, adding compounds here deserves more caution than usual.
No published data on co-administration with any compound. All stacking discussion is mechanism analysis. The additive nephrotoxicity risk, and theoretical interactions with glucose-lowering and lipid-modifying agents, argue for conservatism rather than for inferring a stack.
GLP-1 agonists (semaglutide, tirzepatide, retatrutide)
Completely different mechanisms — GLP-1 drugs reduce appetite and improve metabolic signalling, Adipotide destroys the blood vessels feeding fat. No known drug interaction, but both can cause nausea and dehydration, and those could add up. The practical question is whether it makes sense at all: GLP-1 drugs already produce substantial fat loss with a well-known safety profile, so adding a compound with confirmed kidney toxicity and no human data is a large risk increase for a small possible gain.
Non-overlapping mechanisms: incretin receptor agonism and central appetite suppression versus adipose endothelial apoptosis. No known pharmacological interaction, but overlapping nausea and dehydration risk is additive and dehydration amplifies renal toxicity. Risk-benefit is unfavourable — layering a compound with confirmed primate nephrotoxicity and zero human data onto an agent with established efficacy and a characterised safety profile is a substantial risk escalation for marginal incremental fat loss.
BPC-157
No known interaction, but the mechanisms look contradictory. BPC-157 encourages the growth of new blood vessels, while Adipotide destroys them. Whether they cancel each other out in fat tissue specifically is unknown.
No known interaction. BPC-157 is pro-angiogenic; Adipotide is anti-angiogenic via endothelial apoptosis. Whether the mechanisms offset within adipose tissue is unknown; the targeting domains differ, so direct interaction may not occur, but the pairing is theoretically contradictory.
TB-500
Same situation as BPC-157. TB-500 promotes new blood vessel growth and Adipotide kills blood vessels, so running both at once is at least theoretically working against itself. No known direct interaction.
No known interaction. TB-500 promotes angiogenesis, which is mechanistically opposed to adipose vascular ablation. Different targeting domains mean no direct molecular interaction is expected, but the combination is conceptually contradictory.
Growth hormone peptides (CJC-1295, Ipamorelin, Sermorelin)
No known interaction and different mechanisms. Growth hormone peptides need to be dosed fasted. There is no data on whether growth hormone signalling changes how Adipotide works, or the other way round.
No known interaction; distinct mechanisms. GH secretagogues require a fasted window. No data exist on whether GH/IGF-1 signalling modifies adipose vascular targeting or vice versa.
TRT
No known interaction. As far as current research shows, testosterone does not affect the receptor system Adipotide targets.
No known interaction. Testosterone is not shown to affect the prohibitin-annexin A2 receptor system on current evidence.
Avoid: NSAIDs, high-dose creatine, and other nephrotoxic substances
Anything that adds stress to the kidneys should be kept off while using Adipotide. That includes NSAIDs such as ibuprofen, which can impair kidney function, and high-dose creatine, which raises creatinine in blood tests and can hide the early signs of kidney damage. If you are on any prescription medicine that affects the kidneys, do not use this compound.
Hard avoid for anything adding renal load: NSAIDs (impair renal function), high-dose creatine (elevates serum creatinine and masks the primary monitoring signal), and any other nephrotoxic substance. Concurrent prescription therapy affecting renal function is a contraindication, not a caution.

Common questions

Does Adipotide actually kill fat cells or just shrink them?

Based on the animal data, it kills them. It destroys the blood vessels feeding fat tissue, and the fat cells then die from lack of blood supply. That is cell death, not just emptying out the stored fat, and the body clears the dead cells away. Whether this produces longer-lasting fat loss in people is unknown.

In animal models it kills them. Endothelial apoptosis in adipose vasculature leads to ischaemic secondary apoptosis of downstream adipocytes, which are then cleared — distinct from lipid mobilisation, where the adipocyte survives and can refill. Whether this yields more durable fat loss in humans has never been tested.

Why was the clinical trial stopped?

The Phase 1 trial (NCT01262664) was terminated before it finished and no results were ever published. The reasons were never made public. Given the consistent kidney toxicity in monkey studies and the narrow gap between the effective dose and the toxic dose, safety concerns are the most likely explanation. Arrowhead Research Corporation appears to have abandoned development as of 2019.

NCT01262664 was terminated before completion with no published results and no publicly disclosed rationale. Consistent dose-dependent renal tubular injury in primates and a therapeutic window that sits above the 0.25 mg/kg toxicity threshold make safety the most probable cause. Arrowhead Research Corporation, the commercial rights holder, appears to have discontinued development as of 2019.

Is Adipotide specific to fat tissue?

It is preferential, not specific. The receptor complex it targets is most concentrated on fat tissue blood vessels but exists elsewhere too. The kidneys are the most affected non-target organ in monkey studies. Whether other heavily blood-supplied organs such as the brain, liver, and lungs are affected at effective doses is not well characterised.

Preferential, not specific. Prohibitin and annexin A2 are enriched on white adipose tissue vasculature but not exclusive to it, and the differential expression is what confers selectivity. The kidney is the dominant off-target organ in primate data, consistent with its high endothelial surface area. Effects on other highly vascularised organs at therapeutic doses are poorly characterised.

Does Adipotide affect appetite?

Indirectly, possibly. The 2010 mouse study showed treated animals ate less even though leptin — the fullness hormone — was falling, which would normally increase appetite. The monkey study also showed reduced food intake. Whether that comes from the vessel destruction itself, from an unidentified signal released by dying fat tissue, or simply from feeling unwell is not clear.

Indirectly, possibly. Kim, Woods, and Seeley (2010) reported reduced food intake despite falling leptin, implying an uncharacterised adipose-derived anorexigenic signal acting outside the leptin pathway. Barnhart et al., 2011 also recorded reduced food consumption. Attribution between vascular ablation, that unknown signal, and malaise during treatment remains unresolved — the basis of the Criscione (2012) critique.

Is the kidney damage reversible?

In the monkey study most kidney changes reversed within 28 days of stopping. But that was at controlled doses, in healthy animals, over a short treatment period. Whether damage reverses at higher doses, with longer use, or in someone with any existing kidney weakness is unknown. The Bostin Loyd case suggests that at high enough doses it may not.

In Barnhart et al., 2011 most renal alterations reversed within 28 days of cessation, at controlled doses in healthy animals over a 28-day exposure. Reversibility at supratherapeutic doses, with extended exposure, or against pre-existing renal vulnerability is unestablished. The stage 5 renal failure case at reportedly far higher doses suggests it cannot be assumed.

Why does Adipotide not affect lean animals?

Lean monkeys given effective doses did not lose weight. The likely reason is that obese fat tissue has more blood vessels carrying more of the target receptor, so there is more for the peptide to bind to. Normal fat tissue has less expanded vessel network and less target, so there is less for it to act on.

Lean monkeys at therapeutic doses showed no weight loss. The likely explanation is that obese adipose tissue carries expanded vasculature with higher prohibitin-annexin A2 expression, increasing available binding targets, whereas non-expanded adipose vasculature presents fewer receptors and therefore less substrate for the construct.

How does Adipotide compare to GLP-1 drugs for fat loss?

Completely different mechanisms. GLP-1 drugs reduce appetite and improve metabolic signalling through well-known hormone pathways, with extensive human data and well-characterised safety. Adipotide destroys fat tissue blood vessels, has zero published human data, and has confirmed kidney toxicity in monkeys. For most people wanting fat loss, GLP-1 drugs are the rational choice.

Mechanistically unrelated. Incretin agonists act through established GLP-1 and related receptor pathways with extensive human efficacy and safety data. Adipotide acts peripherally on adipose endothelium with no published human efficacy or safety data and confirmed dose-dependent primate nephrotoxicity. For fat loss specifically, the incretin class dominates on risk-adjusted grounds; Adipotide remains a mechanistically interesting experimental compound.

What monitoring does this compound require?

Get baseline kidney bloodwork before starting — BUN, creatinine, GFR, and a urine test — and repeat it weekly during use. Any rise in creatinine, protein or glucose appearing in urine, or a drop in GFR is a signal to stop immediately. Watch for changes in urine colour, volume, or clarity, lower back pain, swelling in the legs or ankles, and unexplained fatigue. Stay extremely well hydrated throughout, since dehydration was seen at higher doses in monkeys and poor hydration could amplify kidney toxicity.

Baseline renal panel (BUN, creatinine, GFR, urinalysis) before initiation and weekly during use. Creatinine elevation, new proteinuria or glucosuria, or falling GFR are immediate stop signals. Clinical watch-items: urine colour, volume and clarity, flank or lower back pain, peripheral oedema, unexplained persistent fatigue. Aggressive hydration throughout — the primate study recorded dehydration at higher doses and the kidneys are under stress by design, so inadequate hydration could amplify renal toxicity.

References

This entry has been reviewed and expanded with additional reference material. Units are recomputed from the stated protocol.