Adipotide

Fat-Targeted Proapoptotic Peptide: A Comprehensive Research Review Adipotide, also known as FTPP (Fat-Targeted Proapoptotic Peptide) and Prohibitin-TP01, is one of the most mechanistically novel compounds to emerge from obesity research in the past two decades. Rather than suppressing appetite, increasing metabolism, or modulating hormonal pathways, adipotide works by physically destroying the blood vessels that supply white adipose tissue, thereby starving fat cells of oxygen and nutrients and inducing their programmed death. The compound was originally developed as an oncology tool. Researchers studying vascular targeting strategies for tumor ablation discovered that certain homing peptides could selectively bind to endothelial cells in the vasculature of white adipose tissue. When conjugated to a proapoptotic effector sequence, this targeting system produced dramatic fat loss in preclinical models, redirecting the research focus from cancer toward obesity. Preclinical results were striking. Obese mice treated with adipotide lost approximately 30% of total body weight over four weeks. Obese rhesus monkeys showed average weight loss of approximately 11%, with some individuals losing up to 38.7% of body weight, accompanied by meaningful improvements in insulin sensitivity and metabolic markers. A Phase 1 human clinical trial was initiated in 2011 in patients with advanced prostate cancer and comorbid obesity, though clinical development appears to have been formally discontinued by 2019. Adipotide is classified as a chimeric peptide-peptidomimetic construct with a molecular weight of approximately 2 to 3 kDa. It is available through research peptide suppliers in lyophilized powder form and has no approved human use in any jurisdiction. Its mechanism of action is irreversible by nature, which distinguishes it fundamentally from all currently approved weight loss therapeutics and demands careful consideration of its risk profile.

How It Works

Molecular Architecture

Adipotide is a chimeric construct composed of two functionally distinct peptide domains joined by a short linker sequence. The full molecular structure includes a prohibitin-targeting homing peptide domain (KGGRAKD-GG-(D)CKGGRAKDC) and a DKLAKLAK² proapoptotic effector motif. Together, these components form a delivery system that seeks out a specific cellular target and then kills it upon arrival.

The Targeting Domain

The homing sequence binds selectively to prohibitin and annexin A2 (ANXA2), two proteins found on the luminal surface of endothelial cells lining the blood vessels that supply white adipose tissue. Prohibitin expression is notably enriched on adipose vasculature endothelium relative to most other tissues, providing a degree of selectivity that makes targeted delivery theoretically feasible. However, it is important to acknowledge that prohibitin is not exclusively expressed in adipose vasculature. It is present at lower levels on renal endothelium, renal tubular cells, and other vascular beds throughout the body. This incomplete tissue specificity is the root cause of adipotide’s primary toxicity concern.

The Proapoptotic Effector Domain

Once the homing peptide binds prohibitin on an endothelial cell surface, receptor-mediated internalization brings the entire construct inside the cell. The KLAKLAK sequence, which is the effector domain, then disrupts mitochondrial membrane integrity. Mitochondrial membrane disruption triggers the intrinsic apoptosis pathway, leading to endothelial cell death.

Downstream Cascade

The sequence of events demonstrated in animal studies proceeds as follows: the peptide binds prohibitin on adipose tissue endothelial cells, is internalized via receptor-mediated uptake, disrupts mitochondrial membranes through the KLAKLAK domain, induces endothelial cell apoptosis, causes collapse of the adipose-specific microvasculature, and ultimately results in secondary adipocyte death due to loss of blood supply. This is anti-angiogenic fat ablation, not metabolic modulation.

Why Fat Cell Destruction Differs from Fat Cell Shrinkage

Virtually all existing fat loss interventions, including caloric restriction, GLP-1 receptor agonists, and exercise, work by emptying fat cells rather than eliminating them. Adipocytes shrink as their lipid content is mobilized, but they persist. This is one reason why weight regain is so common following cessation of treatment or caloric restriction. The preserved fat cell population can rapidly re-expand when caloric intake increases. Adipotide takes the opposite approach. It destroys fat cells by eliminating their blood supply. Dead cells do not refill. In theory, this could confer a more durable fat loss outcome because the cellular infrastructure no longer exists. Whether this theoretical advantage translates into meaningful long-term benefits in humans remains unknown, as no long-term human data exists.

Reseaerch Benefits

Substantial Fat Mass Reduction in Preclinical Models

The most compelling evidence for adipotide’s efficacy comes from its preclinical performance. Obese mice lost approximately 30% of body weight over four weeks of treatment. Obese rhesus monkeys achieved an average weight reduction of 11% over the same period, with some animals reaching losses of up to 38.7% of initial body weight. These figures exceed what is typically achievable with most pharmacological interventions in primate models.

Preferential Loss of Visceral Adipose Tissue

Preclinical data indicate that adipotide preferentially ablates visceral adipose tissue, the deep abdominal fat depot most strongly associated with insulin resistance, cardiovascular disease, and metabolic syndrome. Preferential visceral fat reduction is a clinically meaningful distinction, as this fat depot is disproportionately harmful relative to subcutaneous fat.

Preservation of Lean Mass

In animal studies, lean body mass was relatively preserved during adipotide treatment. Weight loss appeared to be primarily attributable to fat mass reduction rather than muscle wasting, which is a consistent concern with aggressive caloric restriction and some pharmacological approaches.

Metabolic Improvements

Adipotide treatment in primate studies was associated with improved insulin sensitivity and reductions in fasting triglyceride levels alongside weight loss. These metabolic benefits appeared to track proportionally with the degree of weight reduction achieved, consistent with what would be expected from significant fat mass loss generally.

Mechanism Independence from Appetite and CNS Pathways

Adipotide does not work through appetite suppression, alteration of satiety signals, or central nervous system modulation. Treated animals continued normal eating behavior. This represents a fundamentally different therapeutic avenue that could theoretically be relevant for individuals who cannot tolerate incretin- based therapies or CNS-active weight loss agents, or who have not responded to those approaches.

Persistence of Effects After Treatment Cessation

Unlike receptor agonists that require continuous administration to maintain their effects, vascular destruction is not rapidly reversed. Ablated blood vessels do not regenerate immediately, meaning that some degree of benefit may persist after the treatment period ends. Animal data suggest effects persist beyond the active treatment phase, though the body can generate new fat cells over time, particularly with sustained caloric surplus.

What the Science Shows

Mouse Studies (Kolonin et al., 2004) The foundational adipotide research was published in Nature Medicine in 2004 by Kolonin and colleagues. This work demonstrated that targeted ablation of adipose vasculature in obese mice could reverse obesity without surgical intervention. Treated mice lost approximately 30% of body weight over four weeks. Fat loss was rapid, significant, and accompanied by improvements in metabolic markers. This study established the proof of concept for adipose-targeted vascular ablation as a weight loss strategy and generated considerable scientific interest.

Primate Study (Barnhart et al., 2011) The pivotal nonhuman primate study was published in Science Translational Medicine in 2011. Obese rhesus monkeys received adipotide for four weeks, followed by four weeks of observation without treatment. The results demonstrated an average body weight loss of approximately 11% at four weeks, with some individuals achieving losses of up to 38.7% of initial body weight. Abdominal circumference was measurably reduced. Insulin sensitivity improved significantly. Triglyceride levels declined. Effects were dose dependent, with higher doses producing greater fat loss.

The critical safety finding from this study was dose-dependent kidney toxicity. Proximal tubular injury was the primary dose-limiting adverse effect. Some animals developed proteinuria, elevated serum creatinine, and histological evidence of renal damage. Importantly, kidney function returned to baseline after treatment was discontinued in most animals. However, the narrow separation between effective and nephrotoxic doses was identified as a serious limitation for clinical development. The kidney toxicity observed in this study was the principal factor that ultimately halted further clinical advancement.

Phase 1 Human Trial (NCT01262664, 2011–2012) A Phase 1 clinical trial was initiated in 2011 and registered on ClinicalTrials.gov under identifier NCT01262664. The study enrolled patients with advanced solid tumors who also had comorbid obesity. The primary objectives were safety assessment and dose finding. Published information about the outcomes of this trial remains limited in the public domain. Clinical development of adipotide appears to have been formally discontinued as of 2019, with no subsequent human trials announced. The specific reasons for discontinuation were never publicly detailed, though the toxicity profile identified in primates almost certainly contributed.

Additional Research (Daquinag et al., 2016) A 2016 study published in Molecular Therapy by Daquinag and colleagues examined the effects of targeted proapoptotic peptides depleting adipose stromal cells on tumor growth. This work explored the oncological applications of the adipose vascular targeting approach and provided additional mechanistic insight into how prohibitin-targeting peptides behave in vivo, further characterizing the tumor microenvironment modulation potential of this class of compounds.

Dosing Protocol

Important Preliminary Note

There is no validated human dosing protocol for adipotide. The following information is extrapolated from primate research and represents the closest available reference points for researchers. This compound carries substantially higher risk than most research peptides due to its irreversible mechanism of action and demonstrated nephrotoxicity. Human dosing data is essentially nonexistent.

Route of Administration

All preclinical studies used either controlled intravenous infusion or subcutaneous injection. Subcutaneous injection is the route most commonly referenced in the research community for this compound. Oral administration is not feasible. Adipotide is a peptide of approximately 2 to 3 kDa and would be rapidly degraded by gastrointestinal proteases. It cannot cross the intestinal epithelium intact in any meaningful quantity, and no oral formulation has been explored in published research.

Conservative Protocol

The conservative dosing reference derived from primate studies is 0.5 mg/kg body weight administered once daily via subcutaneous injection. For a 100 kg individual, this equates to 50 mg daily. For an 80 kg individual, this equates to 40 mg daily. For a 70 kg individual, this equates to 35 mg daily.

Higher Dose Reference

The higher dose range used in some primate experiments was 1.0 mg/kg body weight per day. This represents the upper boundary of the dose range that produced significant fat loss in primates and was also the range associated with the most pronounced nephrotoxicity. There is no evidence that doses above 1.0 mg/kg provide additional benefit, and they carry substantially increased toxicity risk.

Cycle Length

The primate studies used four-week treatment periods. Based on this reference point, four weeks is the maximum cycle length that has any preclinical basis. Extended use beyond this period increases the risk of cumulative kidney stress. A minimum of four weeks off between cycles is a reasonable precaution based on the renal recovery timeline observed in primate studies. Shorter cycles with lower doses represent a more cautious approach.

Practical Dosing Considerations and Draw Volumes

At the standard dose of 0.5 mg/kg, the quantities required are substantial. With a 5 mg vial reconstituted in 1 mL of bacteriostatic water to yield a concentration of 5 mg/mL, a single daily dose for a 70 kg individual would require 7.0 mL, necessitating multiple vials. For a 100 kg individual at this dose, 10.0 mL would be required daily. This makes 5 mg vials highly impractical for the standard protocol. Larger vial formats improve practicality. Some researchers have experimented with doses in the microgram range, far below primate protocols, but there is no data indicating whether such sub-therapeutic doses produce meaningful effects or simply reduce both benefit and toxicity.

Reconstitution Instructions

Use bacteriostatic water for reconstitution. Draw the appropriate volume of bacteriostatic water into a sterile syringe. Inject slowly down the inside wall of the vial to minimize foaming. Gently swirl or roll the vial until the powder is fully dissolved. Do not shake. The reconstituted solution should appear clear and colorless. Discard immediately if the solution is cloudy or contains visible particles. Label each vial with the reconstitution date and the resulting concentration. Refrigerate reconstituted vials at 36 to 46 degrees Fahrenheit (2 to 8 degrees Celsius). Use within 28 days of reconstitution.

Side Effects and Safety Profile

Primary Safety Concern: Renal Toxicity

Nephrotoxicity is the principal and most serious documented side effect of adipotide. The kidneys express prohibitin on renal tubular cells and glomerular endothelium, making them a significant off-target tissue for the adipotide homing peptide. In primate studies, dose-dependent proximal tubular injury was the primary dose-limiting toxicity. Findings included proteinuria, elevated serum creatinine, and histological evidence of renal damage at higher doses. While kidney function recovered after treatment cessation in most animals, some subjects developed severe renal impairment. The therapeutic window between effective and nephrotoxic doses is narrow, which was a central reason clinical development was discontinued.

Irreversibility of the Mechanism

Unlike signaling pathway modulators that can be titrated, stopped, or reversed, adipotide’s proapoptotic mechanism is irreversible. Once the KLAKLAK effector domain disrupts mitochondrial membranes, cell death proceeds. There is no pharmacological antidote. Overdosing or mistargeting does not produce a reversible effect that can be corrected. This fundamentally distinguishes adipotide from all currently approved weight loss medications and demands a heightened degree of caution.

Off-Target Apoptosis Risk

Prohibitin is expressed, albeit at lower levels, in tissues beyond adipose vasculature. The renal endothelium is the best-documented example, but other vascular beds throughout the body also carry some expression. Any delivery method, route, or formulation that increases non-selective tissue penetration or bypasses normal prohibitin-mediated selectivity would increase the risk of apoptosis in non-target tissues. This concern is why DMSO-based delivery vehicles would be particularly contraindicated; DMSO enhances membrane permeability non-selectively and could undermine the targeting selectivity that adipotide depends upon for its relative safety.

Signs of Kidney Stress Requiring Immediate Attention

Researchers should monitor closely for any signs of renal dysfunction during and after use. These include changes in urine color, particularly dark or blood-tinged urine; decreased urine output or frequency; lower back pain or flank pain; swelling in the lower extremities; and unexplained fatigue. Any of these symptoms warrant immediate cessation of the compound and prompt medical evaluation. Bringing information about the compound to the treating physician is important for appropriate clinical assessment.

Other Potential Adverse Effects

Additional potential adverse effects include dehydration secondary to renal stress, injection site reactions including local inflammation, and theoretically possible effects on any other highly vascularized tissue expressing prohibitin. Because human data is essentially absent, the full side effect profile in the human context remains incompletely characterized. Unknown off-target effects represent a meaningful risk that cannot be quantified without clinical data.

Contraindications and Precautions

Absolute Contraindications

Adipotide should not be used by individuals with any existing kidney disease or history of kidney problems, given the documented nephrotoxicity. It is also contraindicated in individuals with cardiovascular disease, as the vascular targeting mechanism could affect cardiac and coronary endothelium. Individuals with diabetes and established vascular complications face amplified risk. Active cancer represents a contraindication given the pro-apoptotic mechanism and potential immune and vascular interactions. Pregnancy and breastfeeding are absolute contraindications given the irreversible cellular destruction mechanism and unknown effects on fetal or neonatal development. Any condition primarily affecting blood vessels is a contraindication.

Use With Extreme Caution

Individuals with elevated blood pressure, a history of blood clots, or any metabolic disorder affecting vascular function should approach this compound with extreme caution if they choose to explore it in a research context. These conditions increase baseline vascular vulnerability and may narrow the already tight therapeutic window.

Drug Interactions

No formal interaction studies exist for adipotide. Compounds that affect kidney function, including NSAIDs, certain antibiotics, and diuretics, should be used with particular caution during any research protocol involving adipotide. Medications that alter vascular function or coagulation represent an additional theoretical interaction concern. Given the absence of any interaction data, researchers should be conservative in their concurrent use of any other agents.

Hydration Requirement

The renal toxicity observed in primate studies places hydration in the category of a critical safety measure rather than a recommendation. Significantly increased water intake throughout any research protocol is essential to minimize renal tubular concentration of the compound and support kidney clearance.

Comparison to Other Weight Loss Approaches

Adipotide vs. GLP-1 Receptor Agonists (Semaglutide, Liraglutide) GLP-1 receptor agonists work by mimicking the glucagon-like peptide-1 hormone, enhancing insulin secretion, suppressing glucagon, slowing gastric emptying, and reducing appetite through central nervous system mechanisms. They are fully reversible in their action. Semaglutide (Ozempic, Wegovy) has demonstrated average weight loss of approximately 15% of body weight in clinical trials, with an extensive and well-characterized safety profile built on hundreds of thousands of patient-years of data. Common side effects are gastrointestinal. Adipotide’s mechanism is irreversible and carries nephrotoxicity risk with minimal human safety data. For most individuals, GLP-1 agonists represent the clearly safer and better- evidenced choice.

Adipotide vs. GLP-1/GIP Dual Agonist (Tirzepatide) Tirzepatide (Mounjaro, Zepbound) combines GLP-1 and GIP receptor agonism, producing average weight loss of up to 20 to 22% of body weight in clinical trials, the highest efficacy figures documented for any approved pharmacological weight loss agent to date. Like GLP-1 agonists, tirzepatide is fully reversible, has an established safety profile, and operates through appetite and metabolic signaling rather than tissue ablation. Adipotide cannot match this combination of efficacy and safety profile, particularly given the complete absence of controlled human data.

Adipotide vs. Retatrutide (Triple Agonist, Investigational) Retatrutide, a GLP-1, GIP, and glucagon triple receptor agonist currently in Phase 3 clinical development, has shown weight loss of up to 24% of body weight in Phase 2 trials. Though not yet approved, it already has far more human safety and efficacy data than adipotide. The triple agonist mechanism is also fully reversible, and its side effects are predominantly gastrointestinal.

Where Adipotide Stands

Adipotide occupies a unique scientific niche because of its vascular ablation mechanism. It is the only known compound that achieves fat loss by destroying adipose vasculature rather than modulating metabolic signals. This uniqueness is scientifically interesting but clinically problematic. Its development was not stopped because it failed to work. It was stopped because the risk-benefit ratio was unfavorable given the narrow therapeutic window, irreversible mechanism, nephrotoxicity, and the concurrent advancement of far safer alternatives. For the overwhelming majority of research contexts, the incretin-based therapies represent the rational first choice.

Success Tips for Research Protocols

Prioritize Hydration

Given the kidney toxicity documented in primate studies, aggressive hydration is the single most important harm reduction measure. Significantly increased daily water intake throughout any research protocol helps maintain renal tubular flow and minimize concentration of the compound in the kidneys.

Keep Cycles Short

The four-week treatment period used in primate studies is the only reference point available. Extending cycle length beyond this duration increases cumulative kidney stress with no established benefit. Adequate time between cycles, a minimum of four weeks, allows for renal recovery consistent with the primate recovery timeline.

Start at the Lower End of the Dose Range The conservative protocol of 0.5 mg/kg provides the most preclinical reference data. Starting at this level, rather than the higher dose range, is appropriate for any initial research protocol. There is no basis for exceeding 1.0 mg/kg under any circumstances.

Monitor Closely

Active self-monitoring is essential with this compound. Daily observation of urine color, output volume, and frequency provides a practical early warning system for kidney stress. Any deviation from normal should prompt immediate cessation and medical evaluation. Baseline and periodic kidney function panels, including serum creatinine, BUN, and urinalysis, are appropriate components of any responsible research protocol.

Set Realistic Expectations

The primate data is scientifically impressive, but primate studies were conducted in controlled clinical settings with close veterinary monitoring and immediate intervention capability. Human use of this compound without that level of clinical oversight represents a meaningfully different risk context. The absence of human efficacy and safety data means that outcomes in human research are not predictable from primate results alone.

Consider Alternatives First

Unless there is a specific and considered reason to avoid incretin-based therapies, the evidence base strongly supports exploring those agents before pursuing adipotide. Tirzepatide, semaglutide, and retatrutide collectively offer more substantial weight loss than most prior pharmacological approaches, with well- characterized safety profiles, established dosing protocols, and regulatory approval for clinical use. Adipotide’s uniqueness does not offset the magnitude of the known and unknown risks in the absence of human clinical data.

Storage and Handling

Before Reconstitution (Lyophilized Powder) Store lyophilized vials in the freezer at minus 4 degrees Fahrenheit (minus 20 degrees Celsius) for long- term storage. Short-term storage in the refrigerator at 36 to 46 degrees Fahrenheit (2 to 8 degrees Celsius) is acceptable. Protect from light exposure. Do not use vials past their expiration date. Inspect the powder for any discoloration or unusual appearance before reconstitution and discard any suspect vials.

After Reconstitution

Reconstituted solution must be refrigerated at 36 to 46 degrees Fahrenheit (2 to 8 degrees Celsius). Use within 28 days of reconstitution. Do not freeze reconstituted solution, as freeze-thaw cycles can degrade peptide integrity. Keep the vial stopper clean between uses. Discard immediately if the solution becomes cloudy, discolored, or develops visible particulate matter.

Injection Technique

Wash hands thoroughly before handling any injectable compound. Clean the vial stopper with an alcohol swab and allow it to air dry completely before drawing. Use a sterile insulin syringe appropriate for the planned volume. Clean the injection site with an alcohol swab. Pinch a skinfold and insert the needle at 45 to 90 degrees into subcutaneous tissue. There is no need to aspirate for subcutaneous injections. Inject the solution slowly and steadily. Withdraw the needle and apply light pressure with sterile gauze if needed. Dispose of the syringe immediately in an approved sharps container. Rotate injection sites among the abdomen, outer thighs, and upper arms, maintaining at least one inch separation between sites on rotation.

Legal Status

Adipotide has not been approved by the U.S. Food and Drug Administration for any indication, and clinical development appears to have been formally discontinued as of 2019. It is not approved for human use in any jurisdiction. Adipotide is classified as a research chemical and is commercially available in lyophilized powder form from research peptide suppliers for in vitro and laboratory research purposes. Researchers and institutions should review applicable local, state, and federal regulations regarding the procurement, handling, and use of research chemicals prior to any acquisition or protocol initiation.

Frequently Asked Questions

Why was clinical development discontinued?

The specific business and regulatory decisions that led to discontinuation were never publicly detailed. However, the scientific record provides a clear picture of the contributing factors. The primary concern was the narrow therapeutic window between doses that produced meaningful fat loss and doses that caused kidney damage. The irreversible nature of the mechanism meant that overdosing or off-target effects could not be corrected pharmacologically. The prohibitin receptor is not exclusive enough to adipose vasculature to ensure safety at clinically effective doses. Regulatory approval of a weight loss compound with this risk profile would face a very high hurdle, particularly given the concurrent development of the incretin-based therapies, which offer comparable or superior efficacy with far more favorable safety profiles.

Is the fat loss permanent? In theory, adipotide-induced fat loss may be more durable than that achieved through conventional means because the destroyed fat cells are gone rather than merely emptied. Dead cells do not refill with lipid. However, the human body retains the capacity to generate new adipocytes, a process that is substantially driven by chronic caloric surplus. Long-term human data does not exist for adipotide. New adipose depots can develop over time even if existing cells have been ablated, meaning that without ongoing caloric discipline, the fat loss may not prove to be permanent in practice.

How does adipotide compare to GLP-1 drugs? The GLP-1 agonists and dual/triple agonists have undergone rigorous large-scale clinical trials, have established dosing protocols, and carry FDA approval. Their side effect profiles are well understood and are primarily gastrointestinal in nature. Adipotide has essentially no controlled human clinical data, an irreversible mechanism of action, documented nephrotoxicity, and a narrow therapeutic window. For the overwhelming majority of research and clinical contexts, the incretin-based drugs represent the evidence- based and lower-risk approach to pharmacological weight management.

Are the kidney effects reversible? In primate studies, kidney function returned to baseline after treatment was stopped in most animals. However, some subjects developed severe renal impairment, and the studies were conducted in controlled clinical settings with continuous veterinary monitoring and the ability to intervene rapidly. The applicability of these findings to human use with varying doses, cycle lengths, hydration status, and individual renal health baselines is uncertain. The reversibility demonstrated in primates cannot be assumed to hold universally in human research contexts.

Can lower doses be used effectively? Some researchers experiment with doses significantly below the primate protocol, in the microgram range rather than milligrams per kilogram. There is no published data to indicate whether such doses produce meaningful fat loss in any species. Lower doses may reduce toxicity, but if they fall below the effective range, they would provide neither benefit nor any rational risk justification.

Is DMSO appropriate as a delivery vehicle? DMSO would be fundamentally contraindicated as a delivery vehicle for adipotide. Adipotide’s relative selectivity depends on preferential delivery to adipose vasculature via prohibitin-mediated binding. DMSO enhances membrane permeability non-selectively across all contacted tissues, potentially bypassing the

prohibitin-mediated selectivity mechanism entirely. This would increase intracellular concentrations of the proapoptotic effector sequence in non-target tissues and substantially amplify the risk of off-target apoptosis in the kidneys and other organs.

Is this compound safe for human use? There is insufficient human data to answer this question. The preclinical safety profile demonstrates meaningful and dose-dependent nephrotoxicity with a narrow therapeutic window. The irreversible mechanism of action means that errors in dosing or individual variability in prohibitin expression could produce permanent tissue damage. Researchers considering this compound should do so with full awareness of these unknowns and with robust monitoring protocols in place.

References

1. Kolonin MG, Saha PK, Chan L, Pasqualini R, Arap W. Reversal of obesity by targeted ablation of adipose tissue. Nature Medicine. 2004;10(6):625–632. 2. Barnhart KF, Christianson DR, Hanley PW, et al. A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys. Science Translational Medicine. 2011;3(108):108ra112. 3. Daquinag AC, Tseng C, Salameh A, et al. Targeted proapoptotic peptides depleting adipose stromal cells inhibit tumor growth. Molecular Therapy. 2016;24(11):1–10. 4. Staquicini FI, Tandle A, Libutti SK, et al. Vascular ligand-receptor mapping by direct combinatorial selection in cancer patients. PNAS. 2011;108(46):18637–18642. 5. ClinicalTrials.gov. NCT01262664: Phase 1 Trial of Adipotide in Patients with Advanced Solid Tumors and Obesity. U.S. National Library of Medicine. 2011. 6. Hossen MN, Kajimoto K, Akita H, Hyodo M, Ishitsuka T, Harashima H. Ligand-based targeted delivery of a peptide modified nanocarrier to endothelial cells in adipose tissue. Journal of Controlled Release. 2019;126(3):6–22.