Buy Adipotide (FTPP) 5MG | Fat Loss Research Peptide

Overview

Adipotide (FTPP) is a research peptidomimetic that selectively targets prohibitin on adipose tissue vasculature to deliver a pro-apoptotic sequence, destroying fat-supplying blood vessels and inducing fat cell loss—distinct from traditional metabolic or hormonal methods. Preclinical rodent and primate studies and a Phase 1 human trial showed dose-dependent, largely fat-selective weight loss and metabolic improvements, with potential preferential effects on visceral fat. Clinical development was halted in 2011 due to dose-limiting kidney toxicity, underscoring a narrow therapeutic window. This document details mechanism of action, research history, benefits, dosing and administration protocols, safety and monitoring, contraindications, regulatory/ethical considerations, and research-only product information.

What is Adipotide (FTPP)?

Adipotide peptide , also known as FTPP (Fat-Targeted Proapoptotic Peptide), represents a revolutionary approach to fat loss research through selective vascular targeting. This innovative peptidomimetic compound consists of two functional components: a prohibitin-targeting sequence that directs the peptide to blood vessels supplying white adipose tissue, and a pro-apoptotic sequence that induces programmed cell death in those vessels. The result is a highly selective mechanism for reducing fat mass that differs fundamentally from traditional metabolic or hormonal approaches to weight management.

The development of adipotide emerged from research into tumor vasculature targeting, where scientists discovered that certain peptide sequences could selectively bind to receptors on blood vessels supplying tumors. Researchers recognized that white adipose tissue, like tumors, requires extensive vascularization to maintain its blood supply and nutrient delivery. By adapting vascular targeting technology to adipose tissue, they created ftpp adipotide as a tool for studying targeted fat reduction through blood vessel destruction.

The molecular structure of adipotide peptide is elegantly designed for its purpose. The targeting sequence (CKGGRAKDC) binds specifically to prohibitin, a protein that is preferentially expressed on the surface of endothelial cells lining blood vessels in white adipose tissue. This prohibitin expression pattern provides the selectivity that allows adipotide to distinguish fat tissue vasculature from blood vessels in other organs. Once the peptide binds to prohibitin receptors, it is internalized into the endothelial cells through receptor-mediated endocytosis.

The second component of ftpp adipotide is the pro-apoptotic sequence D(KLAKLAK)2, a synthetic peptide that disrupts mitochondrial membranes when it enters cells. In the bloodstream, this sequence is relatively inactive because it cannot cross cell membranes on its own. However, once the targeting sequence delivers it inside endothelial cells of adipose tissue blood vessels, the D(KLAKLAK)2 peptide disrupts mitochondrial function, triggering apoptosis (programmed cell death) in those specific cells. This leads to destruction of the blood vessels supplying fat tissue.

When blood vessels supplying adipose tissue are destroyed, the fat cells they nourish are deprived of oxygen and nutrients. Without adequate blood supply, adipocytes (fat cells) undergo apoptosis and are gradually cleared by the body’s natural waste removal systems. This process results in reduction of fat mass in areas where adipotide has targeted the vasculature. Importantly, the selectivity of the targeting mechanism means that blood vessels in other tissues are largely spared, providing a degree of specificity not achievable with systemic metabolic interventions.

Research with adipotide has demonstrated remarkable fat loss effects in preclinical models. Studies in obese rhesus monkeys showed that adipotide human trials potential was supported by dramatic weight loss of up to 27% over just 4 weeks of treatment, with fat mass reductions of approximately 39% while lean body mass was preserved. These results were far more dramatic than typically seen with dietary interventions or metabolic compounds, highlighting the potency of vascular targeting as a fat loss mechanism.

Human clinical trials with adipotide peptide progressed to Phase 1 studies in obese patients with type 2 diabetes. These trials demonstrated dose-dependent weight loss, with subjects losing significant amounts of body weight over the treatment period. The fat loss was accompanied by improvements in metabolic parameters including blood glucose control and insulin sensitivity. However, clinical development was ultimately halted in 2011 due to kidney-related safety concerns that emerged at higher doses, though lower doses showed acceptable tolerability.

Despite the discontinuation of clinical development, adipotide remains highly valuable for research purposes. The compound provides unique insights into adipose tissue biology, vascular targeting mechanisms, and the relationship between tissue blood supply and fat mass regulation. Researchers studying obesity, body composition, and metabolic health find ftpp adipotide to be an invaluable tool for understanding how targeted interventions might address fat accumulation more selectively than traditional approaches.

When researchers buy adipotide from PrymaLab, they receive pharmaceutical-grade peptide manufactured to the highest quality standards. Each 5mg vial contains 99% pure adipotide verified by third-party testing, ensuring reliable and reproducible research results. The peptide arrives as lyophilized powder for maximum stability, ready for reconstitution with ++bacteriostatic water++ when research protocols begin.

Understanding Adipose Tissue Vasculature and Fat Biology

To fully appreciate how adipotide peptide works, it’s essential to understand the role of blood vessels in adipose tissue maintenance and growth. White adipose tissue, the primary form of fat storage in the body, is a highly vascularized organ that requires extensive blood vessel networks to function. Each adipocyte must be within close proximity to a capillary to receive oxygen and nutrients and to release stored fatty acids when energy is needed.

Adipose tissue vasculature is dynamic and responds to changes in fat mass. When individuals gain weight, adipose tissue expands through both hypertrophy (existing fat cells growing larger) and hyperplasia (formation of new fat cells from precursor cells). This expansion requires angiogenesis, the formation of new blood vessels, to ensure adequate blood supply to the growing tissue. Without sufficient vascularization, adipose tissue cannot expand effectively, and fat cells in poorly vascularized areas may undergo hypoxia and cell death.

The relationship between adipose tissue and its blood supply is bidirectional. Fat cells secrete factors that promote angiogenesis, including vascular endothelial growth factor (VEGF) and other pro-angiogenic signals. These factors stimulate endothelial cells to proliferate and form new blood vessels that penetrate the expanding fat tissue. Conversely, blood vessels provide not just oxygen and nutrients but also deliver hormones, immune cells, and other factors that regulate adipocyte function.

Importantly, the blood vessels supplying white adipose tissue express distinct molecular markers that differentiate them from vasculature in other tissues. One of these markers is prohibitin, a protein that appears on the surface of endothelial cells in adipose tissue vasculature at higher levels than in most other organs. This differential expression pattern is what makes vascular targeting of fat tissue possible and is the basis for adipotide’s selectivity.

The concept of targeting adipose tissue vasculature for fat loss emerged from cancer research, where scientists developed peptides that could selectively bind to and destroy tumor blood vessels. Tumors, like adipose tissue, require extensive vascularization to grow and survive. By destroying tumor vasculature, researchers could starve tumors of their blood supply, causing tumor regression. The same principle applies to ftpp adipotide and fat tissue — by destroying the blood vessels supplying adipose depots, the compound effectively starves fat cells of their blood supply.

When adipotide destroys blood vessels in adipose tissue, several processes occur. First, the immediate loss of blood flow causes hypoxia (oxygen deprivation) in nearby adipocytes. Fat cells are metabolically active and require oxygen for their various functions, so hypoxia triggers stress responses. Second, the loss of nutrient delivery means adipocytes cannot maintain their normal metabolic activities or respond to hormonal signals effectively. Third, without blood vessel access, adipocytes cannot release stored fatty acids into circulation when the body needs energy.

These combined stresses lead to adipocyte apoptosis, the programmed cell death pathway that allows cells to be removed without causing inflammation or tissue damage. As fat cells die, they are engulfed by macrophages and other immune cells that clear the cellular debris. The fat stored in these cells is metabolized and removed from the body through normal metabolic pathways. Over time, this process results in reduction of fat mass in the targeted areas.

Interestingly, research suggests that adipotide peptide may preferentially affect visceral adipose tissue (fat surrounding internal organs) compared to subcutaneous fat (fat under the skin). Visceral fat is more highly vascularized than subcutaneous fat and may express higher levels of prohibitin on its blood vessels, making it more susceptible to adipotide’s targeting mechanism. This preferential effect on visceral fat is particularly valuable from a health perspective, as visceral adiposity is more strongly associated with metabolic disease, cardiovascular risk, and other health problems than subcutaneous fat.

The selectivity of ftpp adipotide for adipose tissue vasculature, while impressive, is not absolute. At higher doses, the compound can affect blood vessels in other tissues, particularly the kidneys, which led to the safety concerns that halted clinical development. This highlights the importance of dose selection in research protocols and the need for careful monitoring when using this powerful compound. Understanding the balance between efficacy and safety is a key aspect of adipotide research.

Adipotide Mechanism of Action: Vascular Targeting for Fat Loss

The mechanism by which adipotide promotes fat loss involves a sophisticated sequence of molecular events, all stemming from its dual-component design as a vascular targeting agent. Understanding these mechanisms in detail helps researchers design effective protocols and interpret research results accurately.

Primary Mechanism — Prohibitin Targeting:

When adipotide peptide is administered, it enters the bloodstream and circulates throughout the body. The CKGGRAKDC targeting sequence at the N-terminus of the peptide has high binding affinity for prohibitin, a protein expressed on the surface of endothelial cells. While prohibitin is present in various tissues, its surface expression on blood vessel endothelium is particularly high in white adipose tissue, providing the selectivity that makes ftpp adipotide effective for targeted fat loss.

The binding of adipotide to prohibitin receptors on adipose tissue blood vessels is the critical first step in its mechanism. This binding is specific and high-affinity, meaning the peptide preferentially accumulates in adipose tissue vasculature compared to other organs. Once bound, the peptide-receptor complex is internalized through receptor-mediated endocytosis, a process where the cell membrane engulfs the bound peptide and brings it inside the cell in a vesicle.

Cellular Internalization and Pro-Apoptotic Action:

Once inside endothelial cells, the pro-apoptotic component of adipotide peptide becomes active. The D(KLAKLAK)2 sequence is a synthetic peptide designed to disrupt mitochondrial membranes. In the bloodstream, this sequence cannot enter cells on its own because it lacks the ability to cross cell membranes. However, once delivered inside cells by the targeting sequence, it gains access to intracellular compartments including mitochondria.

Mitochondria are the powerhouses of cells, generating the ATP energy that cells need to function. They have a double membrane structure, and the integrity of these membranes is essential for mitochondrial function and cell survival. The D(KLAKLAK)2 peptide disrupts mitochondrial membranes through its amphipathic structure, which allows it to insert into lipid bilayers and create pores or otherwise compromise membrane integrity.

When mitochondrial membranes are disrupted, several catastrophic events occur in the cell. First, the electrochemical gradient across the inner mitochondrial membrane collapses, halting ATP production. Second, pro-apoptotic factors normally sequestered in mitochondria are released into the cytoplasm, including cytochrome c, which activates the caspase cascade leading to apoptosis. Third, reactive oxygen species production increases, causing oxidative stress that further damages cellular components.

Endothelial Cell Apoptosis and Vessel Destruction:

The combined effects of mitochondrial disruption trigger programmed cell death (apoptosis) in the endothelial cells that have internalized adipotide. Apoptosis is a controlled process where cells systematically dismantle themselves without causing inflammation or damage to surrounding tissues. The dying endothelial cells detach from the blood vessel wall, leaving gaps in the vessel lining.

As multiple endothelial cells in a blood vessel undergo apoptosis, the structural integrity of the vessel is compromised. Blood vessels are essentially tubes made of endothelial cells supported by basement membrane and sometimes smooth muscle cells. When the endothelial lining is destroyed, the vessel can no longer maintain blood flow effectively. The vessel may collapse, become blocked by blood clots, or simply cease to function as a conduit for blood.

The destruction of blood vessels in adipose tissue has immediate consequences for the fat cells they supply. Without blood flow, adipocytes are deprived of oxygen (hypoxia) and nutrients (glucose, fatty acids, amino acids). They also lose the ability to release stored fatty acids into circulation or respond to hormonal signals like insulin or catecholamines that normally regulate fat metabolism.

Adipocyte Apoptosis and Fat Mass Reduction:

The hypoxic and nutrient-deprived environment created by blood vessel destruction triggers stress responses in adipocytes. Fat cells attempt to adapt to these conditions, but if blood flow is not restored, they eventually undergo apoptosis themselves. The adipotide results observed in research studies reflect this secondary adipocyte death following vascular targeting.

As adipocytes die, they are recognized and cleared by macrophages, immune cells that specialize in removing dead cells and debris. The lipids stored in dying fat cells are released and metabolized through normal pathways. Some fatty acids are taken up by other tissues for energy, while others may be processed by the liver. The overall effect is a reduction in fat mass in areas where ftpp adipotide has successfully targeted the vasculature.

Selectivity and Tissue Specificity:

The selectivity of adipotide peptide for adipose tissue vasculature is impressive but not absolute. The degree of selectivity depends on the differential expression of prohibitin on blood vessel endothelium in different tissues. White adipose tissue expresses high levels of surface prohibitin, making it a primary target. However, other tissues also express prohibitin to varying degrees, and at higher doses of adipotide, off-target effects can occur.

The kidneys, in particular, showed susceptibility to adipotide effects in clinical trials, with kidney-related side effects being the primary safety concern that halted development. This likely reflects prohibitin expression in renal vasculature or glomerular cells. Understanding this dose-dependent selectivity is crucial for research protocol design, as lower doses may provide adequate fat loss effects while minimizing off-target toxicity.

Temporal Dynamics and Dose-Response:

The time course of adipotide’s effects follows a predictable pattern. After administration, the peptide circulates and binds to target vessels within hours. Endothelial cell apoptosis begins within 24-48 hours, and vessel destruction becomes apparent within several days. Adipocyte apoptosis and fat mass reduction occur over subsequent weeks as the full effects of vascular targeting manifest.

The adipotide dosage used in research directly affects both the magnitude and selectivity of effects. Lower doses may preferentially target adipose tissue with minimal off-target effects, while higher doses produce more dramatic fat loss but increase the risk of affecting other tissues. Research protocols must carefully balance efficacy and safety through appropriate dose selection.

Regeneration and Reversibility:

An important aspect of adipotide’s mechanism is the potential for vascular regeneration after treatment cessation. Blood vessels have the capacity to regenerate through angiogenesis, and adipose tissue is particularly adept at stimulating new vessel formation. After ftpp adipotide treatment ends, surviving adipocytes and adipose tissue stromal cells can secrete pro-angiogenic factors that promote new blood vessel growth.

This regenerative capacity means that the effects of adipotide may not be permanent without ongoing treatment or lifestyle modifications to prevent fat regain. However, it also provides a safety margin — if off-target vascular effects occur, cessation of treatment allows for tissue recovery through revascularization. This reversibility is an important consideration in research protocol design and safety planning.

Clinical Research and Adipotide Studies

Adipotide has been studied extensively in preclinical models and has progressed to human clinical trials, providing substantial data on its effects, safety profile, and potential applications. Understanding this research history helps researchers design effective protocols and interpret their findings in context.

Preclinical Studies — Proof of Concept:

Early research with adipotide peptide in rodent models demonstrated the feasibility of vascular targeting for fat loss. Studies in diet-induced obese mice showed that administration of the compound led to significant reductions in body weight and fat mass. Histological examination of adipose tissue from treated animals revealed evidence of blood vessel destruction and adipocyte apoptosis, confirming the proposed mechanism of action.

These initial studies established several important principles. First, they confirmed that ftpp adipotide could selectively target adipose tissue vasculature with relative sparing of other organs at appropriate doses. Second, they showed that the fat loss achieved was accompanied by improvements in metabolic parameters including insulin sensitivity and glucose tolerance. Third, they demonstrated that the effects were dose-dependent, with higher doses producing greater fat loss but also increased risk of adverse effects.

Primate Studies — Translational Research:

The most dramatic preclinical results came from studies in obese rhesus monkeys, which provided crucial translational data supporting human trials. In these studies, obese monkeys received daily subcutaneous injections of adipotide at doses ranging from 0.25 to 2.5 mg/kg body weight. The results were remarkable, with treated animals losing up to 27% of their body weight over 4 weeks of treatment.

Body composition analysis revealed that the weight loss was primarily fat mass, with approximately 39% reduction in adipose tissue while lean body mass was largely preserved. This selective fat loss distinguished adipotide results from simple caloric restriction, which typically causes loss of both fat and lean tissue. The monkeys also showed reductions in waist circumference, improvements in insulin sensitivity, and decreases in markers of metabolic dysfunction.

Importantly, the primate studies also revealed dose-limiting toxicities. At the highest doses tested (2.5 mg/kg), some animals developed kidney-related problems including increased serum creatinine and proteinuria, indicating kidney damage. These findings suggested that while adipotide was highly effective for fat loss, there was a relatively narrow therapeutic window between effective doses and those causing adverse effects.

Phase 1 Human Clinical Trial:

Based on promising preclinical data, adipotide human trials progressed to Phase 1 studies in humans. These trials enrolled obese patients with type 2 diabetes and tested escalating doses of adipotide peptide administered as daily subcutaneous injections. The primary goals were to assess safety, tolerability, and pharmacokinetics, with secondary endpoints including effects on body weight and metabolic parameters.

The Phase 1 trial demonstrated that adipotide could produce weight loss in humans, with dose-dependent effects on body weight. Subjects receiving the compound lost significantly more weight than those receiving placebo, with the magnitude of weight loss increasing with dose. The fat loss was accompanied by improvements in glycemic control, with reductions in fasting glucose and HbA1c levels in diabetic subjects.

However, the trial also revealed safety concerns that would ultimately halt development. At higher doses, some subjects experienced kidney-related adverse events including increased serum creatinine, proteinuria, and in some cases, more serious kidney dysfunction. These adipotide side effects were consistent with the kidney toxicity observed in primate studies and raised concerns about the compound’s safety profile at doses needed for significant weight loss.

Clinical Development Discontinuation:

In 2011, the pharmaceutical company developing adipotide (Arrowhead Research Corporation, in partnership with The University of Texas MD Anderson Cancer Center) announced the discontinuation of clinical development. The decision was based on the kidney toxicity observed in clinical trials, which suggested that the therapeutic window between effective doses for weight loss and doses causing kidney damage was too narrow for safe therapeutic use.

The company stated that while the compound showed proof-of-concept for vascular targeting as a weight loss mechanism, the safety profile did not support continued development for obesity treatment. The kidney effects appeared to be mechanism-based, resulting from adipotide’s effects on renal vasculature or glomerular cells, rather than off-target toxicity that might be engineered away through structural modifications.

Research Implications and Ongoing Value:

Despite the discontinuation of clinical development, adipotide remains highly valuable for research purposes. The extensive preclinical and clinical data provides important insights into vascular targeting as a fat loss mechanism, the role of adipose tissue blood supply in fat mass regulation, and the challenges of developing selective vascular targeting agents.

The research with ftpp adipotide has informed scientific understanding of adipose tissue biology and has inspired development of next-generation compounds that might achieve similar fat loss effects with improved safety profiles. Understanding why adipotide caused kidney toxicity has helped researchers identify potential strategies for improving selectivity and reducing off-target effects in future vascular targeting agents.

For researchers who buy adipotide today, the peptide serves as a powerful tool for studying adipose tissue vasculature, vascular targeting mechanisms, and the relationship between tissue blood supply and fat mass. The well-characterized mechanism of action and extensive research history make it an ideal compound for controlled research studies exploring these important biological questions.

Lessons from Adipotide Research:

The adipotide research program provides several important lessons for peptide drug development and obesity research. First, it demonstrates that vascular targeting is a viable approach to fat loss, capable of producing dramatic reductions in fat mass. Second, it highlights the importance of selectivity in targeted therapies — even relatively selective compounds can cause off-target effects at higher doses. Third, it shows that the therapeutic window for some mechanisms may be too narrow for safe therapeutic use, even if the mechanism is effective.

These lessons continue to inform research into obesity treatments and vascular targeting approaches. While adipotide peptide itself may not become a therapeutic agent, the principles it demonstrated and the data it generated remain valuable for advancing the field of obesity research and metabolic medicine.

Adipotide Benefits for Fat Loss Research

The adipotide peptide benefits for fat loss research extend across multiple aspects of adipose tissue biology and body composition, making it one of the most innovative tools available for studying targeted fat reduction. Understanding these benefits helps researchers design studies that maximize the compound’s research value.

Dramatic Fat Mass Reduction:

The most obvious benefit of adipotide is its ability to promote substantial reductions in fat mass through a novel mechanism. Preclinical research showed fat mass reductions of up to 39% in obese primates over just 4 weeks of treatment, with body weight decreases of up to 27%. These dramatic effects far exceed what is typically achievable through dietary interventions or traditional weight loss compounds, demonstrating the potency of vascular targeting as a fat loss mechanism.

The magnitude of fat loss with ftpp adipotide makes it particularly valuable for research into maximum fat reduction potential and the limits of adipose tissue targeting. Researchers can study how much fat can be safely removed, how quickly fat loss can occur, and what factors limit the extent of fat reduction achievable through vascular targeting.

Selective Fat Loss with Lean Mass Preservation:

One of the most important adipotide peptide benefits is its selectivity for fat tissue, with relative preservation of lean body mass. Unlike caloric restriction or general metabolic interventions that cause loss of both fat and muscle, adipotide results show predominantly fat loss. In primate studies, approximately 90% of weight loss was fat mass, with lean tissue largely maintained.

This selective fat loss makes adipotide valuable for research into body composition optimization and the mechanisms that determine whether weight loss comes from fat or lean tissue. For adipotide bodybuilding research applications, the ability to reduce fat while preserving muscle is particularly interesting, as it represents an ideal body composition change for athletic performance and aesthetics.

Targeted Fat Depot Reduction:

Research suggests that adipotide peptide may preferentially affect certain fat depots over others, particularly visceral adipose tissue compared to subcutaneous fat. Visceral fat, which surrounds internal organs, is more highly vascularized and may express higher levels of prohibitin on its blood vessels, making it more susceptible to adipotide’s targeting mechanism.

This preferential effect on visceral fat is particularly valuable from a health research perspective. Visceral adiposity is strongly associated with metabolic syndrome, type 2 diabetes, cardiovascular disease, and other health problems. The ability to selectively reduce visceral fat while potentially sparing subcutaneous fat could provide insights into optimal fat distribution for metabolic health.

Metabolic Improvements:

Beyond direct fat loss effects, adipotide research has shown improvements in metabolic parameters. Studies in obese primates and humans demonstrated improvements in insulin sensitivity, glucose tolerance, and glycemic control in diabetic subjects. These metabolic benefits likely result from the reduction in fat mass, particularly visceral fat, which is metabolically active and contributes to insulin resistance.

The metabolic improvements observed with ftpp adipotide make it valuable for research into the relationship between fat mass, fat distribution, and metabolic health. Researchers can study whether the metabolic benefits are simply due to fat loss or whether vascular targeting produces additional effects on adipose tissue function and inflammatory signaling.

Novel Mechanism for Mechanistic Studies:

The unique vascular targeting mechanism of adipotide peptide provides opportunities for research that would not be possible with traditional fat loss approaches. Researchers can study the role of adipose tissue vasculature in fat mass regulation, the consequences of blood vessel destruction in fat tissue, the regenerative capacity of adipose tissue after vascular injury, and the selectivity determinants that allow targeting of fat tissue over other organs.

These mechanistic studies contribute to fundamental understanding of adipose tissue biology and may inform development of next-generation targeted therapies. The ability to selectively manipulate adipose tissue blood supply provides a powerful experimental tool for dissecting the complex biology of fat tissue.

Dose-Response Research:

The dose-dependent effects of adipotide allow for detailed dose-response studies that can establish relationships between dose, fat loss magnitude, selectivity, and adverse effects. Understanding the adipotide dosage that produces optimal fat loss with acceptable safety is crucial for research applications and informs understanding of the therapeutic window for vascular targeting approaches.

Researchers can design studies that test multiple dose levels, different dosing frequencies, and various treatment durations to fully characterize the compound’s effects. This dose-response data is valuable for optimizing research protocols and understanding the limits of vascular targeting as a fat loss mechanism.

Combination Research Potential:

Adipotide can be combined with other research compounds to study synergistic or additive effects on body composition. Researchers might combine it with muscle-building peptides like ++Ipamorelin++ or ++CJC-1295++ to investigate whether simultaneous fat loss and muscle gain can be achieved. Combinations with metabolic compounds could explore whether enhancing fat oxidation alongside vascular targeting produces superior results.

Such combination research could provide insights into optimal approaches for body composition modification and whether different mechanisms of fat loss work additively or synergistically. The ability to study adipotide peptide alongside other compounds from our ++peptides for sale++ collection makes it a valuable component of comprehensive metabolic research programs.

Translational Research Value:

The progression of adipotide from preclinical models through human clinical trials provides a complete translational research dataset. Researchers can compare effects across species, understand how findings in rodents and primates translate to humans, and identify factors that affect translatability of vascular targeting approaches.

This translational perspective is valuable for researchers developing next-generation compounds or studying the principles of targeted therapy development. The adipotide human trials data, despite the program’s discontinuation, provides crucial information about human responses to vascular targeting that informs future research directions.

Research into Safety and Selectivity:

The safety challenges that halted adipotide clinical development make it valuable for research into the determinants of selectivity and off-target effects in targeted therapies. Researchers can study why the compound affects kidney tissue, what factors determine the therapeutic window, and how selectivity might be improved in future compounds.

Understanding the adipotide side effects and their mechanisms contributes to broader knowledge about vascular targeting safety and the challenges of developing selective therapies. This safety research is as valuable as efficacy research for advancing the field and preventing similar problems in future compound development.

Adipotide Dosage Protocols and Administration

Determining appropriate adipotide dosage for research applications requires understanding the available preclinical and clinical data, considering research goals, and carefully balancing efficacy against safety concerns. The narrow therapeutic window observed in clinical trials makes dose selection particularly important for adipotide research.

Preclinical Dosage Data:

Animal studies with adipotide peptide tested a range of doses to establish efficacy and safety:

Rodent Studies:

Doses tested: 0.5-5.0 mg/kg body weight
Administration: Daily subcutaneous injections
Duration: 2-4 weeks typical
Results: Dose-dependent fat loss with higher doses producing greater effects but increased toxicity risk

Primate Studies:

Doses tested: 0.25-2.5 mg/kg body weight
Administration: Daily subcutaneous injections
Duration: 4 weeks in key studies
Results: Dramatic fat loss at 1.0-2.5 mg/kg, but kidney toxicity at highest doses
Optimal dose range: 0.5-1.0 mg/kg showed good efficacy with acceptable safety

Clinical Dosage Data:

Adipotide human trials in Phase 1 studies tested escalating doses:

Phase 1 Dose Escalation:

Starting dose: 0.05 mg/kg body weight
Escalation: Gradual increases to assess tolerance
Maximum tested: Approximately 1.0 mg/kg (specific maximum not publicly disclosed)
Administration: Daily subcutaneous injections
Results: Dose-dependent weight loss, but kidney effects at higher doses limited escalation

Research Dosage Guidelines:

Based on available data, research protocols with adipotide dosing should consider the following ranges:

Conservative Research Protocol:

Dose: 0.25-0.5 mg/kg body weight
Frequency: Daily subcutaneous injection
Duration: 2-4 weeks
Suitable for: Initial research, safety assessment, dose-response studies
Rationale: Lower end of effective range with better safety margin

Standard Research Protocol:

Dose: 0.5-1.0 mg/kg body weight
Frequency: Daily subcutaneous injection
Duration: 4-8 weeks
Suitable for: Efficacy studies, body composition research
Rationale: Effective dose range from primate studies with acceptable risk profile

Advanced Research Protocol:

Dose: 1.0-1.5 mg/kg body weight
Frequency: Daily subcutaneous injection
Duration: 2-4 weeks (shorter duration due to higher dose)
Suitable for: Maximum effect studies, experienced research settings with intensive monitoring
Rationale: Higher efficacy but requires enhanced safety monitoring

Adipotide Dosage Chart: Body Weight Conservative Dose (0.5 mg/kg) Standard Dose (1.0 mg/kg) Advanced Dose (1.5 mg/kg) 60 kg 30 mg (6 vials) 60 mg (12 vials) 90 mg (18 vials) 70 kg 35 mg (7 vials) 70 mg (14 vials) 105 mg (21 vials) 80 kg 40 mg (8 vials) 80 mg (16 vials) 120 mg (24 vials) 90 kg 45 mg (9 vials) 90 mg (18 vials) 135 mg (27 vials) 100 kg 50 mg (10 vials) 100 mg (20 vials) 150 mg (30 vials)

Note: Calculations based on 5mg vials. Use ++PrymaLab’s Peptide Calculator++for precise dosing.

Reconstitution Protocol:

Proper reconstitution of adipotide peptide is essential for accurate dosing and peptide stability:

Reconstitution Steps:

Gather Supplies:
Adipotide 5MG vial(s)
Bacteriostatic water (0.9% benzyl alcohol)
Sterile syringes and needles (insulin syringes recommended)
Alcohol swabs
Sharps container for safe disposal
Prepare Vial:
Remove plastic cap from adipotide vial
Swab rubber stopper with alcohol
Allow to air dry completely (prevents stinging)
Add Bacteriostatic Water:
Draw desired amount of bacteriostatic water into syringe
Common volumes: 2-2.5 mL per 5mg vial
Insert needle through rubber stopper at an angle
Inject water slowly down the side of vial (not directly onto powder)
Avoid creating foam or bubbles
Mix Solution:
Gently swirl vial in circular motion
Do not shake vigorously (can damage peptide structure)
Allow powder to dissolve completely (may take 2-5 minutes)
Solution should be clear and colorless
If cloudiness persists, gently swirl more (do not shake)
Calculate Concentration:
Example: 5mg adipotide + 2mL bacteriostatic water = 2.5mg/mL concentration
Example: 5mg adipotide + 2.5mL bacteriostatic water = 2mg/mL concentration
Use Peptide Calculator for precise calculations
Label vial with concentration and reconstitution date

Administration Technique:

Adipotide requires proper subcutaneous injection technique for optimal absorption and minimal discomfort:

Injection Sites:

Abdomen (2 inches from navel, any direction) — most common site
Upper thighs (front or outer aspects)
Upper arms (outer aspect, if administered by assistant)
Lower back/hip area (if administered by assistant)
Rotate sites with each injection to prevent tissue irritation and lipohypertrophy

Injection Procedure:

Prepare Injection Site:
Select injection site and clean with alcohol swab
Allow alcohol to dry completely (30-60 seconds)
Pinch skin to create fold of subcutaneous tissue
Ensure area is free from bruises, scars, or irritation
Prepare Syringe:
Draw calculated adipotide dose from vial
Remove air bubbles by tapping syringe gently
Verify correct dose in syringe
Ensure no air remains in syringe
Administer Injection:
Insert needle at 45-90 degree angle (depending on body fat thickness)
45 degrees for leaner individuals, 90 degrees for higher body fat
Insert needle smoothly and quickly
Inject slowly and steadily over 5-10 seconds
Do not aspirate (not necessary for subcutaneous injections)
Post-Injection:
Withdraw needle smoothly at same angle as insertion
Apply gentle pressure with clean gauze if needed
Do not rub injection site (can affect absorption)
Dispose of needle safely in sharps container
Record injection site, dose, date, and time

Dosing Frequency and Timing:

Unlike some peptides with longer half-lives, adipotide peptide requires daily administration based on clinical trial protocols:

Daily Dosing Schedule:

Frequency: Once daily subcutaneous injection
Timing: Same time each day for consistency
Preferred time: Morning administration often preferred
Relationship to meals: Can be administered regardless of meal timing
Relationship to exercise: No specific timing requirements relative to training

Timing Considerations:

Morning dosing: Allows monitoring for any acute effects during waking hours
Consistency: Same time daily improves protocol adherence and maintains stable blood levels
Fasting vs fed: No significant difference in absorption or effects
Pre or post-workout: No specific advantage to either timing

Storage and Handling:

Proper storage maintains adipotide potency and stability:

Unreconstituted Peptide:

Storage temperature: 2-8°C (refrigerated) preferred, or -20°C (frozen) for long-term
Protect from light and moisture
Shelf life: 2-3 years when properly stored
Can tolerate room temperature for short periods during shipping
Keep in original packaging until ready to use

Reconstituted Solution:

Storage temperature: 2-8°C (refrigerated) — REQUIRED
Protect from light (store in original vial or wrap in foil)
Shelf life: 14-21 days when refrigerated with bacteriostatic water
Do not freeze reconstituted solution (will damage peptide)
Discard if solution becomes cloudy, discolored, or contains particles

Handling Precautions:

Always use sterile technique when handling
Avoid contamination of vials and solutions
Use bacteriostatic water to extend reconstituted shelf life
Label vials clearly with reconstitution date and concentration
Store away from food and beverages
Keep out of reach of children and pets

Research Protocol Design:

When designing research protocols with adipotide dosage, consider:

Dose-Response Studies:

Test multiple dose levels (e.g., 0.25, 0.5, 1.0 mg/kg)
Include control groups for comparison
Consider both efficacy and safety endpoints
Monitor dose-dependent effects on fat loss and adverse events
Establish optimal dose for specific research objectives

Duration Studies:

Short-term: 2-4 weeks to assess acute effects and tolerance
Medium-term: 4-8 weeks for sustained fat loss
Long-term: >8 weeks requires enhanced safety monitoring
Consider that longer durations may increase toxicity risk

Dose Escalation Protocols:

Start with lower doses and escalate gradually
Allow 3-7 days at each dose level before escalating
Monitor for adverse effects before increasing dose
Have clear criteria for dose reduction or discontinuation
Document rationale for dose adjustments

Safety Monitoring:

Baseline kidney function tests (creatinine, BUN, urinalysis)
Weekly or bi-weekly monitoring during treatment
Blood pressure monitoring
Body weight and composition measurements
Adverse event tracking and documentation

Special Considerations:

Body Weight Adjustments:

Calculate doses based on actual body weight
Recalculate if body weight changes significantly (>5%) during study
Consider using ideal body weight vs actual weight in very obese subjects
Document weight at each dosing time point

Individual Variability:

Response to adipotide peptide may vary based on:
Baseline fat mass and distribution
Adipose tissue vascularization patterns
Genetic factors affecting prohibitin expression
Age and metabolic status
Concurrent medications or compounds
Kidney function and clearance capacity

Combination Protocols:

When combining with other compounds, consider potential interactions
May need to adjust adipotide dosage in combination protocols
Implement enhanced safety monitoring for combinations
Document all concurrent compounds and doses

Research Support Resources:

PrymaLab provides comprehensive support for researchers using adipotide:

Peptide Calculator for accurate adipotide peptide dosage calculations
Bacteriostatic Water for proper reconstitution
Technical support for protocol design and dosing questions
Dosing guidance based on research literature
Quality documentation for research records

When researchers buy adipotide peptide from PrymaLab, they receive detailed reconstitution and administration instructions with their order, ensuring proper handling and use of this valuable research compound.

SAFETY PROFILE AND SIDE EFFECTS

Understanding Adipotide Side Effects

The adipotide side effects profile is well-documented from preclinical and clinical research, providing important safety information for researchers. While the peptide showed promising efficacy for fat loss, kidney-related adverse events led to the discontinuation of clinical development. Understanding these effects is crucial for responsible research use and appropriate safety monitoring.

Preclinical Safety Data

Rodent Studies:

Early safety studies in mice and rats provided initial toxicology data for adipotide peptide:

Common Effects in Rodents:

Injection site reactions (mild redness, occasional swelling)
Transient decreases in food intake at higher doses
Kidney-related changes at doses above 2 mg/kg
Generally good tolerability at doses ≤1 mg/kg

Dose-Limiting Toxicities:

Kidney effects became apparent at doses >2 mg/kg
Histological changes in kidney tissue at high doses
Increased serum creatinine and blood urea nitrogen (BUN)
Proteinuria (protein in urine) at higher doses

Primate Safety Data:

Studies in obese rhesus monkeys provided crucial translational safety data:

Observed Adverse Events:

Kidney-related effects: Most significant safety concern
Increased serum creatinine (marker of kidney function)
Proteinuria (protein leakage into urine)
Histological changes in kidney tissue
Dose-dependent severity, worse at 2.5 mg/kg
Injection site reactions: Mild to moderate
Redness and swelling at injection sites
Resolved within 24-48 hours typically
Gastrointestinal effects: Occasional
Nausea (inferred from behavior)
Decreased appetite at higher doses
Generally mild and transient

Important Findings:

Kidney effects were dose-dependent and reversible upon discontinuation
Lower doses (0.5-1.0 mg/kg) showed better safety profile
Therapeutic window between effective and toxic doses was narrow
Some animals showed good tolerance even at higher doses (individual variability)

Clinical Trial Safety Data

Phase 1 Human Trial:

The adipotide human trials in obese patients with type 2 diabetes revealed the safety profile in humans:

Common Adverse Events:

Kidney-Related Effects (Most Significant):

Increased serum creatinine levels
Proteinuria (protein in urine)
Decreased glomerular filtration rate (GFR)
Dose-dependent severity
Some cases of more significant kidney dysfunction at higher doses

Injection Site Reactions:

Redness, swelling, or discomfort at injection sites
Generally mild and self-limiting
Improved with proper injection technique and site rotation
No serious injection site complications

Gastrointestinal Effects:

Nausea (most common GI effect)
Decreased appetite
Occasional abdominal discomfort
Generally mild to moderate severity

Cardiovascular Effects:

Mild increases in blood pressure in some subjects
Heart rate changes (usually minor)
No serious cardiovascular events reported

Other Effects:

Fatigue or malaise in some subjects
Headaches (occasional)
Dizziness (rare)
Changes in laboratory values (electrolytes, liver enzymes)

Serious Adverse Events:

Kidney dysfunction requiring dose reduction or discontinuation
No deaths or life-threatening events reported in published data
Reversibility of kidney effects upon treatment cessation

Mechanism of Kidney Toxicity

Understanding why adipotide causes kidney effects is important for research safety:

Prohibitin Expression in Kidneys:

The kidney toxicity likely results from adipotide peptide affecting renal vasculature or glomerular cells:

Prohibitin is expressed in kidney tissue, particularly in glomeruli
Glomeruli are the filtering units of kidneys with extensive capillary networks
Adipotide may bind to prohibitin in renal vasculature
Vascular damage in kidneys impairs filtration function
Dose-dependent effect suggests selectivity is lost at higher doses

Glomerular Damage:

Endothelial cell damage in glomerular capillaries
Disruption of filtration barrier
Protein leakage into urine (proteinuria)
Decreased filtration rate
Potential for progressive damage with continued exposure

Reversibility:

Kidney effects were generally reversible upon discontinuation
Suggests functional rather than permanent structural damage
Recovery time varied among individuals
Some subjects showed complete recovery, others partial
Highlights importance of early detection and intervention

Safety Monitoring Recommendations

Researchers using ftpp adipotide should implement comprehensive safety monitoring:

Baseline Assessment:

Before starting research protocols:

Complete medical history with focus on kidney disease
Physical examination including blood pressure
Baseline laboratory tests:
Serum creatinine and blood urea nitrogen (BUN)
Estimated glomerular filtration rate (eGFR)
Urinalysis including protein and microscopy
Complete blood count (CBC)
Comprehensive metabolic panel
Liver function tests
Documentation of any pre-existing conditions
Assessment of risk factors for kidney disease

Ongoing Monitoring:

During research protocols:

Weekly kidney function monitoring:
Serum creatinine
Urinalysis for protein
Calculate eGFR
Bi-weekly comprehensive monitoring:
Complete metabolic panel
Blood pressure measurement
Body weight and composition
Physical examination for adverse effects
Injection site inspection
Symptom assessment and documentation

Warning Signs Requiring Immediate Attention:

Significant increase in serum creatinine (>0.3 mg/dL from baseline)
New or worsening proteinuria
Decreased urine output
Swelling (edema) in legs, ankles, or face
Persistent nausea or vomiting
Severe injection site reactions
Significant blood pressure increases
Any signs of kidney dysfunction

Intervention Criteria:

Mild kidney changes: Consider dose reduction
Moderate kidney changes: Reduce dose or hold treatment
Significant kidney dysfunction: Discontinue treatment immediately
Persistent adverse effects: Discontinue and monitor recovery
Any serious adverse event: Stop treatment and provide appropriate care

Contraindications and Precautions

Certain conditions or circumstances warrant exclusion from adipotide research or require special precautions:

Absolute Contraindications:

Pre-existing kidney disease or impaired kidney function
History of kidney stones or kidney disorders
Uncontrolled hypertension
Pregnancy or breastfeeding (insufficient safety data)
Known allergy to adipotide or components
Active infection or inflammatory conditions
Severe cardiovascular disease
Dehydration or volume depletion

Relative Contraindications (Require Careful Consideration):

Borderline kidney function (eGFR 60-90 mL/min/1.73m²)
Controlled hypertension (requires close monitoring)
Diabetes with kidney involvement (diabetic nephropathy)
Use of nephrotoxic medications
Advanced age (>65 years, higher kidney disease risk)
History of proteinuria
Autoimmune diseases affecting kidneys
Obesity with metabolic syndrome (multiple risk factors)

Special Populations:

Elderly Subjects:

Higher risk of kidney dysfunction
May require lower doses
Enhanced monitoring recommended
Consider baseline kidney function carefully

Diabetic Subjects:

Diabetes increases kidney disease risk
Careful baseline kidney assessment essential
More frequent monitoring may be needed
Watch for diabetic nephropathy progression

Subjects with Multiple Risk Factors:

Combination of risk factors increases adverse event likelihood
May require dose reduction or exclusion
Enhanced safety monitoring essential
Consider risk-benefit carefully

Managing Adverse Effects

If adipotide side effects occur during research, appropriate management strategies include:

For Kidney-Related Effects:

Mild Changes (Creatinine increase <0.3 mg/dL):

Continue monitoring closely
Consider dose reduction (e.g., from 1.0 to 0.5 mg/kg)
Ensure adequate hydration
Avoid nephrotoxic medications
Recheck kidney function in 3-5 days

Moderate Changes (Creatinine increase 0.3-0.5 mg/dL):

Hold treatment temporarily
Increase monitoring frequency
Ensure hydration and avoid nephrotoxins
Consult with medical oversight
Resume at lower dose only if kidney function improves

Significant Dysfunction (Creatinine increase >0.5 mg/dL):

Discontinue treatment immediately
Comprehensive kidney function assessment
Medical evaluation and management
Monitor recovery closely
Do not resume treatment
Document event thoroughly

For Injection Site Reactions:

Rotate injection sites consistently
Use proper injection technique
Apply ice before injection to reduce discomfort
Ensure alcohol has dried before injecting
Consider smaller injection volumes
Use different needle sizes if needed
If reactions persist or worsen, consider discontinuation

For Gastrointestinal Effects:

Take with food if nausea occurs
Use anti-nausea medications if needed
Ensure adequate hydration
Consider dose reduction if effects are bothersome
Monitor for dehydration
Discontinue if severe or persistent

For Blood Pressure Changes:

Monitor blood pressure regularly
Ensure adequate hydration
Consider antihypertensive medication if needed
Reduce adipotide dosage if blood pressure increases significantly
Discontinue if blood pressure cannot be controlled

General Management Principles:

Document all adverse effects thoroughly
Assess severity and relationship to peptide
Consider dose reduction before discontinuation
Provide supportive care as needed
Discontinue if serious adverse effects occur
Follow up after treatment cessation to ensure recovery

Long-Term Safety Considerations

While adipotide peptide clinical development was relatively short-term, researchers should consider potential long-term effects:

Theoretical Long-Term Concerns:

Cumulative kidney effects with prolonged use
Potential for progressive kidney damage
Effects on adipose tissue regeneration and function
Long-term metabolic consequences of vascular targeting
Unknown effects of very long-term use (months to years)
Potential for development of resistance or tolerance

Research Duration Recommendations:

Short-term studies (2-4 weeks): Best supported by safety data
Medium-term studies (4-8 weeks): Reasonable with enhanced monitoring
Long-term studies (>8 weeks): Limited safety data, not recommended without compelling justification
Very long-term use (>12 weeks): Insufficient safety data, significant concerns

Recovery and Reversibility:

Most adverse effects reversed upon discontinuation
Kidney function typically recovered within weeks to months
Some individuals showed faster recovery than others
Importance of early detection and intervention
Long-term follow-up recommended after treatment cessation

Comparison to Other Fat Loss Compounds

The adipotide side effects profile differs significantly from other fat loss research compounds:

Compared to Metabolic Compounds:

Different mechanism means different side effect profile
No stimulant effects (unlike thermogenic compounds)
Kidney toxicity is unique to vascular targeting mechanism
May have advantages in some contexts, disadvantages in others

Compared to Other Peptides:

More significant safety concerns than many peptides
Narrow therapeutic window compared to most research peptides
Requires more intensive safety monitoring
Unique mechanism provides unique research value despite safety challenges

Risk-Benefit Considerations:

Dramatic efficacy must be balanced against safety concerns
Appropriate for research but safety profile prevented therapeutic development
Careful subject selection and monitoring essential
Lower doses may provide better risk-benefit balance

Regulatory and Ethical Considerations

Researchers using adipotide should be aware of regulatory status and ethical obligations:

Regulatory Status:

Not approved for human therapeutic use by FDA or other regulatory agencies
Clinical development discontinued in 2011 due to safety concerns
Available for research purposes only
Not intended for human consumption outside approved research settings
Researchers must comply with all applicable regulations

Research Ethics:

Informed consent essential for any human research
Full disclosure of known risks, including kidney toxicity
Appropriate institutional review board (IRB) approval required
Adherence to good clinical practice (GCP) guidelines
Proper documentation and safety monitoring
Transparent reporting of adverse events

Banned Substance Status:

Prohibited by World Anti-Doping Agency (WADA)
Banned in competitive sports
Athletes subject to drug testing should not use
Researchers working with athletes must ensure compliance

Risk Mitigation Strategies

To minimize risks when conducting research with ftpp adipotide:

Protocol Design:

Start with lowest effective doses
Use shortest duration necessary for research objectives
Include appropriate control groups
Plan for comprehensive safety monitoring
Have clear stopping criteria for safety concerns
Design dose escalation protocols carefully

Subject Selection:

Rigorous screening to exclude high-risk individuals
Thorough kidney function assessment at baseline
Exclusion of those with contraindications
Assessment of all risk factors
Documentation of inclusion/exclusion criteria
Informed consent with clear risk communication

Monitoring and Follow-Up:

Frequent safety assessments during research
Prompt attention to any adverse effects
Documentation of all safety-related observations
Follow-up after research completion to ensure recovery
Long-term monitoring if indicated by adverse events

Quality Assurance:

Use pharmaceutical-grade peptide from reputable sources
Verify peptide identity and purity through testing
Proper storage and handling to maintain quality
Accurate dosing and administration
Sterile technique for all injections
Regular equipment calibration and maintenance

Emergency Preparedness

Research protocols should include plans for managing potential emergencies:

Kidney Dysfunction:

Severe Adverse Reactions:

Clear protocols for recognition and management
Access to emergency medical care
Immediate discontinuation of treatment
Appropriate medical intervention
Documentation and reporting requirements
Communication with oversight bodies

Allergic Reactions:

Recognition of symptoms (rash, difficulty breathing, swelling)
Immediate discontinuation
Emergency medical treatment if severe
Documentation and reporting
Exclusion from further research

Safety Documentation

Proper documentation of safety aspects is essential:

Required Documentation:

Informed consent forms with detailed risk disclosure
Medical history and screening results
Baseline safety assessments
All monitoring data (kidney function, blood pressure, etc.)
Adverse event reports with severity and causality assessment
Dose modifications and reasons
Follow-up assessments
Final safety summary

Reporting Requirements:

Adverse events to appropriate oversight bodies
Serious adverse events to IRB/ethics committee immediately
Safety data in research publications
Transparency about risks and benefits
Contribution to scientific understanding of peptide safety

When researchers buy adipotide for sale from PrymaLab, comprehensive safety information is provided with each order, including known side effects, monitoring recommendations, kidney function assessment guidelines, and emergency management protocols. This ensures researchers have the information needed for responsible and safe research use of this powerful but potentially toxic vascular targeting compound.

FREQUENTLY ASKED QUESTIONS

What is Adipotide (FTPP)?

Adipotide , also known as FTPP (Fat-Targeted Proapoptotic Peptide), is an innovative research peptide that promotes fat loss through a unique vascular targeting mechanism. Unlike traditional fat loss compounds that work through metabolic or hormonal pathways, adipotide peptide selectively targets and destroys blood vessels supplying white adipose tissue. The compound consists of two functional components: a prohibitin-targeting sequence that directs it to adipose tissue vasculature, and a pro-apoptotic sequence that induces cell death in those blood vessels. By cutting off the blood supply to fat tissue, ftpp adipotide causes fat cells to die and be cleared from the body, resulting in significant fat mass reduction. Preclinical research in obese primates showed dramatic weight loss of up to 27% with fat mass reductions of approximately 39% over just 4 weeks. While clinical development was discontinued in 2011 due to kidney-related safety concerns, adipotide remains valuable for research into adipose tissue biology, vascular targeting mechanisms, and body composition modification.

How does Adipotide work for fat loss?

Adipotide peptide works through a sophisticated vascular targeting mechanism that is fundamentally different from traditional fat loss approaches. When administered, the peptide circulates in the bloodstream and selectively binds to prohibitin receptors that are preferentially expressed on endothelial cells lining blood vessels in white adipose tissue. Once bound, adipotide is internalized into these endothelial cells through receptor-mediated endocytosis. Inside the cells, the pro-apoptotic D(KLAKLAK)2 component disrupts mitochondrial membranes, triggering programmed cell death (apoptosis) in the endothelial cells. This leads to destruction of the blood vessels supplying fat tissue. Without adequate blood supply, adipocytes (fat cells) are deprived of oxygen and nutrients, causing them to undergo apoptosis as well. The dead fat cells are then cleared by the body’s natural waste removal systems, resulting in fat mass reduction. This vascular targeting approach allows ftpp adipotide to selectively reduce fat while preserving lean muscle mass, making it particularly interesting for body composition research.

What are the benefits of Adipotide for research?

The adipotide peptide benefits for research are substantial and unique. Most notably, the compound produces dramatic fat loss through a novel vascular targeting mechanism, with preclinical studies showing fat mass reductions of up to 39% while preserving lean body mass. This selective fat loss makes adipotide valuable for studying body composition optimization and the mechanisms determining whether weight loss comes from fat or muscle. Research suggests the compound may preferentially target visceral adipose tissue (fat around organs) over subcutaneous fat, which is particularly valuable since visceral fat is more strongly associated with metabolic disease. Adipotide results have also shown improvements in metabolic parameters including insulin sensitivity and glucose control. The unique mechanism provides opportunities for research into adipose tissue vasculature, the role of blood supply in fat mass regulation, and the development of targeted therapies. For adipotide bodybuilding research applications, the ability to reduce fat while maintaining muscle mass represents an ideal body composition change. The compound’s progression through preclinical and clinical trials provides valuable translational research data for understanding how vascular targeting approaches translate across species.

What is the recommended Adipotide dosage?

Adipotide dosage recommendations are based on preclinical and clinical trial data, with careful consideration of the narrow therapeutic window between effective and toxic doses. Preclinical studies in obese primates showed optimal results at doses of 0.5-1.0 mg/kg body weight administered daily via subcutaneous injection, with higher doses (up to 2.5 mg/kg) producing greater fat loss but increased kidney toxicity risk. Adipotide human trials in Phase 1 studies tested escalating doses starting at 0.05 mg/kg and increasing gradually, though specific maximum doses tested were not fully disclosed publicly. For research protocols, conservative approaches might use 0.25-0.5 mg/kg daily, standard protocols 0.5-1.0 mg/kg daily, and advanced protocols up to 1.0-1.5 mg/kg daily with enhanced safety monitoring. An adipotide dosage chart would show that for an 80 kg subject, a 0.5 mg/kg dose equals 40 mg daily (8 vials of 5mg), while 1.0 mg/kg equals 80 mg daily (16 vials). Researchers should use ++PrymaLab’s Peptide Calculator++ for precise adipotide peptide dosage calculations. The adipotide dosing frequency is daily based on clinical protocols, with treatment durations typically ranging from 2-8 weeks depending on research objectives and safety monitoring capabilities.

How do I reconstitute and administer Adipotide?

To reconstitute adipotide peptide , you’ll need ++bacteriostatic water++ and sterile syringes. Remove the plastic cap from the Adipotide 5MG vial and swab the rubber stopper with alcohol, allowing it to dry completely. Draw 2-2.5 mL of bacteriostatic water into a sterile syringe and inject it slowly down the side of the vial, not directly onto the powder, to avoid damaging the peptide structure. Gently swirl the vial in a circular motion until the powder completely dissolves — never shake vigorously. The solution should be clear and colorless. For a 5mg vial with 2mL of water, you’ll have a concentration of 2.5mg/mL. For administration, adipotide requires daily subcutaneous injection into areas like the abdomen (2 inches from navel), upper thighs, or upper arms. Clean the injection site with alcohol and allow it to dry, pinch the skin to create a fold, insert the needle at a 45-90 degree angle depending on body fat thickness, and inject slowly over 5-10 seconds. Rotate injection sites daily to prevent tissue irritation. Store reconstituted solution refrigerated at 2-8°C and use within 14-21 days. Calculate your specific adipotide dose using ++PrymaLab’s Peptide Calculator++ based on your body weight and desired mg/kg dose.

What are Adipotide side effects?

The adipotide side effects profile is well-documented from preclinical and clinical research, with kidney-related effects being the most significant concern. In adipotide human trials , the most common adverse events were kidney-related including increased serum creatinine (indicating reduced kidney function), proteinuria (protein in urine), and decreased glomerular filtration rate. These effects were dose-dependent and led to the discontinuation of clinical development in 2011. Other reported adipotide side effects included injection site reactions (redness, swelling), gastrointestinal effects (nausea, decreased appetite), mild blood pressure increases, and occasional fatigue or headaches. The kidney toxicity likely results from adipotide peptide affecting renal vasculature or glomerular cells, as prohibitin is expressed in kidney tissue. Importantly, most adverse effects were reversible upon discontinuation of treatment, though recovery time varied among individuals. Researchers using ftpp adipotide must implement comprehensive safety monitoring including baseline and regular kidney function tests, blood pressure monitoring, and careful dose selection. The narrow therapeutic window between effective doses for fat loss and doses causing kidney toxicity requires careful protocol design and subject selection, with exclusion of anyone with pre-existing kidney disease or risk factors for kidney dysfunction.

Where can I buy Adipotide for research?

You can buy adipotide for research purposes from PrymaLab, a trusted supplier of pharmaceutical-grade research peptides. Our Adipotide (FTPP) 5MG vials contain 99% pure peptide verified by third-party testing, ensuring reliable and reproducible research results. Each vial arrives as lyophilized powder for maximum stability during shipping and storage. When you buy ftpp adipotide from PrymaLab, you receive comprehensive documentation including certificates of analysis, reconstitution instructions, detailed dosing guidelines with adipotide peptide dosage chart , and extensive safety information including kidney monitoring protocols. We also provide research support resources including our ++Peptide Calculator++ for accurate dosing calculations and ++bacteriostatic water++ for proper reconstitution. Fast, discreet shipping ensures your research materials arrive quickly and securely. Adipotide for sale at PrymaLab is intended for research purposes only and is not for human consumption outside approved research settings. We provide technical support for protocol design and can answer questions about adipotide dosing and safety monitoring to ensure responsible research use of this powerful vascular targeting compound.

What were the results of Adipotide human trials?

Adipotide human trials progressed to Phase 1 studies in obese patients with type 2 diabetes before clinical development was discontinued. While complete results were not fully published, available data showed that adipotide produced dose-dependent weight loss in human subjects, with those receiving the compound losing significantly more weight than placebo-treated controls. The fat loss was accompanied by improvements in metabolic parameters including better glycemic control, with reductions in fasting glucose and HbA1c levels in diabetic subjects. These adipotide results demonstrated that the dramatic fat loss effects observed in preclinical primate studies (up to 27% body weight loss and 39% fat mass reduction) could translate to humans. However, the trials also revealed dose-limiting kidney toxicity, with subjects experiencing increased serum creatinine, proteinuria, and decreased kidney function at higher doses. These adipotide side effects were consistent with preclinical findings and ultimately led to the discontinuation of clinical development in 2011. The narrow therapeutic window between effective doses for weight loss and doses causing kidney damage was deemed too narrow for safe therapeutic use. Despite the program’s termination, the human trial data provides valuable proof-of-concept for vascular targeting as a fat loss mechanism and informs ongoing research into adipose tissue biology and targeted therapies.

Is Adipotide safe for research use?

Adipotide safety for research use requires careful consideration of the known risks, particularly kidney toxicity. While preclinical and clinical data demonstrate that the compound can be used in research settings, it has a narrow therapeutic window and requires comprehensive safety monitoring. The kidney-related adipotide side effects that halted clinical development — including increased creatinine, proteinuria, and decreased kidney function — were dose-dependent and generally reversible upon discontinuation, but they represent significant safety concerns. For research purposes, adipotide peptide can be used safely with appropriate precautions including rigorous subject screening to exclude anyone with pre-existing kidney disease or risk factors, comprehensive baseline kidney function assessment, frequent monitoring during treatment (weekly kidney function tests, urinalysis, blood pressure), clear protocols for dose reduction or discontinuation if adverse effects occur, and use of lower doses that provide better safety margins. Research protocols should start with conservative doses (0.25-0.5 mg/kg) and escalate gradually only with careful monitoring. The compound should not be used in pregnant or breastfeeding individuals, those with kidney disease, uncontrolled hypertension, or other contraindications. When used responsibly with proper precautions and monitoring, ftpp adipotide provides valuable research insights while maintaining acceptable safety margins, though researchers must remain vigilant for kidney-related adverse effects.

How does Adipotide compare to traditional fat loss methods?

Adipotide peptide differs fundamentally from traditional fat loss methods in both mechanism and effects. Traditional approaches including caloric restriction, increased physical activity, and metabolic compounds work by creating an energy deficit or enhancing fat oxidation through systemic metabolic changes. In contrast, ftpp adipotide uses vascular targeting to selectively destroy blood vessels supplying adipose tissue, cutting off the blood supply to fat cells and causing them to die. This mechanism allows for more selective fat loss with better preservation of lean muscle mass — preclinical studies showed approximately 90% of weight loss was fat mass, compared to typical 60-75% with caloric restriction. Adipotide results also suggest preferential targeting of visceral adipose tissue over subcutaneous fat, which is advantageous since visceral fat is more metabolically harmful. The magnitude of fat loss with adipotide far exceeds what’s typically achievable with traditional methods, with primate studies showing 27% body weight loss and 39% fat mass reduction in just 4 weeks. However, this dramatic efficacy comes with significant safety concerns, particularly kidney toxicity, that traditional methods don’t have. For adipotide bodybuilding research, the selective fat loss with muscle preservation represents an ideal body composition change that’s difficult to achieve through diet and exercise alone. The unique mechanism makes adipotide valuable for research into targeted fat reduction, though the safety profile prevented its development as a therapeutic agent.

What is the difference between Adipotide 5MG and 10MG?

The difference between Adipotide 5MG and adipotide 10mg formulations is simply the amount of peptide per vial, which affects dosing convenience and cost-effectiveness for research protocols. Both contain the same adipotide peptide with identical purity and quality standards. The 5MG vials are suitable for lower-dose protocols or shorter research studies, while 10MG vials may be more economical for higher-dose protocols or longer studies requiring larger total amounts. When calculating adipotide dosage , researchers should consider their total peptide needs based on body weight, desired mg/kg dose, treatment duration, and dosing frequency. For example, an 80 kg subject using 1.0 mg/kg daily would need 80 mg per day, which equals 16 vials of 5MG or 8 vials of 10MG. The adipotide ftpp 10mg vials would provide more doses per vial, potentially reducing the number of reconstitutions needed and simplifying protocol administration. However, once reconstituted, peptide solutions should be used within 14-21 days, so researchers must balance vial size against usage timeline to minimize waste. Use ++PrymaLab’s Peptide Calculator++ to determine which vial size best suits your research protocol. Both formulations are available in our ++peptides for sale++ collection, and researchers can buy adipotide online in either concentration based on their specific needs.

Can Adipotide be combined with other research peptides?

Yes, adipotide peptide can potentially be combined with other research compounds to study synergistic or complementary effects on body composition, though such combinations require careful protocol design and enhanced safety monitoring. Researchers might combine ftpp adipotide with muscle-building peptides like ++Ipamorelin++ or ++CJC-1295++ to investigate whether simultaneous fat loss and muscle gain can be achieved more effectively than with either compound alone. The different mechanisms — vascular targeting for fat loss versus growth hormone enhancement for muscle growth — might work synergistically to optimize body composition. Combinations with metabolic compounds could explore whether enhancing fat oxidation alongside vascular targeting produces superior results. However, combination protocols require several important considerations: potential interactions between compounds must be evaluated, adipotide dosage may need adjustment when combined with other peptides, safety monitoring must be enhanced to detect adverse effects from either compound or their interaction, and researchers should start with lower doses of each compound when combining. The kidney toxicity risk with adipotide is particularly important to consider in combinations, as some other compounds might also affect kidney function. When designing combination research, include appropriate control groups receiving each compound individually to distinguish synergistic from additive effects. PrymaLab’s comprehensive ++peptides for sale++ collection provides researchers access to multiple compounds for combination studies exploring optimal approaches to body composition modification.

What monitoring is required when using Adipotide?

Comprehensive monitoring is essential when using adipotide due to the kidney toxicity risk that led to clinical development discontinuation. Before starting research, baseline assessment must include complete medical history, physical examination, and laboratory tests including serum creatinine, blood urea nitrogen (BUN), estimated glomerular filtration rate (eGFR), comprehensive urinalysis with protein measurement, complete blood count, comprehensive metabolic panel, and liver function tests. During research protocols with adipotide peptide , weekly monitoring should include serum creatinine, urinalysis for protein, and eGFR calculation to detect early kidney function changes. Bi-weekly monitoring should include comprehensive metabolic panel, blood pressure measurement, body weight and composition assessment, and physical examination for adverse effects. Researchers must establish clear intervention criteria: mild kidney changes (creatinine increase <0.3 mg/dL) warrant close monitoring and possible dose reduction, moderate changes (0.3-0.5 mg/dL increase) require holding treatment temporarily, and significant dysfunction (>0.5 mg/dL increase) mandates immediate discontinuation. Warning signs requiring immediate attention include significant creatinine increases, new or worsening proteinuria, decreased urine output, swelling in legs or face, persistent nausea, or severe injection site reactions. The adipotide dosing protocol should include plans for dose reduction or discontinuation based on monitoring results. After treatment cessation, follow-up monitoring should continue until kidney function returns to baseline, which may take weeks to months. This intensive monitoring is necessary to ensure early detection of adipotide side effects and prevent serious kidney damage. When researchers buy adipotide peptide from PrymaLab, detailed monitoring protocols and safety guidelines are provided to support responsible research use.

About the Author

Name: Michael Phelps

Title: Marketing Director & Biochemistry Specialist at Prymalab

Michael is an Air Force veteran and the Marketing Director at Prymalab. With a specialized background in biochemistry and over 10 years in the biotech industry, he applies military-grade precision to research standards and quality control. Michael is dedicated to bridging the gap between complex scientific studies and practical application, providing accurate, science-backed information on peptide protocols like Muscle Groth Peptides.