Adipotide (FTTP) — Research, Dosing & Price Guide

Adipotide (FTTP — Fat-Targeted Proapoptotic Peptide) is a peptidomimetic that selectively destroys the blood vessels feeding white adipose tissue, causing targeted fat cell death through vascular disruption. Originally developed at MD Anderson Cancer Center using cancer drug delivery technology repurposed for obesity, it produced dramatic fat loss in primate studies — 11% body weight reduction in 28 days. However, it carries significant renal risks and is considered one of the more aggressive fat loss compounds in the research peptide space.

Adipotide is a chimeric peptide with two functional domains working in concert. The targeting sequence (CKGGRAKDC) binds specifically to prohibitin, a protein overexpressed on the surface of endothelial cells lining blood vessels in white adipose tissue. This targeting peptide was identified through phage display screening and shows high selectivity for the adipose vasculature over blood vessels in other organs. Once the targeting domain binds prohibitin, the entire complex is internalized via receptor-mediated endocytosis. The second domain — the proapoptotic peptide D(KLAKLAK)2 — then triggers apoptosis by disrupting the mitochondrial membrane. This amphipathic peptide sequence inserts into the inner mitochondrial membrane, causing membrane depolarization, cytochrome c release, caspase cascade activation, and ultimately endothelial cell death. As the microvasculature supplying fat tissue is systematically destroyed, adipocytes are starved of oxygen and nutrients, undergoing apoptosis through ischemia. The dead fat cells are then cleared by macrophages. This mechanism is largely irreversible for the affected tissue — the destroyed vasculature and adipocytes do not rapidly regenerate, producing potentially lasting fat reduction. However, this same potency makes it a high-risk compound, as off-target effects on renal vasculature have been documented.

• A 2011 study published in Science Translational Medicine demonstrated that treated rhesus monkeys lost 11% of body weight and had a 10% decrease in BMI over just 28 days of treatment.
• MRI imaging confirmed selective loss of white adipose tissue with preservation of lean mass and organ tissue, validating the targeting mechanism.
• Abdominal circumference was significantly reduced in treated primates, indicating preferential visceral and subcutaneous abdominal fat loss.
• Reversible proximal renal tubular changes were observed in treated animals — mild kidney damage that resolved after treatment cessation, likely due to prohibitin expression in renal vasculature.
• The phage display technology used to discover adipotide's targeting sequence has since been validated in cancer drug delivery applications, confirming the tissue-targeting approach.
• Metabolic parameters including insulin sensitivity improved in parallel with fat loss in treated primates.

• Primate study protocol: 0.43 mg/kg subcutaneous injection daily for 28 days, which produced 11% body weight loss in rhesus monkeys.
• No established human dosing protocol exists — this compound is strictly research-use only and has not entered human clinical trials.
• Anecdotal research community protocols suggest starting at significantly lower doses (0.1–0.2 mg/kg) to assess individual tolerance before any escalation.
• Kidney function monitoring (serum creatinine, BUN, urinalysis) is absolutely essential before, during, and after any research use, given documented renal effects.
• Hydration should be maintained at high levels during use to support renal function and facilitate clearance of cellular debris from fat cell apoptosis.
• Should not be used without direct medical supervision due to the inherent risks of vascular disruption in a non-targeted-therapy setting.
• Typical research cycle: no longer than 28 days, with pre- and post-cycle blood work including comprehensive metabolic panel and urinalysis.

Known Side Effects

• Renal tubular damage — the most significant and well-documented side effect. Prohibitin is expressed in renal vasculature, making the kidneys a partial off-target site. Manifests as elevated creatinine, proteinuria, and potential acute kidney injury.
• Dehydration — the rapid destruction of adipose tissue and associated inflammatory response increases fluid requirements significantly.
• Injection site reactions — pain, redness, and swelling at injection sites are commonly reported.
• Fatigue and malaise — the systemic inflammatory response to widespread fat cell death can produce flu-like symptoms.
• Nausea and reduced appetite — likely related to the systemic inflammatory burden and renal stress.
• Potential for irreversible fat loss in treated areas — while this is the intended effect, it means dosing errors or asymmetric application could theoretically produce cosmetically uneven results.

Safety Profile

Adipotide carries one of the highest risk profiles of any research peptide. The primary concern is renal toxicity — prohibitin is not exclusively expressed on adipose vasculature, and the kidneys appear to be a significant off-target tissue. In primate studies, reversible proximal tubular damage was documented, but the long-term renal consequences of repeated exposure are unknown. Individuals with any pre-existing kidney disease, diabetes (with potential subclinical nephropathy), or those taking nephrotoxic medications should absolutely avoid this compound. There is no human clinical trial data, no established safety margins, and no antidote if adverse effects occur. The mechanism is inherently aggressive — it kills cells — and unlike most peptides, its effects may be partially irreversible. It is contraindicated in anyone with renal impairment, cardiovascular disease, clotting disorders, or who is pregnant/breastfeeding. This compound should only be considered in a supervised research context with comprehensive blood work monitoring.

Days 1–5: Injection site reactions are common. Systemic effects are minimal as the vascular disruption process begins at the molecular level. Increased thirst and mild fatigue may occur. Days 6–14: Fat loss becomes noticeable and surprisingly rapid. Users in research contexts report visible reduction in abdominal fat. Fatigue and flu-like symptoms may peak as the inflammatory response to fat cell death is greatest. Urine output should be monitored. Days 15–28: Continued aggressive fat loss. Primate studies showed peak effects during this period. Renal markers should be monitored at least weekly. Body composition changes are dramatic compared to any other peptide. Post-cycle: Fat loss effects may persist as destroyed vasculature and adipocytes are slowly cleared. Full renal recovery should be confirmed through blood work. Some fat loss may be permanent in treated areas due to the irreversible nature of the mechanism.

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