Adipotide Dosage Guide: Protocols, Calculator & Safety

Dosage for Adipotide varies by protocol. Consult a qualified healthcare provider.

Administration frequency depends on the specific protocol. Consult current research literature.

Cycling requirements depend on the protocol. Follow established research guidelines.

There is no published human safety data for adipotide. The only registered human trial enrolled 4 of a planned 39 participants, was terminated, and has no posted results (ClinicalTrials.gov NCT01262664). Everything below is from monkeys, mice or cell culture. **Kidney injury is the dose-limiting finding in monkeys.** In a Good Laboratory Practice toxicology study in lean rhesus macaques given 0.25, 0.43 or 0.75 mg/kg daily for 28 days, kidney lesions were present at necropsy in a dose-dependent pattern and absent in controls: minimal to mild at the low dose, minimal to mild in most middle-dose animals, and minimal to moderate at the high dose. The lesions were classified as degenerative or necrotic (single-cell necrosis) and as reactive or regenerative. After four weeks off the drug, minimal tubular degeneration was still present in one middle-dose animal and two high-dose animals. The authors summarised the primary side effect as relatively mild, predictable and reversible renal injury with altered tubular function (PMID: 22072637). **Laboratory changes in monkeys.** Serum creatinine rose in a slight to moderate, dose-dependent way at doses above 0.25 mg/kg, without a matching rise in blood urea nitrogen. Serum phosphorus and serum potassium fell in a time- and dose-dependent way. Urine showed mild to marked glucosuria, mild to moderate proteinuria, and a slight to mild increase in transitional or renal epithelial cells. Treated monkeys produced more urine and mild dehydration was noted at the highest doses. Most of these changes reversed within 28 days of stopping, with slight residual creatinine and urinary glucose elevation in one treated animal per study at the end of recovery (PMID: 22072637). **Food intake and the nausea question.** Monkeys on adipotide stayed alert and active, interacted normally with handlers, and showed no overt nausea, vomiting or food aversion, but the number of chow biscuits they ate fell in proportion to dose and to weight lost. The authors stated that mild nausea could not be completely ruled out as a contributor (PMID: 22072637). A published comment argued that the weight loss may reflect a direct effect on food consumption rather than vascular ablation, and the authors replied in the same issue (PMID: 22539771). **What was looked for and not found in monkeys.** Lipid profiles stayed normal and free fatty acids trended downward rather than upward during treatment. Abnormal lipid accumulation, including hepatic steatosis, was not seen in any monkey that received adipotide. The authors also reasoned against increased faecal fat loss, since the oily stool and incontinence seen with fat absorption inhibitors did not occur, though faecal lipids were not measured (PMID: 22072637). **Acute lethality in monkeys.** In safety work across 52 cynomolgus macaques for this class of compounds, single doses of adipotide up to 100 mg/kg, about 133 times the therapeutic dose, did not cause death (PMID: 22072637). **Mice.** The original mouse report described obesity reversal without detectable adverse effects (PMID: 15133506). That is a 2004 statement about a mouse experiment, not a safety conclusion for any other species. **The killer half is cytotoxic by design.** D(KLAKLAK)2 on its own kills fungal cells through mitochondrial injury with reactive oxygen species accumulation and caspase-like activity (PMID: 24098573) and disrupts bacterial membranes with loss of membrane potential (PMID: 23345420). Whatever selectivity adipotide has comes from the homing motif, not from the toxic one.

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