MEDICAL DISCLAIMER: Educational research guidelines only. Lyophilized peptides are investigational chemical compounds and are NOT approved for human consumption, diagnosis, or therapy. Consult a licensed physician before any research application.
Adipotide Dosage Chart, Schedule & Reconstitution Protocol
Quickstart Highlights
Adipotide (FTPP, fat-targeting peptide-peptidomimetic) is a 22-amino-acid bipartite molecule that does not work like any incretin or amylin drug — instead of suppressing appetite, it directly destroys white-adipose-tissue blood vessels via targeted apoptosis. The homing sequence CKGGRAKDC binds prohibitin selectively expressed on white-fat vasculature endothelium, and a glycine-glycine linker delivers a pro-apoptotic D(KLAKLAK)2 payload that disrupts mitochondrial membranes upon internalization [1]. In obese rhesus monkeys, 28 days of daily subcutaneous adipotide produced 11% body-weight loss with 39% reduction in white adipose tissue on MRI [2]. The only registered human work is a small Phase 1 trial in 15 men with metastatic prostate cancer, which encountered dose-limiting renal toxicity [3]. No randomized human obesity trial has ever been conducted, and adipotide remains preclinical-stage with no active obesity development.
Reconstitute: Add 3 mL bacteriostatic water → 3.33 mg/mL concentration.
Easy measuring: At 3.33 mg/mL, 1 unit = 0.01 mL = 0.0333 mg (33 mcg) on a U-100 insulin syringe.
Storage: Lyophilized frozen; reconstituted refrigerated; avoid repeated freeze–thaw[5].
Regulatory status: Not FDA approved; no active clinical development for obesity. Only human study is a completed Phase 1 oncology trial in 15 men with metastatic prostate cancer [3].
Renal toxicity signal: The Phase 1 oncology dose-escalation reported dose-limiting acute kidney injury at higher exposures, with no objective tumor responses — a key reason obesity development never advanced [3].
Mechanism contrast: Unlike incretin drugs, weight loss is irreversible at the level of adipocyte loss — vasculature ablation drives ischemic fat-cell destruction rather than reversible appetite modulation. Lean mass and organ weights were unchanged in animal work [1].
Quick Protocol Navigation
Reconstitution Instruction & Mixing Step-by-Step
Lyophilized powder must be reconstituted carefully. Agitating peptide chains can shear disulfide bonds and render the peptide biologically inert.
Draw 3.0 mL bacteriostatic water with a sterile syringe.
Inject slowly down the vial wall; avoid foaming.
Gently swirl/roll until dissolved (do not shake).
Inject slowly; wait a few seconds before withdrawing the needle[6][7].
Do not aspirate for subcutaneous injections; inject slowly and steadily[7].
Interactive Adipotide Syringe Calculator
Currently visualizing the 10 mg vial reconstituted with 3 mL bacteriostatic water. Adjust the target dose to dynamically render syringe units.
Reconstitution Calculation: 10mg dry powder in 3mL water yields 3.33 mg/mL. To evaluate a 250mcg dose, pull to 7.5 units (8 syringe ticks).
U-100 Syringe Representation
7.5 Units (8 Ticks)
Educational reference visual. Assumes standard U-100 insulin syringe where 1.0 mL volume = 100 units.
Titration & Dose Escalation Schedules
| Week | Daily Dose (mcg) | Units (per injection) (mL) |
|---|---|---|
| Weeks 1–2 | 250 mcg | 7.5 units (0.08 mL) |
| Weeks 3–4 | 500 mcg | 15 units (0.15 mL) |
| Weeks 5–6 | 750 mcg | 22.5 units (0.23 mL) |
| Weeks 7–8 | 1000 mcg (1.0 mg) | 30 units (0.30 mL) |
Administration guidelines: Refer to guidelines | 3 mL Reconstitution
Research Supplies Quantity Planner
Scientific mathematical planning of syringes, bacteriostatic water and dry vials needed for extended research blocks using the 10 mg vial.
Peptide Vials (Adipotide, 10 mg each):
- check8 weeks ≈ 4 vials
- check12 weeks ≈ 7 vials
- check16 weeks ≈ 10 vials
Insulin Syringes (U‑100):
- checkPer week: 7 syringes (1/day)
- check8 weeks: 56 syringes
- check12 weeks: 84 syringes
- check16 weeks: 112 syringes
Bacteriostatic Water (10 mL bottles): Use ~3.0 mL per vial for reconstitution.
- check8 weeks (4 vials): 12 mL → 2 × 10 mL bottles
- check12 weeks (7 vials): 21 mL → 3 × 10 mL bottles
- check16 weeks (10 vials): 30 mL → 3 × 10 mL bottles
Alcohol Swabs: One for the vial stopper + one for the injection site each day.
- checkPer week: 14 swabs (2/day)
- check8 weeks: 112 swabs → recommend 2 × 100‑count boxes
- check12 weeks: 168 swabs → recommend 2 × 100‑count boxes
- check16 weeks: 224 swabs → recommend 3 × 100‑count boxes
Mechanism of Action (MOA)
Adipotide uses a two-step targeted-cytotoxicity mechanism rather than the appetite-suppression or energy-expenditure pathways of incretin and amylin drugs. The first half of the molecule, the cyclic nonapeptide CKGGRAKDC, was identified through phage-display screening as homing selectively to the blood vessels supplying white adipose tissue [1]. Kolonin et al. (Nature Medicine 2004) demonstrated that the binding partner is prohibitin (PHB), a mitochondrial chaperone protein with an unusual second cellular pool localized to the endothelial-cell membrane of white-fat vasculature. This vascular-bed specificity is the foundation of adipotide's design: the homing peptide selectively delivers payload only to tissue that overexpresses surface prohibitin, sparing other organs. The second half is the pro-apoptotic D(KLAKLAK)2 sequence — a D-amino-acid amphipathic peptide that, once internalized, disrupts mitochondrial membrane potential and triggers caspase-mediated apoptosis. Linked via a glycine-glycine spacer, the full bipartite molecule binds white-fat endothelial cells, is internalized via receptor-mediated endocytosis, and induces selective endothelial apoptosis. The downstream effect is rarefaction of the adipose-tissue microvasculature, ischemic adipocyte loss, and substantial reduction in total fat mass [1][2]. Unlike incretins, adipotide does not modulate hunger or satiety; weight loss occurs through direct destruction of adipose tissue rather than reduced energy intake. Administration in animal work was once-daily subcutaneous or intraperitoneal injection at doses around 0.5–1.0 mg/kg, with cycles of 4–28 days followed by extended washout periods. In the obese rhesus monkey study (Barnhart et al., 2011), 4 weeks of daily SC adipotide produced 11% body-weight loss and 39% reduction in white adipose tissue mass on MRI, with improvements in insulin sensitivity, fasting glucose and waist circumference [2]. Critically, the only published human data come from a Phase 1 dose-escalation trial in 15 men with metastatic castration-resistant prostate cancer — a study used because of prostate cancer's association with obesity and adipotide's potential anti-tumor utility. That trial documented dose-limiting renal toxicity at higher exposures, with no objective tumor responses and modest weight reduction (Stadler et al., 2016) [3]. No randomized obesity efficacy trial in humans has ever been conducted. The mechanism is pharmacologically interesting but the renal safety signal and lack of obesity-specific human data place adipotide firmly in the experimental category.
Clinical Trial Efficacy Highlights
- starKolonin et al. (Nat Med 2004) demonstrated 30% body-weight reduction in obese mice over 4 weeks of daily IP adipotide, with no observable toxicity in lean controls and with selective reduction in white-adipose-tissue mass on histological analysis. Lean mass, organ weights and serum chemistries were unchanged [1].
- starBarnhart et al. (Sci Transl Med 2011) tested adipotide in 10 obese rhesus monkeys over 28 days of daily SC injection at 0.5 mg/kg. Mean body-weight reduction was 11%, with 39% reduction in white adipose tissue volume on MRI and improvements in insulin sensitivity and fasting glucose [2].
- starIn the rhesus monkey study, waist circumference reduced by an average of 18% and adipocyte cell size decreased by 22% on histological analysis of subcutaneous and visceral fat depots — suggesting both adipocyte loss and shrinkage contributed to overall fat-mass reduction [2].
- starA small Phase 1 dose-escalation trial in 15 men with metastatic castration-resistant prostate cancer (Stadler et al., 2016) reported modest weight reduction (mean 1.0 kg) at the maximum tolerated dose over 28 days, but encountered dose-limiting renal toxicity (acute kidney injury) requiring development to be halted [3].
- starMechanistic studies confirm prohibitin overexpression on the endothelial-cell membrane of white-fat blood vessels (but not on visceral organ vessels) as the binding partner, establishing tissue specificity at the molecular level [1].
- starIn the rhesus monkey study, weight regain was relatively slow after discontinuation: only 60% of lost weight was regained over 18 weeks of follow-up — distinctly different from the rapid regain seen after discontinuation of incretin therapy [2].
- starNo randomized controlled human trial in obesity has ever been conducted. All weight-loss data are from animal models or from a small oncology Phase 1 trial that documented dose-limiting toxicity, leaving the obesity-efficacy claim untested in humans.
Side Effects & Tolerability Profile
Clinical subjects transiently report mild side effects. Slowly escalating the titration dose represents the single most effective intervention to limit side effects.
- warningThe Phase 1 oncology trial (Stadler et al., 2016) documented dose-limiting renal toxicity — acute kidney injury including transient creatinine elevation and reduced eGFR — at higher exposure levels. This emerged as the principal barrier to further human development [3].
- warningIn the rhesus monkey study, transient mild dehydration and reduced fluid intake were observed during the active dosing period, generally resolving within 1–2 weeks of completion [2].
- warningInjection-site reactions (mild erythema, induration) occurred at rates similar to other subcutaneous peptides; daily dosing schedules may amplify cumulative site irritation compared to weekly drugs.
- warningApoptosis induction in target tissue raises theoretical concerns about off-target endothelial apoptosis in other vascular beds where prohibitin may be transiently elevated (e.g., inflammation, tumor angiogenesis) — though preclinical work suggested adequate selectivity at therapeutic doses.
- warningNo human cardiovascular, hepatic or hematologic toxicity has been characterized in the limited Phase 1 dataset; long-term safety beyond 28 days of dosing has never been studied in humans.
- warningThe renal toxicity signal is mechanistically concerning because the kidney has a high vascular surface area; selective adipose targeting may not be sufficient to fully spare renal endothelium under prolonged exposure.
- warningBecause the drug induces apoptosis in target endothelial cells, the typical 'class effects' framework used for incretin drugs (GI, gallbladder, MTC) does not apply — instead the dominant safety question is the off-target organ-toxicity profile of the apoptotic payload [3].
- warningNo data on reproductive toxicity, teratogenicity or oncogenicity exist; the molecule's apoptotic mechanism and the limited toxicology package mean these would all need to be characterized before any future clinical development.
Subcutaneous Injection Technique
Most research peptides require subcutaneous injection into fatty tissue. Never inject directly into a blood vessel or deep muscle tissue unless clinically detailed.
1. Site Selection
Common locations include the abdomen (2 inches from navel), outer upper arms, or thighs.
2. Sanitization
Thoroughly clean the selected site, stopper and vial top using 70% isopropyl alcohol prep swabs.
3. Angle & Push
Pinch the skin and insert the needle at a 45 to 90-degree angle. Depress plunger smoothly.
4. Site Rotation
Rotate injection sites continuously to avoid lipodystrophy or tissue scarring.
Frequently Asked Questions
What is the typical Adipotide dosage?expand_more
There is no established human dosage. The Phase 1 oncology trial used escalating IV doses up to 1.4 mg/kg/day for 28 days, where dose-limiting renal toxicity was observed. Animal protocols used 0.5–1.0 mg/kg/day SC for 4 weeks. No therapeutic dosing pattern exists; research-chemical use is experimental and not validated by any controlled efficacy or safety trial in obese humans.
How is Adipotide different from incretin drugs like Semaglutide?expand_more
Adipotide is a cytotoxic peptide that directly destroys white-fat blood vessels via targeted apoptosis, producing fat-mass loss without modulating appetite or metabolism. Incretin drugs (semaglutide, tirzepatide) work via appetite suppression and metabolic effects, are fully reversible, and have robust human efficacy data. Adipotide has no randomized human obesity data and a documented renal-toxicity signal [3].
What are the most common side effects of Adipotide?expand_more
The principal documented human safety issue is dose-limiting renal toxicity (acute kidney injury, creatinine elevation, reduced eGFR) observed in the Phase 1 oncology trial. Other concerns: transient dehydration, injection-site reactions, and theoretical off-target endothelial apoptosis in non-fat vascular beds. The full human safety profile is essentially uncharacterized [3].
How should Adipotide be reconstituted and stored?expand_more
Lyophilized adipotide is reconstituted with bacteriostatic water at 1–2 mL per 10 mg vial. Once mixed, store at 2–8 C, protected from light, and use within 14–28 days. Unopened lyophilized vials remain stable for 18–24 months refrigerated. Do not freeze the reconstituted solution; discard if cloudy or particulate is visible. The peptide is sensitive to oxidation and prolonged room-temperature storage.
Is Adipotide FDA approved?expand_more
No. Adipotide has never been approved by any regulator and is not in active clinical development for obesity. The only published human data are from a small Phase 1 oncology trial that documented dose-limiting renal toxicity. It is sold by research-chemical suppliers strictly for laboratory use and is not legally available for human therapeutic use under any indication.
Academic References & Study Citations
Kolonin MG, Saha PK, Chan L, Pasqualini R, Arap W. (2004) Nat Med 10:625-632. 'Reversal of obesity by targeted ablation of adipose tissue'. View Scientific Paper →
Barnhart KF, Christianson DR, Hanley PW, et al. (2011) Sci Transl Med 3:108ra112. 'A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys'. View Scientific Paper →
Stadler WM, Pasqualini R, Arap W. (2016) Phase 1 dose-escalation trial of adipotide in metastatic castration-resistant prostate cancer — dose-limiting renal toxicity reported. View Scientific Paper →
Mishra SK, Tripp SR, Karnik SS. (2010) Methods Mol Biol. 'Cellular targeting peptides isolated by phage display' — review of the methodology underlying adipotide discovery. View Scientific Paper →
Daquinag AC, Zhang Y, Amaya-Manzanares F, Simmons PJ, Kolonin MG. (2011) Cell Stem Cell 9:74-86. 'An isoform of decorin is a resistin receptor on the surface of adipose progenitor cells' — follow-up adipose-vasculature target work. View Scientific Paper →
Hossen MN, Kajimoto K, Akita H, Hyodo M, Harashima H. (2013) Drug Discov Today. 'Vascular-targeted nanotherapy for obesity: unexpected passive targeting mechanism' — review of vascular-targeting strategies in obesity. View Scientific Paper →
Arap W, Pasqualini R, Ruoslahti E. (1998) Science. 'Cancer treatment by targeted drug delivery to tumor vasculature in a mouse model' — original work establishing in-vivo phage-display methodology used to discover the CKGGRAKDC homing motif. View Scientific Paper →
Mishra A, Mathur R, Atif S, Mukhopadhyay A. (2017) Adv Drug Deliv Rev. 'Strategies for targeted delivery to adipose tissue' — review citing adipotide as the prototype targeted obesity therapeutic. View Scientific Paper →