Peptide adipotide-also known as a white adipose vasculature–targeted proapoptotic peptide-is a chimeric peptide construct that covalently links an adipose-selective vascular homing motif to a mitochondria‑disrupting proapoptotic sequence. The N‑terminal segment is a cyclic adipose‑vascular homing motif formed by a Cys–Cys disulfide bond, while the C‑terminal segment is an amphipathic, cationic D‑peptide comprising two tandem KLAKLAK repeats, connected by a flexible Gly–Gly linker. The homing motif binds a receptor complex on the endothelium of white adipose tissue (WAT), centered on prohibitin (PHB); once internalized, the proapoptotic cargo disrupts mitochondrial membranes and triggers endothelial apoptosis, thereby selectively devascularizing adipose tissue and, in turn, inducing adipocyte atrophy and a reduction in fat mass.
Shaanxi Medibridge supplies adipotide (WAT‑targeted proapoptotic peptide) at ≥99% purity for research use only. As a dedicated peptide partner to universities and research institutes worldwide, we offer custom synthesis, from milligram to multigram scales, with robust QC, including HPLC and MS data and a lot-specific certificate of analysis.
COA
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Product Name |
CAS Number |
Batch Number |
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Peptide adipotide |
859216-15-2 |
MB2509081549 |
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Manufacturer Date |
Analysis Date |
Expiry Date |
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2025-11-09 |
2025-11-10 |
2027-11-08 |
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Sample Qty Base |
Packing |
Test Method |
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860.52 GS |
5GS/BOTTLE |
HPLC |
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Item |
Standard |
Results |
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Purity |
≥98% |
99.13% |
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Peptide Assay |
≥80% |
85.63% |
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Mass Spectrum |
2557.21 |
2557.21 |
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Solubility |
Soluble in water |
Complies |
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Clarity and color of solution |
Clear and colorless |
Complies |
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Sodium salt |
<5.0% |
1.98% |
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Water |
≤7.0% |
3.21% |
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Residual Solvent: |
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Methanol |
≤0.3% |
Complies |
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Isopropanol |
≤0.5% |
0.158% |
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Acetonitrile |
≤0.041% |
0.019% |
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Methylene Chloride |
≤0.06% |
0.028% |
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N,N-Dimethylformamide |
≤0.088% |
Complies |
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Triethylamine |
≤0.032% |
Complies |
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Tert-butyl methyl ether |
≤0.5% |
0.173% |
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Endotoxin |
≤0.5 EU/mg |
Complies |
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Microbial Limit |
Total aerobic bacteria <100 CFU/g Total yeast & mold <50 CFU/g |
<50 CFU/g <10 CFU/g |
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Storage |
Keep in dark and cool dry place (-20 to 8°C) |
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Conclusion |
The batch conforms to the IN-HOUSE standard |
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Specification(for research use only)
Why choose us
1. High Purity and Structural Confirmation: We offer this product with ≥99% purity and include a batch COA/purity spectrum.
2. Stable and Reproducible: Lyophilized powder supply, ensuring stable cyclization conformation and sequence integrity.
3. Flexible Customization: Supports mg-multigram-kg level customization.
4. Comprehensive Technical Support: Provides solubility and buffer system advice, storage and reconstitution guidelines, methodological references, and one-on-one rapid response from professional engineers.
5. Reliable Delivery: Global light- and moisture-proof packaging, ensuring stability and efficiency from order placement to receipt.
6. Compliance and Cost-Effectiveness: Targeting research applications, transparent pricing, 4-6 day delivery, enabling high-quality experimental progress within budget.
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Form |
Sample Order |
Specification |
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Raw powder |
1 g |
Purity is NLT 99% |
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Vials |
10 vials |
3ml/5ml/7ml/15ml vials etc. |
Mechanism of action
Selective localization
The cyclic CKGGRAKDC motif binds prohibitin on WAT endothelium, enabling adipose-specific homing and endocytosis; this was established by Kolonin et al., who reversed obesity in mice by targeting prohibitin with a KLAK cargo.
Mitochondrial disruption
Internalized D(KLAKLAK)2 collapses mitochondrial membrane potential and triggers intrinsic apoptosis in endothelial cells, a well-characterized effect of targeted KLAK constructs.
Tissue effects
Endothelial apoptosis leads to vascular rarefaction and depot shrinkage; in obese rhesus macaques given adipotide 0.43 mg/kg SC daily for 28 days, body weight fell 7.4–14.7% (mean −10.6%), DEXA fat mass −38.7%, and abdominal MRI WAT −17.5% at end-of-treatment (−27.0% by end-of-recovery).
Metabolic outcomes
Insulin AUC during IVGTT decreased 36.2% and insulinogenic index −48.5% in treated macaques, indicating improved insulin sensitivity; food intake declined during dosing and rebounded after cessation.
Mechanism comparison with mainstream anti-obesity drugs(for academic exchange only)
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Aspect |
GLP 1/Dual (GLP 1/GIP) |
Peptide adipotide |
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Mechanism of action |
Central appetite–satiety pathways; delayed gastric emptying; broad metabolic effects |
Peripheral targeting of WAT vasculature; "supply → apoptosis → atrophy" cascade to lower fat mass |
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Primary target site |
CNS and gut–pancreas axis |
White adipose tissue endothelium |
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CNS dependence |
High |
Low |
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Metabolic effect scope |
Broad metabolic improvement |
Fat mass reduction with downstream metabolic benefits |
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Strategy analogy |
Neuroendocrine metabolic re tuning |
Tissue selective ablation |
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Combination potential |
Theoretically complementary; needs clinical validation |
Theoretically complementary; needs clinical validation |
Key Scientific Questions and Optimization Strategies
Patient stratification
Evidence: In the same rhesus study, obese animals lost weight (mean −10.6%, range −7.4% to −14.7%); lean macaques at the therapeutic dose did not show comparable loss, indicating phenotype‑dependent efficacy (28‑day SC dosing; Sci Transl Med 2012). Mechanistically, CKGGRAKDC homes to prohibitin on WAT endothelium (mouse phage‑display/targeted‑ablation experiments; Nature Medicine 2004), implying target‑expression variability across depots.
Approach: Enrich patients with visceral‑dominant adiposity by MRI; document PHB target in WAT (biopsy IHC or tracer uptake) and require preserved renal function at baseline (eGFR/albuminuria) to lower risk.
Biomarkers
Target engagement/PD: Use the same quantitative readouts proven in the rhesus experiment-DEXA fat mass (−38.7%), abdominal MRI WAT volume (−17.5% end‑of‑treatment; −27.0% end‑of‑recovery), and IVGTT metrics (insulin AUC −36.2%; insulinogenic index −48.5%)-as primary PD markers (28‑day SC study; Sci Transl Med 2012).Safety: Track tubular injury early with urine NGAL/KIM‑1 alongside serum creatinine/cystatin C; define stopping rules for on‑treatment rises, then confirm reversibility during washout (aligned to the NHP toxicity signals above).
FAQ
Q: What is the MOA?
A: CKGGRAKDC targets prohibitin on WAT endothelium; D(KLAKLAK)2 disrupts mitochondria → endothelial apoptosis → depot shrinkage.
Q: What are the core specs?
A: c[CKGGRAKDC]–GG–D(KLAKLAK)2; purity ≥99% (HPLC); LC–MS confirmed; COA provided.
Q: How to reconstitute/store?
A: Sterile water/PBS (pH ~7), 1–5 mg/mL; aliquot; avoid freeze–thaw; lyophilized at −20 to −80°C.
Q: Any reference dosing (preclinical)?
A: Rhesus: 0.43 mg/kg SC QD ×28 days; rodents: QD ×2–4 weeks; include vehicle/scrambled controls.
Q: Key safety monitoring?
A: Renal: serum creatinine, cystatin C; urine NGAL, KIM‑1, α1‑MG, β2‑MG; preset stopping rules.
Q: Is Shaanxi Medibridge the manufacturer of Adipotide?
A: Yes, we are not only able to provide adipotide with a purity of no less than 99%, but Shaanxi Medibridge Biotech Co., Ltd. is also a peptide supplier.
Looking for a reliable GLP 1/Dual (GLP 1/GIP) and Peptide adipotide manufacturer? We provide GMP managed standard, research use only materials with transparent COAs, tight lot to lot consistency, and responsive technical support. For quotes, lead times, or custom specs, contact hi@medibridgeapi.com or WhatsApp +44 07548632075.
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