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Free U.S. shipping on orders over $150Adipotide, also called Prohibitin-targeting peptide 1, is a 25-amino acid peptide designed to attach to a protein called prohibitin [1]. Prohibitin protein is multi-functional, with roles in cell growth and survival, and apoptosis. It is found in several cellular compartments, including the cell membrane [1].
Adipotide peptide has three main components [2]:
It works mainly by targeting specific blood vessels that supply white fat tissue, cutting off fat cell oxygen and nutrient supply, and leading to apoptosis [1]. This approach is highly selective, sparing other tissues [1].
Adipotide peptide kills fat cells indirectly, by attacking the blood vessels that keep fat tissue alive rather than killing the fat cells outright [2].
Adipotide has a homing sequence that specifically binds prohibitin and ANXA2 proteins, which are found on the surface of endothelial cells that line blood vessels supplying fat tissue [2]. This makes the peptide highly selective for fat tissue vasculature [3].
Once bound to prohibitin, the peptide is pulled into endothelial cells and disrupts mitochondria to cause cell death [4]. With the blood vessel destroyed, fat cells lose their supply of oxygen and nutrients [2]. This ischemic stress triggers a secondary apoptosis in the fat cells themselves, leading to resorption of white fat tissue [2].
In short, Adipotide kills the support system that fat cells rely on, causing them to die and be broken down by the body [2]. This process also seems to improve brain signals that reduce appetite and further enhance fat loss [3].
Adipotide peptide acts to reduce white fat mass, impacting metabolic health by augmenting the processing and response to insulin [2]. When adipotide peptide destroys blood vessels that feed adipose tissue, the fat cells gradually die and are resorbed by the body [1]. This shrinking of fat tissue can impact the release of certain inflammatory and hormone-like molecules, called adipokines, which are linked to insulin resistance [2].
In animal studies, adipokine peptide lowered fasting insulin levels without changing blood sugar levels, suggesting that the body became more sensitive to insulin and did not need to overproduce it to control blood sugar levels [3].
Rodent studies also found that adipotide-induced fat loss did not trigger the typical drop in metabolic rate that often accompanies weight loss [3]. In some cases, energy expenditure even increased [3]. This means the body continues burning calories at the same or even slightly higher rate. This helped sustain weight loss and maintain metabolic improvements.
By reducing fat mass, improving insulin sensitivity, and potentially maintaining or even boosting energy use, adipotide peptide directly addresses key metabolic problems associated with weight management [3].
Adipotide peptide acts on blood vessels via a two-part mechanism that is highly selective for those that supply white fat tissue [2].
The first part is a “homing” sequence of amino acids (CKGGRAKDC) that recognizes and binds to prohibitin, a protein located on the surface of cells that line blood vessels in white adipose tissue [2]. This targeting is very specific – prohibitin is especially accessible in the vasculature of white fat, making it a unique marker for those blood vessels [2].
Once bound to prohibitin, the peptide is taken inside endothelial cells [2]. Attached to the targeting sequence is a proapoptotic peptide (D[KLAKLAK]₂) that disrupts the cell's mitochondria (structures that produce energy) [2]. This mitochondrial damage activates apoptosis, or programmed cell death, in endothelial cells [2].
When enough endothelial cells in a vessel die, the blood vessel collapses and is destroyed [2]. Without such vascular supply, white fat tissue loses both oxygen and nutrient flow, causing a breakdown and resorption of fat [2].
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). Adipotide is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
Every lot undergoes our 6-panel testing protocol: identification by ESI-MS, purification by RP-HPLC, conformity, sterility screening, quantification of net peptide content, and LAL endotoxin screening. Full analytical data is published in the Certificate of Analysis for each lot.
Lyophilized peptides should be stored at -20°C or below for long-term stability. Once reconstituted, peptides should be stored at 2–8°C and used within a reasonable timeframe depending on the specific compound. Avoid repeated freeze-thaw cycles. Always store in a dry environment away from direct light.
Orders are processed within 1–3 business days after payment confirmation. Orders placed after 3:00 PM Pacific time or on weekends and holidays will begin processing the next business day. We offer free standard shipping on orders over $150. All orders are shipped in insulated packaging with ice packs when necessary. Standard delivery typically takes 2–4 business days within the continental US.
No. All compounds sold by Genesis Peptides are strictly for in vitro and preclinical laboratory research purposes only. They are not approved for human consumption, therapeutic use, or diagnostic purposes. By purchasing, you confirm the products will be used solely for legitimate research applications.
A Certificate of Analysis (COA) is a document issued by our analytical laboratory that reports the results of all quality control tests performed on a specific lot of product. Each COA includes HPLC chromatograms, mass spectra, endotoxin results, and quantification data where applicable. COAs are available in our COA Library for every lot we have shipped.
Yes. We offer volume pricing for universities, research institutions, and laboratories with recurring needs. Discounts begin at 100+ units and scale with volume. Contact our team for a custom quote tailored to your research requirements.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.
What is ARA 290 peptide? ARA 290, also known as Cibinetide, is a synthetic peptide derived from the structure of erythropoietin (EPO) but engineered to exclude EPO’s hematopoietic, red-blood-cell–stimulating effects [1]. Instead, ARA 290 selectively targets the innate repair receptor (IRR), a heteromeric EPOR/CD131 complex involved in cellular protection, inflammatory resolution, and tissue homeostasis [2]. By isolating the non-erythropoietic region of the EPO molecule, researchers created a peptide that retains EPO’s cytoprotective and pro-repair signaling without impacting hematocrit or erythropoiesis. As a result, ARA 290 has gained significant attention as a research peptide used to study pathways related to cellular stress, microvascular function, and immune modulation. ARA 290 Peptide Benefits ARA 290 Neuropathic Pain and Nerve Health ARA 290 has been studied for its influence on nerve integrity and health. Its activity centers on the innate repair receptor (IRR), a heteromeric EPOR/CD131 complex that becomes activated in response to cellular stress [2, 3]. IRR activation has been shown to modulate inflammatory cascades that contribute to neuronal hypersensitivity. A Phase 2 RCT in adults with type 2 diabetes and painful small-fiber neuropathy evaluated whether ARA 290 can mitigate neuropathic pain [1]. This study followed a parallel timeline, where 48 participants first received ARA 290 4 mg subcutaneously (SC) daily for 28 days, or matched placebo, followed by 28 days of observation. Results showed that ARA 290: Significantly improved glycemic control: A1C –0.21% ± 0.09 after 56 days (p = 0.002) Improved cholesterol/HDL ratio (p = 0.039) Decreased triglycerides (p = 0.043) Significant improvements in pain (tingling, thermal, and allodynia) sensitivity (p < 0.037) Noticeable improvements in reported quality of life There were minimal significant adverse events, and no anti–ARA 290 antibodies detected. These findings support ARA 290 as a potential disease-modifying agent for diabetic small-fiber neuropathy, with benefits extending to widespread metabolic regulation. Similar neuroprotective effects of ARA290 have been found in models of radiation induced injury and peripheral nerve damage [4, 5]. ARA 290 Metabolic and Cardiovascular Benefits Beyond its effects on neural pathways, ARA 290 has been investigated for its influence on metabolic and cardiovascular homeostasis through its selective activation of the innate repair receptor (IRR). A randomized, controlled preclinical trial determined whether ARA290 could affect cardiac aging and function in 48 advanced-age Fischer x Brown Norway rats [6]. Rats were assigned to chronic ARA 290 or saline control from 18-33 months of age. Results showed that ARA 290 administration: Significantly decreased age-associated inflammatory changes, including: non-myocyte:myocyte ratio Infiltrating leukocytes and monocytes Pro-inflammatory cytokines Total NF-κB and phosphorylated NF-κB (p-NF-κB) Displayed cellular level benefits, including: Increased autophagy flux Decreased lipofuscin accumulation (less cellular aging) Improved longevity, such as: Avoiding age-associated rises in blood pressure Maintaining left ventricular ejection fraction (LVEF) Reduced structural deterioration over time Long-term administration of ARA290 attenuates multiple hallmarks of cardiac aging. By preserving cardiomyocyte function, ARA290 appears to extend healthspan and mitigate the systemic decline associated with advanced age. Immune Function and Tissue Healing ARA 290 plays a distinct role in immune modulation and tissue recovery through the activation of the IRR pathway, among others. ARA290 activation influences macrophage polarization, encouraging a shift from pro-inflammatory M1 macrophages toward M2 macrophages that facilitate debris clearance, extracellular matrix organization, and overall tissue restoration [7]. An in vitro preclinical study evaluated whether using an elastin-like peptide (ELP) fusion can increase stability of ARA290 and enhance wound healing in a full-thickness diabetic wound model [8]. After establishing that ELP fusion preserved biological activity, results showed that: In diabetic wounds, ARA290-ELP: Accelerated closure rate Increased angiogenesis in the wound bed Improved early tissue regeneration compared to controls Fusing ARA290 to elastin-like peptide generates stable, proteolytically resistant, bioactive therapeutics suitable for the harsh environment of chronic diabetic wounds. ARA290 has also shown efficacy in non-diabetic injury models, including ischemic/reperfusion injury in kidney models and surface burns [9, 10]
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What is BPC-157? BPC-157 is a synthetic pentadecapeptide composed of 15 amino acids, with the sequence Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val. It is a portion of a protein that occurs naturally in human gastric juice, commonly referred to as Body Protection Compound (BPC). Native BPC helps maintain gastrointestinal integrity under normal physiological conditions. BPC-157 is stable and soluble in water. As a synthetic peptide, BPC-157 is not produced endogenously in this exact form but is designed to replicate a biologically active fragment of the parent protein found in gastric secretions [1]. The peptide has been the subject of extensive preclinical research, particularly in the context of cellular proliferation, angiogenesis, and tissue repair mechanisms. BPC-157 has been studied in animal and in vitro models as a tool for investigating pathways associated with: Gastrointestinal homeostasis Vascular modulation Cytoprotection Inflammation modulation All research involving BPC-157 remains within the domain of experimental studies, and it is not approved for human therapeutic use. What does BPC-157 do? The research Inflammation and pain modulation BPC-157 has been extensively studied in preclinical models for its modulatory effects on inflammation, particularly in relation to tissue injury and repair processes [1]. In various rodent studies, administration of BPC-157 reduced markers of inflammation in models of gastrointestinal, musculoskeletal, and neural injury. By modulating inflammation, rat studies suggest that various BPC variants modulate pain, while BPC-157 predominantly reduces acute pain in incisional and formalin-induced pain [2]. In a rat model of allodynia, it also reduced pain by protecting nerve integrity from capsaicin [3]. BPC may also modulate the nitric oxide (NO) system. It counteracts both excessive and deficient NO activity, supporting endothelial integrity and attenuating leukocyte infiltration in inflamed tissues. This dual regulation may contribute to its observed ability to balance pro-inflammatory and anti-inflammatory signaling cascades [4]. In experimental colitis models, for example, BPC-157 administration was associated with: Reduced mucosal damage Decreased myeloperoxidase activity (a marker of neutrophil infiltration) Normalization of cytokine profiles BPC-157 also promotes angiogenesis (blood vessel growth) and stabilizes vascular function at sites of injury. This angiogenic support not only facilitates tissue repair but may also limit secondary inflammation resulting from ischemia and oxidative stress [5]. Research in tendon and ligament injury models similarly highlights reductions in edema and inflammatory cell presence following BPC-157 exposure. These findings are derived from animal studies, and while promising, they await confirmation in human clinical research to fully understand its therapeutic relevance. Tissue healing and stem cells BPC-157 can facilitate regeneration across various tissue types, including: Tendon Muscle Ligament Bone Nerve A key feature identified in these models is BPC-157’s capacity to modulate cellular and immune environments in ways that promote structural integrity and restoration of injured sites. In rat models of tendon fibroblasts, BPC-157 significantly upregulated growth hormone receptor expression, and enhanced the responsiveness of these cells to endogenous growth hormone [6]. This interaction promotes cell proliferation and tissue regeneration, increasing expression of proliferation markers: Proliferating cell nuclear antigen (PCNA) JAK2 signaling pathway These results suggest a supportive role in tendon repair processes at the molecular level, enhancing the body's natural regenerative mechanisms. BPC-157 may influence stem cell activity indirectly by optimizing the local microenvironment of injured tissues. While direct stimulation of stem cell differentiation by BPC-157 has not been definitively proven, its actions on surrounding tissues, blood vessels, and extracellular matrix components are believed to indirectly enhance stem cell-mediated repair processes. Gut health BPC-157 has been extensively studied in preclinical models for its protective and regenerative effects on the gastrointestinal (GI) tract [7]. Research in rat models of ileoileal anastomosis healing, for instance, shows that BPC-157: Modulates local immune responses Enhances granulation tissue formation Increases collagen and reticulin deposition Promotes re-epithelialization Supports the regeneration of muscular tissue strands at anastomotic sites. BPC-157 reduced adhesion formation and necrosis, while accelerating the resolution of edema and inflammatory infiltrates in treated animals compared to controls. Additional experimental models of intestinal injury, including those involving perforations, fistulas, or induced colitis, report that BPC-157 administration supported gut integrity by: Promoting angiogenesis Mitigating tissue necrosis Stabilizing microvascular structures The peptide’s influence on nitric oxide pathways and its modulation of endothelial function are proposed mechanisms underlying these benefits. While clinical trials in humans remain limited, the consistent findings across animal models offer a compelling basis for future investigation into its application in gut health contexts. BPC-157 in bees Bees are crucial pollinators whose populations are in significant declines. Research suggests that BPC-157 may help to improve bee health and survival. In bees, BPC-157 improves colony strength and enhances certain aspects of immune responses [8]. Supplementation of bee diets with the peptide reduced the infection load of the Nosema ceranae, a one-celled fungal parasite. BPC-157 also attenuates gut damage from N. ceranae infections [8]. Overall, BPC-157 may be beneficial in beekeeping.