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Free U.S. shipping on orders over $150Vilon is a short synthetic dipeptide composed of lysine bound to glutamic acid (Lys-Glu).
Vilon is considered a thymic peptide analogue, meaning it mimics biological activity associated with peptides produced by the thymus gland, an organ essential to immune system development.
Like other bioregulatory peptides, Vilon has been studied for its ability to regulate protein synthesis and normalize cellular homeostasis, particularly in tissues affected by stress, aging, or immune dysfunction.
While Vilon is not approved for medical use outside research settings, its small molecular structure enables high bioavailability and cell membrane permeability, characteristics that have made it an important subject in peptide-based therapy research.
Vilon shows immunomodulatory properties, particularly its effects on thymus-dependent immune pathways.
In an in vitro study using human monocytic THP-1 cells, Vilon treatment resulted in [1]:
In Type 1 diabetes patients, administering Vilon resulted in [2]:
Vilon has been investigated within the field of bioregulatory peptide research for its potential role in cellular repair, longevity regulation, and tissue regeneration.
A case series examined 250 adults aged 65–87 with chronic periodontitis along with type II diabetes, atherosclerosis, and other cardiovascular diseases. Subjects received 10–20 µg daily submucosally for 5–10 days. The treatment significantly improved immune, oxidative stress, and coagulation parameters. Vilon treatment also reduced periodontal pocket depths by 1.2 Ramfjord index points and papillary marginal alveolar index by 10 times. These benefits, however, happened to a lesser degree in younger people with chronic periodontitis [3].
Age-associated declines in phosphorylated CREB (pCREB) reduce levels of arylalkylamine N-acetyltransferase (AANAT), contributing to age-related declines in melatonin, circadian rhythm, and sleep disruption.
Rat pinealocytes were treated with either control (no treatment), norepinephrine (NE) 1 µg/ml (positive control), or peptide-treated cultures (epithalone or Vilon) at 100 ng/ml. Subsequently, cultures were incubated for up to 3 hours at 36.7°C in 5% CO2 [4].
Results showed that Vilon:
Vilon peptide transiently enhances early transcriptional activation (pCREB) and enzyme induction (AANAT) in pinealocytes, suggesting it plays a regulatory role in stimulating melatonin synthesis at the initial phase of the signaling cascade.
Aging is often associated with increased chromatin condensation (heterochromatinization), which suppresses gene expression.
Another cell study investigated the effects of Vilon on chromatin organization in cultured lymphocytes obtained from elderly individuals [5]. The results demonstrated that Vilon loosened chromatin both globally and in the nucleolus, restoring access to genes silenced during aging.
Vilon plays an apoptoregulatory role, helping to protect somewhat damaged healthy cells. However, in cancer cells, Vilon seems to increase apoptotic cell death, which can help prevent further cancer progression.
In a cell study, administration of Vilon administered to rat spleen lymphocytes post-radiation induced significantly less apoptosis [6]. To date, the exact mechanisms by which apoptosis is inhibited has not been elucidated.
In rats transplanted with carcinoma, Vilon stimulated apoptosis in both young and old rats, suggesting that instead of protecting damaged cells, Vilon plays a more apoptoregulatory role [7].
Because dysregulated apoptosis is a hallmark feature of carcinogenesis, some studies have explored Vilon’s effects in oncological research settings.
Early experimental reports from Russian investigators suggest that Vilon could serve as an adjuvant to cancer therapy, resulting in [8]:
However, such studies remain experimental, and no clinical evidence currently supports Vilon for use in oncology.
Vilon’s role in apoptoregulation continues to be a subject of research in the broader field of cellular homeostasis and peptide-based cytoprotection.
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). Vilon 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.
Snapshot Vasoactive Intestinal Peptide (VIP) is a neuropeptide that, when administered exogenously, activates VPAC receptors to support vasodilation, immune balance, tissue repair, and neuroprotection. Its targeted signaling influences respiratory, metabolic, and microvascular pathways, offering broad metabolic use cases that require further clinical validation. What Is Vasoactive intestinal Peptide (VIP)? Vasoactive Intestinal Peptide (VIP) is a naturally occurring neuropeptide produced throughout the gastrointestinal tract, pancreas, cardiovascular system, and central nervous system. In the body (endogenously), it plays key roles in: Smooth-muscle relaxation Circadian rhythm coordination Immune modulation Secretory activity in the gut and lungs Endogenous VIP levels can be measured through laboratory blood testing. Beyond its endogenous functions, exogenous VIP administration has become an area of growing scientific interest. When delivered as a peptide analogue, VIP acts through VPAC1 and VPAC2 receptors, which are widely distributed across neural, vascular, and immune pathways and tissues, to influence cellular signaling in a controlled, dose-dependent manner. VIP Benefits and Side Effects Immunomodulatory Actions Exogenous VIP administration has been widely studied for its ability to influence immune balance through selective activation of VPAC1 and VPAC2 receptors on lymphocytes, macrophages, dendritic cells, and endothelial tissues. VIP can shift cytokine patterns toward anti-inflammatory profiles, downregulating pro-inflammatory mediators while enhancing immune tolerance [1]. VIP has also been explored for its role in T-cell modulation, influencing immune responses. A cell study characterized how VIP receptors (VPAC1 and VPAC2) behave during activation of human Th cells under healthy and inflammatory (early arthritis) conditions [2]. Experiments showed that: VIP Receptors are differentially expressed: VPAC1 expression remained stable during Th cell activation. VPAC2 was significantly upregulated during activation. Receptors are found in different parts of the cell: VPAC1 is located in the nucleus while VPAC 2 is on the plasma membrane. Both VPACs activated PKA-dependent signaling and showed strong immunomodulatory effects. These findings provide new mechanistic insights and identify VIP receptor signaling as a potential therapeutic target in inflammatory and autoimmune diseases. Tissue Repair and Epithelial Integrity One of VIP’s key actions involves tight-junction regulation, a critical determinant of epithelial barrier integrity. An in vitro study used human bronchial epithelial cells (HBECs) to evaluate effects of VIP on wound repair [3]. A mechanical wound model in cultured HBECs was used to simulate epithelial injury. Compared to controls, VIP administration: Significantly accelerated closure of the wounded epithelial area. Enhanced chemotactic migration of bronchial epithelial cells. Increased cell proliferation. Increased both E-cadherin mRNA and protein levels. VIP promotes bronchial epithelial wound healing by increasing migration and proliferation of HBECs. These protective and reparative effects are VPAC1-dependent and are associated with upregulation of E-cadherin, supporting enhanced epithelial integrity. Metabolic and Cardiovascular Benefits A core aspect of VIP’s cardiovascular role is its ability to promote nitric oxide-mediated vasodilation, improving microcirculatory flow and reducing vascular tension. An interventional study in 6 healthy volunteers used continuous IV infusion of VIP to characterize its hemodynamic and cardiovascular effects [4]. Participants underwent continuous VIP infusion at 400 pmol/kg/hour for 100 minutes, resulting in: Sustained vasodilation, with reductions in: Total peripheral resistance by 30% Mean arterial pressure by 12% Forearm vascular resistance by 65% Increased cardiovascular output, including heart rate, and left ventricular contractility More clinical studies are needed to determine whether this can be used in pathologies of heart failure to improve cardiovascular outcomes. Neuroprotection VIP shows the ability to buffer neuroinflammatory signaling. This reduces the biochemical strain that prolonged inflammation can impose on the brain. A preclinical animal study used the MPTP murine model of Parkinson’s disease to evaluate neuroprotective and anti-inflammatory effects of VIP [5]. VIP administration resulted in: Significantly reduced MPTP-induced loss of dopaminergic neurons Preservation of nerve fiber density in the striatum Prevention of microglial activation induced by MPTP, and significant reductions in inflammatory mediators (iNOS, IL-1β, TNF-α) These findings position VIP as a promising therapeutic candidate for neurodegenerative diseases, with human studies needed to validate. Side Effects Exogenous VIP administration is well-tolerated, though some individuals may experience temporary reactions as the peptide engages VPAC receptors throughout the body. Reported responses include: Mild flushing Lightheadedness Nasal congestion Digestive changes These effects are usually short-lived and reflect VIP’s physiologic roles in vasodilation and gut motility rather than toxic or harmful processes. References 1 Gonzalez-Rey, E. and Delgado, M. (2005) Role of vasoactive intestinal peptide in inflammation and autoimmunity. Curr. Opin. Investig. Drugs, Curr Opin Investig Drugs 6, 1116–1123 2 Villanueva-Romero, R., Gutiérrez-Cañas, I., Carrión, M., González-Álvaro, I., Rodríguez-Frade, J. M., Mellado, M., et al. (2019) Activation of Th lymphocytes alters pattern expression and cellular location of VIP receptors in healthy donors and early arthritis patients. Sci. Rep., Nature Publishing Group 9, 7383 3 Guan, C.-X., Zhang, M., Qin, X.-Q., Cui, Y.-R., Luo, Z.-Q., Bai, H.-B., et al. (2006) Vasoactive intestinal peptide enhances wound healing and proliferation of human bronchial epithelial cells. Peptides, Elsevier BV 27, 3107–3114 4 Frase, L. L., Gaffney, F. A., Lane, L. D., Buckey, J. C., Said, S. I., Blomqvist, C. G., et al. (1987) Cardiovascular effects of vasoactive intestinal peptide in healthy subjects. Am. J. Cardiol., Elsevier BV 60, 1356–1361 5 Delgado, M. and Ganea, D. (2003) Neuroprotective effect of vasoactive intestinal peptide (VIP) in a mouse model of Parkinson’s disease by blocking microglial activation. FASEB J., Wiley 17, 944–946
What is adipotide? Adipotide, 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]: A “fat-homing” section that helps find white fat tissue Two identical sections that trigger cell death A short connecter linking the two main compartments together 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]. What does adipotide do? The research Adipotide and fat cell apoptosis 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 and metabolic health 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]. How Adipotide acts on Blood Vessels 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].
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]