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Free U.S. shipping on orders over $150KPV is a short bioactive peptide composed of three amino acids: lysine (K), proline (P), and valine (V) [1]. It is derived from the larger parent molecule α-melanocyte-stimulating hormone (α-MSH), a peptide hormone that modulates inflammation, pigmentation, circadian rhythm, and immune responses [1].
Unlike the full α-MSH sequence, KPV represents the minimal active fragment capable of exerting anti-inflammatory and protective effects in experimental settings.
Because of its small size, KPV is more stable and potentially more amenable to topical or localized delivery compared to its larger parent peptide [2].
KPV is a promising subject of investigation in areas where inflammation and tissue degeneration play central roles, including aging-related disorders.
KPV is thought to act through interactions with the melanocortin 1 receptor (MC1R), a G-protein-coupled receptor expressed in a variety of tissues, including skin, intestinal epithelial cells, and immune cells [3].
One of the most consistent findings across KPV research is its anti-inflammatory activity, particularly in epithelial tissues such as the gut and skin.
In preclinical studies, KPV downregulates pro-inflammatory cytokines, including:
At the same time, KPV enhanced anti-inflammatory mediators, helping to restore immune balance in tissues that were chronically stressed or damaged.
Wound healing is a complex process that requires coordinated activity between keratinocytes, fibroblasts, immune cells, and vascular networks [7]. With aging, this regenerative capacity declines, delaying healing and increasing the risk of chronic wounds and scarring.
Research on KPV suggests that it may play a role in supporting tissue repair by modulating inflammation and stimulating cellular regeneration [8].
Animal studies indicate that KPV significantly accelerates keratinocyte migration and proliferation, which promote the re-epithelialization of damaged skin and cornea [9]. By dampening the inflammatory cascade, KPV creates a more favorable environment for tissue recovery [1].
In parallel, KPV has been shown to influence fibroblast activity and extracellular matrix remodeling, processes that underpin scar formation, collagen deposition, and the restoration of skin integrity [10].
In mouse models, KPV accelerates full-thickness wound closure and reduces scarring compared to untreated controls [11]. KPV accomplishes this through increased angiogenesis and collagen deposition.
The peptide appears to limit oxidative and inflammatory injury and enhance reparative signaling, striking a balance between protecting cells from further damage and promoting regeneration.
In the gut, inflammation disrupts epithelial barrier integrity, leading to increased permeability and impaired nutrient absorption [12]. KPV may counteract this by supporting epithelial repair and reducing inflammatory signaling via inhibiting NF-𝛋B and MAPK signaling pathways [4].
In murine models of inflammatory bowel disease, KPV led to significantly earlier recovery and stronger regain of body weight. The peptide preserved epithelial integrity, reduced oxidative injury, and supported mucosal repair [13].
In dermatological research, KPV has demonstrated the ability to:
In animal models of dermatitis and wound healing, KPV has demonstrated the ability to reduce redness, irritation, and swelling [14]. By balancing cytokine activity and oxidative stress, KPV may treat inflammatory skin conditions and restore healthy skin.
KPV may also be particularly relevant to skin aging, where low-level chronic inflammation accelerates collagen degradation, barrier dysfunction, and visible changes [15].
These effects are consistent with its origin as a fragment of α-MSH, a peptide historically studied for its skin-protective properties.
KPV is generally well tolerated in experimental settings [16]. Unlike full-length α-MSH or other melanocortin peptides, KPV does not significantly influence pigmentation, reducing the risk of unwanted skin-darkening effects.
Preclinical studies report no major systemic toxicity or adverse events, and topical or localized administration appears safe. Although extremely rare, applications of proteins or peptides may run the risk of local irritation or allergic reactions [17].
The evidence base remains limited, with most data derived from animal models, in vitro experiments, or small pilot human studies. Long-term safety, optimal dosing, and potential interactions of KPV with other compounds have yet to be fully established.
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). KPV 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 Liraglutide? Liraglutide (Victoza/Saxenda) is a synthetic analogue of glucagon-like peptide-1 (GLP-1), a hormone involved in appetite regulation, glucose balance, and metabolic signaling [1]. As a modified form of native GLP-1, liraglutide is engineered to resist rapid enzymatic breakdown, allowing it to remain active in the bloodstream far longer than the naturally occurring peptide. This extended activity enables more sustained engagement of GLP-1 receptors, which are found throughout the: Gastrointestinal tract Pancreas Brainstem Peripheral tissues GLP-1 plays a central role in coordinating how the body manages satiety cues, blood-glucose excursions, and nutrient utilization. Liraglutide mechanism of action and benefits Weight loss Liraglutide’s influence on weight regulation stems from its ability to activate GLP-1 receptors involved in: Central satiety signaling of the hypothalamus and brainstem Delayed gastric emptying leading to meal satisfaction Nutrient partitioning A systematic review analyzed the efficacy and safety of liraglutide for weight loss in non-diabetic obese or overweight adults, by synthesizing outcomes from 11 RCTs and 1,328 total participants [2]. The average age of participants was 44.5 years, and the population skewed female (~ 79%). Liraglutide administration resulted in: Significantly greater weight loss versus control (–4.59 kg) Significant reduction in waist circumference (–3.22 cm) Significant improvement in BMI (–1.71 kg/m²) No significant reduction in HbA1c (–0.43%, p > 0.05) The pooled evidence shows that Liraglutide is effective in promoting clinically meaningful weight loss in non-diabetic overweight and obese adults. Metabolic and Cardiovascular Liraglutide’s extended engagement of GLP-1 receptors influences several pathways tied to metabolic efficiency and cardiovascular balance. An RCT evaluated whether liraglutide 1.8 mg/day over 26 weeks improves diabetic cardiomyopathy in 49 type 2 diabetes (DM2) patients without known cardiovascular disease [3]. At the end of the intervention, Liraglutide showed: Significant improvements in diastolic function (reduction in left ventricle (LV) filling pressures) Significant improvements in systolic function - 9mL reduction in stroke volume - 3% reduction in ejection fraction Liraglutide reduced early LV diastolic filling and LV filling pressures, effectively unloading the left ventricle in patients with type 2 diabetes without cardiovascular disease. Although small reductions in stroke volume and ejection fraction occurred, they remained within normal limits. Bone and Joint Health Although best known for its effects on appetite and metabolic regulation, liraglutide has also been studied for its influence on pathways relevant to bone and joint health. GLP-1 receptors are present not only in metabolic tissues but also on osteoblasts, osteoclasts, and chondrocytes, suggesting a broader role in skeletal homeostasis. A meta-analysis evaluated 17 animal studies to determine whether liraglutide improves bone pathology in animal models of osteoporosis [4]. Results showed that Liraglutide: Partially improved bone pathology by enhancing density and maximum mechanical load Significantly improved bone turnover markers (p < 0.05) Increased bone formation (Osteocalcin and P1NP levels) Decreased bone resorption (CTX-I levels) Liraglutide seems to improves osteopenia by: Enhancing osteoblast activity via Wnt signaling and p-AMPK/PGC-1α pathway Suppressing osteoclast activity by inhibiting OPG/RANKL/RANK pathway These findings support liraglutide as a potentially valuable therapy for osteoporosis in diabetic patients, although higher-quality human studies are needed. Other Health Benefits Liver Health Liraglutide has also been shown to improve liver markers in mice models of non-alcoholic fatty liver. Significant reductions were noted in triglyceride content, fasting blood glucose, and LDL [5]. Microbiome By extension of Liraglutide’s gastrointestinal effects, there has been evidence of gut microbiome modulation. Liraglutide increases levels of eubacteria like Bacteroidales and Akkermansia while reducing harmful bacteria like Bacteroides and Lachnospiraceae [5]. Neurocognitive GLP-1 receptors are expressed in several brain regions involved in reward, mood regulation, and cognitive processing. Liraglutide’s protection of brain insulin receptors has been associated with reversal of cognitive impairment and memory loss in mice [6]. These emerging lines of research reflect liraglutide’s broader physiologic relevance, positioning it as a valuable tool for understanding how GLP-1 agonists influence interconnected systems across the body.
Research-grade compound with certificate of analysis. Full analytical testing on every lot.
What is Melanotan I? Melanotan I, a synthetic analogue of α-MSH, acts as an agonist on melanocortin receptors, primarily MC1R [1]. This receptor plays an important role in normal skin pigmentation, found on the surface of skin pigment cells (melanocytes) [1]. Compared to Melanotan II, Melanotan I has a longer duration of action and is more resistant to enzymatic breakdown [2]. Because of its selectivity for MC1R, Melanotan I primarily influences skin pigmentation with minimal central nervous system penetration [2]. Melanotan I Effects & Benefits Tanning & Photoprotection Melanotan I stimulates tanning by binding to MC1R receptors in skin cells, increasing the production of eumelanin, the dark pigment that protects against UV damage [3]. This process enhances photoprotection. Conversely, those with mutations to this receptor produce more pheomelanin, tend to tan poorly, and have an increased risk for sunburn and skin cancer [4]. Melanotan I has been explored for photoprotection in those with these genetic conditions that heighten UV sensitivity [5]. Phase 1 studies have been conducted on Melanotan 1, in which participants received daily injections across 1-4 weeks and then exposed to limited UV-B or sunlight on specific parts of their skin [6]. Those who received the injections developed faster, darker tans than those exposed to light alone, which lasted three weeks longer and required less sun exposure to achieve. They also showed fewer sunburned skin cells, suggesting better skin protection. Neuroinflammation & Cognition Preliminary research has suggested that melanocortin activation may influence neuroprotective pathways in the brain through anti-inflammatory and neuroprotective actions. Animal studies show reductions in brain damage, improved recovery, and limited inflammation when given soon after a stroke [7]. A phase IIa clinical trial found that Melanotan I was safe and well-tolerated in patients who suffered strokes, with no serious side effects [7]. Most patients had improved brain scans and neurological recovery, suggesting a role in protecting brain tissue, stabilizing the blood-brain barrier, and supporting neuroplasticity even when administered up to 20 hours after stroke onset [7]. Blood Pressure & Vascular Health By mimicking the effects of α-MSH, Melanotan 1 may help support vascular health by improving endothelial function and nitric oxide production, which supports blood vessel relaxation [8]. Activation of MC1 receptors found on endothelial cells may enhance circulation, reduce stiffness, and protect against vascular dysfunction associated with metabolic stress [8]. However, current data is sparse. Unlike Melanotan II, it does not significantly activate central melanocortin receptors involved in autonomic control.