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Free U.S. shipping on orders over $150Insulin-like Growth Factor 1 Long Arg3 (IGF-1 LR3) is a synthetic analog of human IGF-1, a naturally occurring peptide hormone that plays a critical role in growth, repair, and metabolic regulation.
Structurally, IGF-1 LR3 consists of 83 amino acids, whereas native IGF-1 has 70 amino acids. IGF-1 LR3 has two additional key modifications: the substitution of arginine for glutamic acid at position 3, and the addition of a 13–amino acid extension at the N-terminus [1].
LGF
These alterations significantly extend its half-life and reduce its binding affinity to IGF-binding proteins, enhancing its biological availability in circulation.
By activating IGF-1 receptors, LGF-LR3 can initiate various intracellular signaling pathways, including PI3K/Akt/mTOR and MAPK/ERK, which are central to [2, 3]:
IGF-1 stimulates satellite cell activation and differentiation, key processes for muscle hypertrophy and repair following injury or intensive exercise [4]. However, these effects have yet to be studied in LGF-LR3 specifically.
LGF-LR3 enhances amino acid uptake, which can theoretically increase protein synthesis, and promotes the fusion of myoblasts into mature muscle fibers, contributing to muscle growth.
An animal study examined whether infusion of IGF-1 LR3 could improve growth and metabolic parameters in fetuses affected by placental insufficiency and fetal growth restriction (FGR) [5].
Fourteen fetal sheep were divided into two groups: one receiving IGF-1 LR3 infusion (1.17 μg/kg·h) and a control group receiving only the vehicle over one week. Glucose-stimulated insulin secretion (GSIS) tests were performed at the end of the treatment period to assess β-cell function.
Results showed:
IGF-1 LR3 did not enhance fetal growth or insulin dynamics in growth-restricted fetuses under these experimental conditions.
The observed decline in amino acid levels suggested possible increased tissue uptake or utilization, suggesting higher metabolic demand without adequate substrate availability.
Supplemental amino acids, glucose, or oxygenation may be necessary to optimize IGF-1-mediated growth responses in FGR scenarios.
IGF-1 LR3 has drawn increasing interest for its neuroprotective and cognitive-enhancing potential, reflecting the broader role of IGF signaling in the central nervous system (CNS).
Endogenous IGF-1 is widely expressed in both neurons and glial cells [6].
A study in 5XFAD mice (a transgenic model that rapidly develops amyloid-β (Aβ) pathology of Alzheimer’s disease) evaluated whether intranasal LR3-IGF-1 could mitigate cognitive decline and reduce AD-related pathology [7].
Wild-type and 5XFAD mice were treated intranasally with LR3-IGF-1 or vehicle solution from 3 to 10 months of age.
Results showed that LR3-IGF-1 treatment:
Although LR3-IGF-1 did not prevent cognitive decline, it produced measurable benefits in amyloid plaque remodeling and microglial function, implying a partial neuroprotective effect at the cellular level.
While human data remain limited, these findings point to IGF-1 LR3 as a promising anti-aging agent for the brain.
IGF-1 LR3 plays a pivotal role in energy balance and glucose metabolism, closely mirroring the physiological actions of insulin.
An animal study explored how short-term exposure to IGF-1 LR3 affects insulin secretion dynamics [8].
Ten fetal sheep were infused intravenously for 90 minutes with either IGF-1 LR3 (n = 5) or vehicle control (n = 5).
Results showed that:
Acute IGF-1 LR3 infusion transiently suppressed insulin secretion in vivo, without damaging β-cells.
This suggests that the inhibitory effects are reversible and may have therapeutic use for intrauterine growth restriction (IUGR) or metabolic modulation during development.
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). IGF1-Lr3 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 Ipamorelin Peptide and What Is It Used For? Ipamorelin is a synthetic pentapeptide that stimulates the pituitary to release growth hormone (GH). Since its discovery in 1998, it has gained a lot of attention as the first selective GH secretagogue. It stimulates GH release without affecting other pituitary hormones such as adrenocorticotropic hormone, follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone, and prolactin. Ipamorelin has primarily been researched preclinically for muscle gain and weight loss, as well as for counteracting corticosteroid side effects and postoperative complications [1]. Ipamorelin Benefits Ipamorelin has an intriguing mechanism of action that mimics some aspects of ghrelin (hunger hormone). It’s a selective agonist, which activates the ghrelin receptor pathway [2]. This interaction activates GH release from the pituitary gland, essentially initiating anabolic processes, including: Appetite regulation Fat metabolism and lipolysis Energy utilization on the whole In rodents, ipamorelin increases appetite, hunger, and caloric intake, suggesting that it may be helpful in patients with cachexia or other conditions where weight gain is beneficial [3]. However, in humans, its effect on appetite appears to vary between individuals. Bodybuilding and Muscle Growth Ipamorelin-induced GH may act on muscles through insulin-like growth factor-1 (IGF-1) to increase muscle protein synthesis, inhibit protein degradation, stimulate satellite cell activity, and counteract myostatin signals [4]. In rats treated with glucocorticoid (GC), ipamorelin significantly increased maximum muscle tension and the rate of periosteal bone formation by fourfold [5]. These findings suggest that ipamorelin may mitigate the decline in muscle strength and bone formation typically observed in GC-treated rats. In young rats, chronic administration of ipamorelin does not lead to desensitization of the GH response, helping to increase body weight. However, chronic administration of ipamorelin on pituitary cell culture did lead to a dampened GH response over time, suggesting a desensitization response [6]. Bone Health GH is essential for linear body growth during childhood, bone remodeling throughout life, and bone preservation in aging adults. GH and its downstream effector IGF-1 are central to skeletal growth and homeostasis. They activate osteoblasts and increase calcium storage and bone collagen. In adult rats, 12 weeks of continuously administered ipamorelin significantly increased body weight, bone mineral content, and femur and vertebra L6 bone volume [6]. Another rat study found that ipamorelin increased linear growth rate and body weight in a dose-dependent manner. However, the ipamorelin treatment did not alter levels of IGF-1, IGFBPs, or serum markers of bone formation or resorption [7]. Body Weight The effect of ipamorelin on weight has been paradoxical. Although GH is a crucial hormone for weight loss, most rodent studies found that ipamorelin assists with weight and body fat gain. Ipamorelin has been shown to exert effects beyond muscle mass regulation. Experimental studies demonstrated that it significantly increased insulin secretion (p < 0.04) from the pancreas in both normal and diabetic rats. These findings suggest that ipamorelin may influence glucose metabolism and insulin-dependent anabolic processes [8]. Gut Health and Pain Ipamorelin demonstrated gastrointestinal effects that are mediated through activating ghrelin receptors. In a rodent model of postoperative ileus, a painful bowel paralysis after surgery, ipamorelin was shown to accelerate gastric emptying by enhancing gastric contractility [9]. A clinical trial on 114 patients who had undergone bowel resection surgery compared twice-daily ipamorelin administration with placebo to assess its effects on shortening the time to the first solid meal. Although there was no statistically significant difference between ipamorelin and the placebo, no safety concerns were observed [10]. Ipamorelin Side Effects In a Phase 2 placebo-controlled trial, ipamorelin had lower but nonsignificant differences in incidents of side effects than placebo (87.5% in the ipamorelin group vs. 94.8% in the placebo group) [10]. Adverse effects observed in this trial included headache, gastrointestinal symptoms, and injection site reactions. The study did not report severe side effects specific to ipamorelin. The one report of risk for immunogenicity was linked to a production-related impurity in an IV administration [11].
Snapshot: Kisspeptin activates the KISS1R receptor, which regulates gonadotropin-releasing hormone (GnRH) secretion and various other targets. Exogenous kisspeptin-10 directly stimulates GnRH release and influences tumor cell behavior. Kisspeptin may also influence sexual and emotional brain processing, metabolic signaling, vascular and renal biology, and in tumor-cell migration and metastatic pathways. What Is Kisspeptin? Kisspeptins are biologically active peptides encoded by the KISS1 gene, which produces several biologically active peptides, including kisspeptin-54 and kisspeptin-10 [1]. All active fragments bind to the same G-protein-coupled receptor, KISS1R [2]. Kisspeptin-10 is the smallest active form of kisspeptin, with the amino acid sequence YNWNSFGLRFamide. Exogenously-administered kisspeptin-10 can directly stimulate GnRH, suggesting that it may have potential therapeutic effects in reproductive medicine and sexual health [3, 4]. KISS1 was originally identified as a metastasis suppressor gene, based on early findings that its expression could inhibit the spread of melanoma and breast cancer cells [5]. The gene is expressed in multiple tissues, including the hypothalamus, gonads, pancreas, adrenal gland, liver, and brain, reflecting both central and peripheral physiological roles [6]. Kisspeptin exerts primary endocrine effects through KISS1R-mediated stimulation of gonadotropin-releasing hormone (GnRH) neurons in the hypothalamus [2]. When it binds to KISS1R, the receptor activates G-protein-coupled intracellular signalling cascades, which increase the activity and firing of GnRH-secreting neurons [1]. GnRH is released into the hypothalamic-pituitary portal circulation and stimulates the anterior pituitary to release luteinizing hormone (LH) and follicle-stimulating hormone (FSH) [1]. Research suggests kisspeptin is a key upstream regulator of reproductive hormone activation, particularly around the onset of puberty, and the full extent of its regulatory control remains an active area of research [2, 7]. Kisspeptin Peptide Benefits Beyond its central role in controlling reproductive hormones, kisspeptin is also studied for possible effects on sexual behavior and emotional processing, metabolic function, and in cancer biology. Sexual Function & Psychology Kisspeptin is best known for its central role in activating the reproductive hormone axis via stimulation of GnRH neurons, which in turn drives LH and FSH release and supports sexual maturation and fertility [6]. In a small clinical study enrolling 4–5 subjects per group per gender, subjects received subcutaneous bolus or IV infusion of kisspeptin-10. Healthy male participants had elevated LH and FSH in response to low-dose IV bolus at 0.3 and 1.0 nmol/kg. In contrast, female participants had no serum gonadotrophin responses during their follicular phase, even at doses as high as 720 pmol/kg/min. However, during their preovulatory phases, the serum LH and FSH were elevated after IV bolus of kisspeptin at 10 nmol/kg [3]. In a small comparative study enrolling 5 healthy men per group, vehicle, kisspeptin-10, kisspeptin-54, and GnRH were compared at doses of 0.1, 0.3, and 1.0 nmol/kg/h. Subjects received 3 hours of intravenous therapy. Subsequently, their LH and FSH were tested. The study found that GnRH produced about three-fold the LH and FSH elevation relative to kisspeptin-10, and twice that of kisspeptin-54 [8]. Emerging research also indicates that kisspeptin may influence aspects of emotional processing, bonding, and sexual behavior through its actions in the limbic and hypothalamic brain regions involved in motivation and affective regulation [6]. Both the hormonal and emotional effects appear to operate within reproductive and motivational circuits, rather than broad psychological pathways [6]. Metabolic Effects Kisspeptin signalling has been identified in several peripheral metabolic tissues, including the pancreas and adipose tissue, suggesting roles beyond reproduction. Experimental work in rodents and humans demonstrated that kisspeptin and its receptor are expressed in pancreatic islets and in vivo models, without affecting basal insulin release [6]. These findings support a context-dependent, glucose-linked action instead of a continuous insulin-stimulatory effect. Consistent with this, animals created without kisspeptin signalling show increased adiposity, higher leptin levels, and impaired glucose tolerance [6]. This raises the possibility that loss of peripheral kisspeptin signalling may contribute to energy imbalances and metabolic dysregulation [6]. Current evidence supports a modulatory, rather than primary, metabolic role with kisspeptin influencing insulin signaling, adiposity, and glucose tolerance under specific physiological conditions, particularly those linked to reproductive or hormonal status [6]. Anticancer Effects Kisspeptin was first discovered in cancer research, where restoring KISS1 gene expression in highly metastatic melanoma cells strongly reduced the spread of tumors in animal models, without stopping the original tumor from growing [9]. This led to its classification as a metastasis-suppressor gene [9]. Cell-based studies suggest it does not mainly act by killing cancer cells, but by reducing their ability to move, invade, and migrate [9]. Kisspeptin peptides can slow chemotaxis and invasion, influence matrix-remodelling enzymes, and change cell shape and cytoskeleton dynamics in ways that make cells less mobile and more adhesive [9]. Clinical expression across several cancer types, including melanoma, breast, ovarian, bladder, esophageal, and endometrial cancers, consistently shows that lower KISS1 expression is associated with more advanced or metastatic disease, whereas higher expression is more common in earlier-stage tumors [9]. Current evidence primarily indicates that kisspeptin impacts metastatic potential rather than tumor growth itself, acting as a regulator of how readily cancer cells spread through the body [9]. References 1 Messager, S., Chatzidaki, E. E., Ma, D., Hendrick, A. G., Zahn, D., Dixon, J., et al. (2005) Kisspeptin directly stimulates gonadotropin-releasing hormone release via G protein-coupled receptor 54. Proc. Natl. Acad. Sci. U. S. A., Proceedings of the National Academy of Sciences 102, 1761–1766 2 Rønnekleiv, O. K. and Kelly, M. J. (2013) Kisspeptin excitation of GnRH neurons. Adv. Exp. Med. Biol., Springer New York 784, 113–131 3 Jayasena, C. N., Nijher, G. M. K., Comninos, A. N., Abbara, A., Januszewki, A., Vaal, M. L., et al. (2011) The effects of kisspeptin-10 on reproductive hormone release show sexual dimorphism in humans. J. Clin. Endocrinol. Metab., The Endocrine Society 96, E1963–72 4 Thurston, L., Hunjan, T., Ertl, N., Wall, M. B., Mills, E. G., Suladze, S., et al. (2022) Effects of kisspeptin administration in women with hypoactive sexual desire disorder: A randomized clinical trial: A randomized clinical trial. JAMA Netw. Open, American Medical Association (AMA) 5, e2236131 5 Lee, J. H., Miele, M. E., Hicks, D. J., Phillips, K. K., Trent, J. M., Weissman, B. E., et al. (1996) KiSS-1, a novel human malignant melanoma metastasis-suppressor gene. J. Natl. Cancer Inst., Oxford University Press (OUP) 88, 1731–1737 6 Bhattacharya, M. and Babwah, A. V. (2015) Kisspeptin: beyond the brain. Endocrinology, The Endocrine Society 156, 1218–1227 7 Skorupskaite, K., George, J. T. and Anderson, R. A. (2014) The kisspeptin-GnRH pathway in human reproductive health and disease. Hum. Reprod. Update 20, 485–500 8 Jayasena, C. N., Abbara, A., Narayanaswamy, S., Comninos, A. N., Ratnasabapathy, R., Bassett, P., et al. (2015) Direct comparison of the effects of intravenous kisspeptin-10, kisspeptin-54 and GnRH on gonadotrophin secretion in healthy men. Hum. Reprod., Oxford University Press (OUP) 30, 1934–1941 9 Mead, E. J., Maguire, J. J., Kuc, R. E. and Davenport, A. P. (2007) Kisspeptins: a multifunctional peptide system with a role in reproduction, cancer and the cardiovascular system: Kisspeptins are multifunctional peptides. Br. J. Pharmacol., Wiley 151, 1143–1153
What Is KPV Peptide? KPV 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 Peptide Mechanism of Action 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]. Anti-Inflammatory Activity 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: Tumor necrosis factor-α (TNF-α) [4, 5] Interleukin-1β (IL-1β) [6] Interleukin-6 (IL-6) [4] At the same time, KPV enhanced anti-inflammatory mediators, helping to restore immune balance in tissues that were chronically stressed or damaged. Wound Healing 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. KPV Peptide Benefits and Side Effects Gut Barrier Protection 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]. Skin Health and Repair In dermatological research, KPV has demonstrated the ability to: Reduce swelling Accelerate wound closure Promote keratinocyte migration Promote fibroblast activity 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. Safety/Side Effect Profile 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.