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Free U.S. shipping on orders over $150Selank is a 7-amino acid peptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP). It was developed at the Russian Institute of Molecular Genetics in the 1990s for its potential anxiolytic, neuroprotective, and nootropic properties. The peptide is an analog of the tuftsin molecule, which is naturally produced in the human body. It works primarily by allosterically modulating GABA receptors, similarly to benzodiazepines but without the same impairing side effects.
Selank can function as a neuropsychotropic, antidepressant, and antistress, nootropic and immunomodulatory drug due to its anxiolytic activity [1].
Selank has similar effects to tranquilizers like benzodiazepines at low doses without the unwanted side effects such as dependence, withdrawal, and amnesia. Moreover, animal studies suggest that Selank relieves aggression and fear reaction [1].
In addition, Selank modulates the expression of genes that influence different types of immune responses, suggesting that it may also work through immunomodulation [2]. A rat study suggests that Selank may help maintain immune homeostasis during stress [3].
The pharmacological investigation of Selank has primarily focused on its anxiolytic and antidepressant properties. In patients with anxiety and depressive disorders, Selank effectively reduced anxiety, mood swings, and somatic symptoms [4].
In the experimental model of chronic mild stress, the combination of Selank with benzodiazepines was the most effective in reducing anxiety levels, and Selank independently was the most efficient in reducing anxiety levels after individual stressful events [5].
Adults living in Ukraine with adjustment disorder who were admitted to hospital for routine check ups were either given Selank or placebo. Selank reduced complaints in patients with adjustment disorders. Even two weeks after treatment, patients receiving Selank reported reduced somatic symptoms, nutritional problems, and alcohol misuse [6].
A 2016 rat study [1] examined the effect of intranasal Selank and GABA on the expression of genes related to neurotransmission in the frontal cortex. The study concluded that Selank exerts a significant and time-dependent effect on the expression of genes related to neurotransmission, supporting its pivotal role in modulating anxiolytic and antidepressant pathways.
Moreover, Selank works as a GABA receptor modulator. If administered together, Selank and benzodiazepines can regulate the activity of GABA receptors in a peculiar manner, which is not cumulative and is different from either substance individually. Thus, Selank's anti-anxiety mechanism of action is also concentration-dependent allosteric modulation of GABA receptors [7].
A rat study suggests that intranasal selank may improve memory and learning by increasing BDNF in the hippocampus [1, 8].
Another study examined rats with strong alcohol preference fed with 10% ethanol as the only fluid source for 30 weeks to induce attention and memory disturbances mimicking chronic alcohol intoxication. Subsequently, both alcohol-fed and age-matched control rats received Selank intraperitoneally at 0.3 mg/kg. Both alcohol-fed and control rats experienced a cognitive stimulating effect with increased exploration time and reduced discrimination index in novel object recognition tests. In control animals, BDNF was unchanged. However, in alcohol-fed animals, alcohol cessation after 30 weeks elevated BDNF in the hippocampus and cortex, while administration of selank restored BDNF levels to values comparable to those of the control group. In conclusion, Selank helps modulate BDNF and other reparative processes in rats cognitively impaired from chronic alcohol [9].
A Russian article investigated the effects of Selank on behavior and serotonin/noradrenalin concentrations in the brains of adult rats exposed to hypoxia during 14-16 days of gestation. Intraperitoneal Selank resulted in [10]:
These results suggest that Selank has a normalizing impact on neurobehavioral functions impaired by prenatal hypoxia, indicating its potential role in enhancing stress resilience and supporting recovery of serotonergic and noradrenergic system activity. Moreover, Selank was shown to have positive emotional effects and antistress actions [11].
Inflammation is a complex process mediated by the interaction of various immune cells and cytokines including IL-1β, IL-6, and TGF-β1. A recent study [12] has evaluated the effect of Selank on the level of the cytokines in rats that have been exposed to inflammatory stress. There was a significant decrease in the concentration of IL-1β and IL-6 and restoration of the level of IL-4, as well as suppression of the production of TGF-β1 and TNF-α in the serum of rats treated with Selank.
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). Selank 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 Semax and what is it used for? Semax is a synthetic peptide derived from the adrenocorticotropic hormone (ACTH) fragment Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP) [1]. It was originally developed in Russia in the 1980s as part of a government initiative to create neuroprotective agents with both cognitive-enhancing and therapeutic potential [1]. Unlike the parent ACTH peptide, Semax does not exhibit hormonal activity, which reduces concerns about systemic endocrine effects while preserving its neuromodulatory properties [1]. Research has focused on Semax primarily as a nootropic and neuroprotective compound. It has been investigated in both preclinical and clinical contexts for conditions such as: Cerebrovascular disease Ischemic stroke Cognitive impairment Neuropathic disorders Because of its stability and ability to cross the blood-brain barrier, Semax has drawn attention as a candidate for regulating processes tied to neuroinflammation, oxidative stress, and neurotransmitter balance. Semax benefits Neuroprotection and cognitive enhancement One of the most widely studied effects of Semax is its role in neuroprotection and cognitive function. Preclinical studies have demonstrated that Semax influences neurotrophic factors, particularly brain-derived neurotrophic factor (BDNF), which is essential for [2]: Synaptic plasticity Memory consolidation Neuronal survival In an animal study with six Wistar rats, a single intranasal spray of Semax at 50 μg/kg resulted in a 1.4 fold increase of BDNF protein levels in the hippocampus, a memory forming area of the brain. Rats were subsequently able to learn significantly more conditioned avoidance reactions (p < 0.05) [3]. An animal study of ~70 rats investigated whether Semax could counteract the negative effects of acute restraint stress on cognitive function and anxiety-related behavior. Semax was administered intraperitoneally at 0.1 mg/kg 30 minutes prior to stress exposure (electric bell sounds) [4]. Pretreatment with Semax significantly prevented stress-induced deficits in reaction time and latency, maintaining performance similar to controls (p < 0.01). Semax exposure also significantly decreased anxiety-like behavior (p < 0.04). These effects appear to result from enhanced synaptic signaling and reduced neuronal apoptosis in regions such as the hippocampus. In a randomized controlled trial, 110 patients who recently suffered from ischemic stroke received 6 mg of Semax twice daily for 10 days. Semax significantly increased plasma BDNF levels and was highly correlated with early rehabilitation and faster improvement of motor outcomes [5]. Stress resilience and mood regulation Overactive stress responses can induce pathogenic immune changes, which contribute to the mechanisms of diseases that may be exacerbated by stress, such as cardiovascular disease, digestive disorders, autoimmune diseases, and skin conditions. Semax has been studied for its ability to modulate stress responses and mood-related pathways. Semax helps balance monoamine neurotransmitters, dopamine, and serotonin, which play central roles in emotional regulation and resilience to psychological stress [6]. By stabilizing these systems, Semax may mitigate the negative cognitive and behavioral consequences of chronic stress. A rat study investigated the immunomodulatory effects of Semax during chronic social stress. After 20 days of social stress (sensory contact and daily intermale confrontations), rats were treated intranasally with Semax (150 μg/kg/day) [7]. After Semax administration, investigators observed: Normalized immune hyperactivity: Delayed type hypersensitivity reactions (DTH) decreased by 30–40%, with antibody titers reduced by 30–60%. Restored phagocytic balance: Phagocytic index returned closer to baseline (p<0.001). Recovered leukocyte counts: Total leukocytes increased by 30–50% compared to stressed animals. Improved immune organ health: Thymus and spleen weights increased by 40–100% compared to stressed animals (p<0.01 to p<0.001). Semax demonstrated immunocorrective and immunomodulatory properties in this rat model by restoring both cellular and humoral immune responses. The findings suggest that Semax may be useful for counteracting stress-induced immune imbalance. Antioxidant and antiinflammatory benefits Semax also exerts antioxidant and anti-inflammatory effects. Studies in PC12 cells and in rats suggest that semax may reduce markers of oxidative damage, including lipid peroxidation products, while enhancing the activity of endogenous antioxidant enzymes such as superoxide dismutase and catalase [8, 9]. These findings suggest that the peptide helps maintain redox balance during cellular stress and injuries. Semax also modulates cytokine activity, reducing the release of pro-inflammatory mediators like TNF-α and IL-6 [10]. These actions not only limit secondary damage in ischemic injury but also contribute to preserving neuronal integrity under chronic inflammatory conditions. Taken together, the antioxidant and anti-inflammatory properties of Semax highlight its potential relevance in research on cerebrovascular and neurodegenerative conditions.
What is Sermorelin? Sermorelin is a synthetic analog of growth hormone–releasing hormone (GHRH). GHRH is a naturally occurring peptide secreted by the hypothalamus to stimulate growth hormone (GH) production in the anterior pituitary gland. Structurally, sermorelin is a 29–amino acid peptide fragment of GHRH that retains full biological activity in terms of binding to pituitary receptors and triggering GH release [1]. Originally, sermorelin was developed as a diagnostic tool to assess pituitary function. Over time, its use has expanded into research exploring potential roles as a secretagogue in endocrine regulation, metabolism, and aging biology. Sermorelin benefits, safety, and side effects Height increase and catchup growth Sermorelin stimulates the pituitary to produce and secrete GH, which in turn drives the liver and peripheral tissues to generate insulin-like growth factor-1 (IGF-1), the primary mediator of bone elongation and linear growth. Clinical trials in children with impaired growth velocity have shown that sermorelin administration can increase growth rate and promote catch-up growth. Specifically, once-daily subcutaneous Sermorelin (30 µg/kg body weight) at bedtime was effective in treatment of prepubertal children with idiopathic GH deficiency [2]. Although sermorelin-treated children demonstrated less height improvements compared to 30 µg/kg/day of somatropin (bioidentical GH), sermorelin was likely safer and better tolerated. Unlike direct GH therapy, sermorelin does not appear to excessively elevate circulating GH or IGF-1 levels, potentially lowering the risk of disproportionate bone growth or metabolic complications. In this context, sermorelin is best understood as a diagnostic and therapeutic tool that can support normal developmental trajectories in children with specific types of growth impairment. However, long-term data remain limited, and not all forms of growth delay respond equally, underscoring the importance of careful patient selection in research and clinical settings. Anti-carcinogenesis Preclinical studies suggest that GHRH analogs similar to sermorelin can exert anti-proliferative effects in certain cancer models. Mechanistically, these peptides appear to influence signaling pathways that regulate apoptosis, angiogenesis, and cell cycle progression [3]. A transcriptomic screen for candidate compounds in treatment-resistant glioma patients identified sermorelin as a candidate compound effective against the glioma [4]. Among screened compounds, sermorelin emerged as the most promising agent for recurrent gliomas, especially those with high-grade tumors, IDH-wildtype status, and 1p/19q non-codeletion. This study suggests that sermorelin may inhibit glioma cell proliferation by blocking the cell cycle, although clinical validation is required. Bone health and muscle mass GH and IGF-1 support osteoblast activity, increase bone turnover, and may help reverse age‐related loss of bone mass. These hormones also support muscle growth and maintenance along with tissue repair [5, 6]. As a GH secretagogue, sermorelin may mitigate some aspects of age-related decline in bone health. However, specific trials of sermorelin in aging adults focused on bone density remain limited. A single-blind, randomized, placebo-controlled trial of 19 people investigated the effects of nightly subcutaneous sermorelin at 10 µg/kg for 16 weeks. Results showed [7]: Significant increases in GH release over 2 hours post-injection and in 12-hour mean GH levels Increased IGF-1, IGFBP-3, and GHBP levels until week 12 Significantly increased lean body mass in men (+1.26 kg) No significant changes in body weight, body fat mass, or dietary intake Increased skin thickness in both genders after 16 weeks Improved insulin sensitivity While body weight, fat mass, and testosterone levels remained stable, these findings suggest sermorelin may mitigate age-related GH/IGF-1 decline and corresponding muscle mass loss. Side effects In clinical and research use, sermorelin has generally been regarded as safe and well tolerated, especially in comparison to direct recombinant growth hormone therapy. Because it acts as a secretagogue, stimulating the body’s own pulsatile growth hormone release rather than providing supraphysiologic doses, its endocrine profile is considered closer to natural physiology. The most frequently reported adverse effects are mild and transient, such as injection site reactions, flushing sensation, and nausea. Serious side effects are rare in published reports, and no consistent evidence suggests long-term harm at research dosages. However, as with other growth hormone-modulating therapies, caution is advised in individuals with active malignancy, since GH and IGF-1 pathways can influence cell proliferation. Overall, the safety data indicate a favorable risk profile for sermorelin within short- to medium-term use, though robust long-term clinical studies are limited.
Summary Sermorelin + GHRP-6 + GHRP-2 combines complementary upstream signals within the growth hormone axis. Sermorelin activates GH synthesis through the GHRH receptor, while GHRP-6 and GHRP-2 stimulate the ghrelin receptor GHS-R1a to amplify GH pulse release. Together, they enhance endogenous, pulsatile growth hormone signaling through dual-pathway stimulation, along with some gastric ghrelin effects. What Is Sermorelin? Sermorelin is a synthetic 29-amino acid fragment of growth hormone–releasing hormone [1]. It represents the shortest, completely functional portion of the endogenous GHRH. Sermorelin works via upstream mechanisms rather than supplying growth hormone directly [1]. It acts through the GHRH receptor on somatotroph cells in the anterior pituitary to increase growth hormone synthesis and pulsatile secretion [2]. Sermorelin remains under normal physiologic regulation through negative feedback from somatostatin, which helps modulate growth hormone output and preserve its natural pulsatile release pattern [2]. In addition to stimulating secretion, sermorelin also supports transcription of the growth hormone gene, helping to maintain the integrity of the growth hormone neuroendocrine axis [3]. Because it stimulates endogenous growth hormone production rather than replacing growth hormone directly, sermorelin is considered a more physiologic approach to enhancing growth hormone signalling [3]. What Is GHRP-2? Growth hormone–releasing peptide-2 (GHRP-2), is a synthetic hexapeptide that functions as a growth hormone secretagogue [4]. It agonises ghrelin receptor GHS-R1a, a G-protein-coupled receptor expressed in the hypothalamus and anterior pituitary [4]. When GHRP-2 binds GHS-R1a, intracellular signalling pathways activate, increasing calcium flux and downstream second-messenger activity to stimulate pulsatile growth hormone release from pituitary somatotroph cells [5]. GHS-R1a receptor activation also increases the amplitude of growth hormone pulses and can raise circulating Insulin-like Growth Factor (IGF-1) [6]. In addition to growth hormone, GHRP-2 may stimulate adrenocorticotropic hormone (ACTH), suggesting broader HPA-axis engagement [7]. Because it works via receptor-mediated stimulation rather than direct hormone replacement, GHRP-2 is widely used in research and in diagnostics to assess growth hormone reserve [8]. Its unique pharmacologic profile makes it a tool for studying ghrelin receptor signalling, endocrine feedback regulation, and somatotrophic axis dynamics [7]. What Is GHRP-6? Growth hormone–releasing peptide-6 (GHRP-6) is a synthetic hexapeptide that also functions as a growth hormone secretagogue [9]. Like GHRP-2, GHRP-6 acts as an agonist of the G-protein-coupled ghrelin receptor GHS-R1a, expressed in the hypothalamus and anterior pituitary [9]. This binding mimics the action of endogenous ghrelin and stimulates intracellular signalling cascades that increase calcium mobilization and promote pulsatile growth hormone release from pituitary somatotroph cells [10]. This mechanism enhances both the amplitude and frequency of growth hormone pulses [10]. The effects of GHRP-6 appear to be influenced by metabolic context, with insulin augmenting the growth hormone response, while concurrent carbohydrate or lipid intake can blunt it [11]. Interestingly, GHRP-6 is one of the only GHRPs that can actively increase hunger and food intake. Because it stimulates endogenous growth hormone release via receptor activation rather than direct hormone administration, GHRP-6 is primarily used in research contexts to study ghrelin signalling, somatotropic regulation, and downstream metabolic effects [11]. Sermorelin, GHRP-2, and GHRP-6 Synergy The combination of sermorelin with growth hormone–releasing peptides produce complementary effects through stimulation of growth hormone release via two unique upstream receptors that converge on the same pituitary somatotroph output [12]. Sermorelin activates the GHRH receptor to promote growth hormone synthesis and physiologic, pulsatile secretion [2]. Conversely, GHRP-2 and GHRP-6 act as ghrelin receptor agonists, which increase intracellular signalling and calcium-dependent pathways that also drive pulsatile growth hormone release [5,10]. Pairing a GHRH-pathway signal from sermorelin with a ghrelin pathway signal from GHRPs may produce a stronger growth hormone pulse than either agent alone through stimulating the axis from two distinct areas rather than one. Dosage and Balance Considerations There is some in vitro evidence to suggest that GHRP-2 and GHRP-6 each act synergistically with GHRH to stimulate growth hormone release, supporting the rationale for combining a GHRH analogue like sermorelin with a GHRP [12]. Equal dosing in this formulation is designed to provide a balanced stimulation across both regulatory arms of the somatotropic axis to support a coordinated GH pulse rather than disproportionally driving one pathway. References: 1 Prakash, A. and Goa, K. L. (1999) Sermorelin: A review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency. BioDrugs, Springer Nature 12, 139–157 2 Ishida, J., Saitoh, M., Ebner, N., Springer, J., Anker, S. D. and von Haehling, S. (2020) Growth hormone secretagogues: history, mechanism of action, and clinical development. JCSM Rapid Communications, Wiley 3, 25–37 3 Walker, R. F. (2006) Sermorelin: a better approach to management of adult-onset growth hormone insufficiency? Clin. Interv. Aging, Dove Medical Press Ltd. 1, 307–308 4 Moulin, A., Brunel, L., Verdie, P., Gavara, L., Martinez, J. and Fehrentz, J.-A. (2014) Ghrelin Receptor Ligands: Design and Synthesis of Pseudopeptides and Peptidomimetics. Curr. Chem. Biol., Bentham Science Publishers Ltd. 7, 254–270 5 &na; (2004) Pralmorelin: GHRP 2, GPA 748, growth hormone-releasing peptide 2, KP-102 D, KP-102 LN, KP-102D, KP-102LN. Drugs R. D., Springer Nature 5, 236–239 6 Furuta, S., Shimada, O., Doi, N., Ukai, K., Nakagawa, T., Watanabe, J., et al. (2004) General pharmacology of KP-102 (GHRP-2), a potent growth hormone-releasing peptide. Arzneimittelforschung, Georg Thieme Verlag KG 54, 868–880 7 Kimura, T., Shimatsu, A., Arimura, H., Mori, H., Tokitou, A., Fukudome, M., et al. (2010) Concordant and discordant adrenocorticotropin (ACTH) responses induced by growth hormone-releasing peptide-2 (GHRP-2), corticotropin-releasing hormone (CRH) and insulin-induced hypoglycemia in patients with hypothalamopituitary disorders: evidence for direct ACTH releasing activity of GHRP-2. Endocr. J., Japan Endocrine Society 57, 639–644 8 McDowell, R. S., Elias, K. A., Stanley, M. S., Burdick, D. J., Burnier, J. P., Chan, K. S., et al. (1995) Growth hormone secretagogues: characterization, efficacy, and minimal bioactive conformation. Proc. Natl. Acad. Sci. U. S. A., Proceedings of the National Academy of Sciences 92, 11165–11169 9 Camanni, F., Ghigo, E. and Arvat, E. (1998) Growth hormone-releasing peptides and their analogs. Front. Neuroendocrinol., Elsevier BV 19, 47–72 10 McGirr, R., McFarland, M. S., McTavish, J., Luyt, L. G. and Dhanvantari, S. (2011) Design and characterization of a fluorescent ghrelin analog for imaging the growth hormone secretagogue receptor 1a. Regul. Pept., Elsevier BV 172, 69–76 11 Peñalva, A., Carballo, A., Pombo, M., Casanueva, F. F. and Dieguez, C. (1993) Effect of growth hormone (GH)-releasing hormone (GHRH), atropine, pyridostigmine, or hypoglycemia on GHRP-6-induced GH secretion in man. J. Clin. Endocrinol. Metab., The Endocrine Society 76, 168–171 12 Cheng, J., Wu, T. J., Butler, B. and Cheng, K. (1997) Growth hormone releasing peptides: a comparison of the growth hormone releasing activities of GHRP-2 and GHRP-6 in rat primary pituitary cells. Life Sci., Elsevier BV 60, 1385–1392