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Free U.S. shipping on orders over $150Pinealon is a synthetic, bioactive, tripeptide (Glu-Asp-Arg) derived from the pineal gland [3]. It is classified as a peptide bioregulator due to its unique ability to bypass typical cell-surface or cytoplasmic receptors [3]. Instead, evidence suggests that it’s exceptionally small structure enables the molecule to cross both cellular and nuclear membranes [3]. Lab studies find that Pinealon can enter the cell nucleus, where it is thought to interact with DNA or DNA-associated proteins [3]. This ability to reach the genome provides a potential explanation for its wide-ranging effects, which align better with gene-expression changes rather than modulating traditional signalling pathways [3].
Inside the nucleus, Pinealon seems to modulate genes involved in antioxidant defenses, cell repair, and protection from cellular stress [1]. Animal model research reveals reductions in reactive oxygen species and apoptosis, and increased activity of endogenous antioxidant enzymes [4]. It appears to reduce the activity of caspase-3, an enzyme involved in programmed cell death, across several tissue types, suggesting a potential role in supporting cell survival under stressful conditions [4]. Pinelon may impact pathways related to healthy cell cycling and interact with the pineal gland to influence its function and regulate circadian rhythm [5].
Its unique mechanism, which bypasses conventional cell-surface receptors, has led to growing interest in its potential roles in neuroprotection, metabolism, stress resilience, and cognitive support.
Through directly interacting with DNA to influence gene expression involved in neural function, Pinealon may support learning and memory. Studies suggest it can reduce oxidative stress in brain tissue, preserve neuronal viability, and modulate pathways related to information retention.
In a study of prenatal rats exposed to high levels of homocysteine, maternal administration of Pinealon improved offspring cognitive function, enhancing performance in spatial orientation and navigation tasks while reducing reactive oxygen species and neuronal necrosis in the cerebellum [6]. Another found Pinealon was able to produce improvements in the Morris labyrinth task, showing faster acquisition of navigation tasks compared to untreated controls and those treated with a comparator peptide [7]. Improvements were also accompanied by reductions in caspase-3 activity in brain regions, suggesting that this peptide supports neuronal survival and resilience under hypoxic stress [4].
In a review, authors highlight findings to suggest that Pinealon enhances learning indices, decreases age- and stress-related neuronal apoptosis, and improves overall memory performance in animal models. It is thought these benefits are related to Pinealon’s ability to penetrate the nucleus and modulate gene expression, upregulating protective pathways and antioxidant systems while stabilizing cell-cycle and cell-death processes [8].
Studies have found that Pinealon may help protect neurons through multiple and complementary mechanisms, primarily demonstrated in preclinical models. One major pathway involves reducing oxidative stress, a key contributor to neuronal injury and neurodegeneration. In cell studies, Pinealon was found to decrease ROS accumulation, reduce necrotic cell death, and modulate ERK1/2 activation, a signalling pathway involved in cell survival and stress response [1]. These findings suggest Pinealon may help maintain neuronal integrity under conditions of metabolic or oxidative stress, through direct genomic interactions that influence cell-cycle regulation [1].
Experimental hypoxia models further demonstrate neuroprotective effects. In hypobaric hypoxia and aged rat studies, Pinealon was able to increase neuronal resistance to oxygen deprivation, potentially by stimulating superoxide dismutase and glutathione peroxidase, and by limiting NMDA receptor-mediated excitotoxicity [7]. Pinealon was also found to normalize pro-inflammatory cytokines such as IL-6 and TNF‑α, indicating a dual role reducing programmed cell death and neuroinflammation [4].
At a molecular level, Pinealon is thought to modulate gene expression pathways associated with neurodegeneration [8]. Evidence suggests it can interact with histones and RNA, influencing pathways such as MAPK/ERK, as well as pro-apoptotic proteins and antioxidant genes [8]. This makes it a candidate for further study in neurodegenerative conditions.
Pinealon shows promise as an antioxidant and cellular longevity support. It supports brain cell viability by reducing reactive oxygen species (ROS) and limiting cell death, while also influencing cell survival pathways like ERK1/2 [1].
It also shows benefits for strengthening cell membranes and preventing lipid peroxidation, helping support the brain’s resistance to oxidative stress [8]. Pinealon has been shown to modulate the activity of antioxidant enzymes, including SOD and GPx, and support antioxidant genes like SOD2 and GPX1 [8]. In aging and low-oxygen models, it protects neurons by reducing excitotoxicity, lowering caspase‑3 activity, and normalizing inflammatory signals, which supports cell survival and new neuron growth [4].
In human neurons from older donors, it also reduces DNA damage and helps maintain dendritic structures [9]. Overall, Pinealon combines antioxidant, anti-aging, and anti-inflammatory effects, though human studies are still limited.
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). Pinealon 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.
PT-141 peptide benefits PT‑141, also known as bremelanotide, is a synthetic cyclic heptapeptide structurally derived from α‑melanocyte‑stimulating hormone (α‑MSH). It acts primarily as an agonist at melanocortin receptors MC3R and MC4R, in the central nervous system [1]. By doing so, it activates hypothalamic pathways, resulting in downstream signals that influence sexual arousal and associated neurobiologic responses. Mechanistic target of PT-141 PT‑141 exerts its effect through binding and activation of melanocortin receptors, especially within the hypothalamus. Evidence from animal studies indicates that systemic administration of PT‑141 induces penile erection and activates hypothalamic neurons, as shown by increased c‑Fos immunoreactivity [1]. By working on sexual arousal and desires in the brain, PT-141’s mechanism of action differs from phosphodiesterase‑5 (PDE-5) inhibitors, which cause peripheral vasodilation. Instead, PT‑141 stimulates arousal via central neurochemical cascades, including increased dopamine release in key brain regions governing sexual function. This also means combining PT-141 with PDE5 inhibitors can have additive effects. Also, PT-141 is more effective in females than PDE5. PT-141 and erectile dysfunction Male erectile function Across preclinical and clinical studies, PT-141 demonstrated the ability to increase sexual arousal in both men and women, with dose-dependent efficacy and an acceptable safety profile in the controlled research setting. A randomized, double-blind, placebo-controlled clinical trial was combined with preclinical animal studies to investigate the effects of PT-141 on sexual dysfunction [1]. Preclinical results suggests that PT-141: Activated MC3 and MC4 melanocortin receptors in the central nervous system. Produced sexual arousal behaviors in rodents without directly affecting the vascular system. The parallel clinical trial found that intranasal PT-141 up to 20 mg, produced significant improvements in erectile function compared to placebo. The erectile response rates were dose-dependent, with higher doses achieving a significant increase in rigidity and duration of erection (p < 0.05). Adverse events were generally mild to moderate, with the most common being dose-dependent, transient nausea and flushing. Phase I data shows that subcutaneous doses of PT‑141 (10 mg, 20 mg) increased duration of base rigidity ≥ 80% in healthy males. Phase 2A results indicated significantly longer durations at the 20 mg dose, with common adverse events including flushing and nausea. PT-141 and female libido Two identical Phase 3 RCTs enrolled a total of 2,449 premenopausal women with hypoactive sexual desire disorder (HSDD). 1,247 participants were included in the safety population, and 1,202 in the modified intent-to-treat efficacy analysis [3]. Participants were randomized 1:1 to receive either bremelanotide 1.75 mg or placebo administered subcutaneously on an as-needed basis over 24 weeks. Bremelanotide administration resulted in: Increases in Female Sexual Function Index (FSFI) desire domain scores versus placebo (p < 0.01) Reductions in Female Sexual Distress (FSDS-DAO) scores (p < 0.01) The most common adverse events (≥10% in both studies) were nausea, flushing, and headache. Most events were mild to moderate in severity. These findings support the potential of bremelanotide in modulating sexual desire in female populations. PT-141 safety and side effect profile Preclinical and clinical evidence indicate that PT‑141 (bremelanotide) is generally safe in research settings, with most adverse events being mild to moderate and transient. Adverse events The most frequently reported side effects include nausea, flushing, and headaches [4]. Cardiovascular effects PT-141 is associated with transient and mild cardiovascular effects, including: Blood pressure elevation ( ~3 mm Hg systolic and 2 mm Hg diastolic) Heart rate reduction These effects peaked within a few hours and returned to baseline within approximately 8–10 hours. Importantly, there was no net increase in overall myocardial workload [5]. Pigmentation Activation of melanocortin receptors can contribute to hyperpigmentation on the face, gums, and breasts. This was rare with dosing protocols in research settings (fewer than eight doses per month). However, this became more common with daily consecutive dosing [6]. Rare events A single case of acute hepatitis was reported in a participant after approximately 20 subcutaneous doses over one year. Significant elevations in aminotransferases and mild hyperbilirubinemia, resolved after discontinuation of PT‑141 [6].
What is Selank? Selank 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 peptide benefits 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]. Anxiolytic and antidepressant properties 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]. Cognitive enhancement and neuroprotection 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]. Stress resilience and recovery 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]: 2–3-fold increase in sensory attention 1.5-fold changes in learning capacity Normalized exploratory activity in the open field and hole board Recovered balance of serotonergic and noradrenergic brain system activity 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]. Immune and inflammation modulation 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.
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.