PRODUCTS SOLD ON PEPTIDESLABIRELAND.COM ARE FOR RESEARCH PURPOSES ONLY AND ARE NOT FOR HUMAN OR VETERINARY USE.
PRODUCTS SOLD ON PEPTIDESLABIRELAND.COM ARE FOR RESEARCH PURPOSES ONLY AND ARE NOT FOR HUMAN OR VETERINARY USE.
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Selank Ireland – Buy Online | In Stock & Ready to Ship
Buy Selank in Ireland with fast shipping and guaranteed ≥99% purity — verified with COA and HPLC documentation. A trusted choice for peptides Ireland research teams rely on, with no customs delays or international wait times. Whether you’re searching for Selank Ireland suppliers or looking to buy peptides Ireland-wide, we have you covered. Irish research teams can count on consistent stock, rapid fulfilment and full batch documentation every time.
For research use only. Not intended for human or veterinary use.
Selank is a synthetic heptapeptide anxiolytic and nootropic research compound and one of the most mechanistically distinctive centrally active peptides available to laboratories in Ireland — a stabilised analogue of the endogenous immunomodulatory tetrapeptide tuftsin conjugated to a proline-containing C-terminal extension that confers metabolic stability, designed and characterised by the Institute of Molecular Genetics of the Russian Academy of Sciences as a peptide anxiolytic with a pharmacological profile combining anxiolytic, nootropic, antidepressant, and immunomodulatory properties through mechanisms involving modulation of GABAergic neurotransmission, enhancement of brain-derived neurotrophic factor expression, regulation of serotonin and dopamine metabolism, and modulation of the enkephalin degradation system, making it an indispensable research tool for studying peptide-mediated anxiolytic pharmacology and GABA-A receptor modulation, neurotrophic factor regulation by short peptides, the neurobiology of anxiety and stress resilience, serotonergic and dopaminergic system modulation by tuftsin-related peptides, immunomodulatory neuropeptide biology, cognitive enhancement and memory consolidation mechanisms, and the emerging research biology of metabolically stabilised synthetic peptides as centrally active neuromodulators with combined anxiolytic and cognitive-enhancing profiles that distinguish them mechanistically from classical benzodiazepine and SSRI pharmacology. Researchers and institutions across Ireland can source verified, research-grade Selank directly from our Irish peptide supply, with domestic-speed dispatch and complete batch documentation.
✅ ≥99% Purity — HPLC & Mass Spectrometry Verified
✅ Batch-Specific Certificate of Analysis (CoA) Included
✅ Sterile Lyophilised Powder | GMP Manufactured
✅ Fast Dispatch to Ireland | Peptides Ireland Stock
Selank — designated Thr-Lys-Pro-Arg-Pro-Gly-Pro in its amino acid sequence, with the systematic designation TP-7 — is a synthetic heptapeptide developed at the Institute of Molecular Genetics of the Russian Academy of Sciences through a rational design strategy combining the immunomodulatory tetrapeptide tuftsin (Thr-Lys-Pro-Arg) with a C-terminal Pro-Gly-Pro extension derived from the IgG heavy chain hinge region, where the extension serves the dual function of conferring metabolic stability against rapid proteolytic degradation that limits the in vivo utility of tuftsin itself and introducing additional pharmacological activity through the Pro-Gly-Pro sequence’s independent effects on enkephalin-metabolising enzymes and neurochemical regulation. The compound has been characterised through an extensive Russian and Eastern European research programme spanning several decades — with the majority of foundational mechanistic and behavioural pharmacology research conducted at Russian academic and government research institutions — and has subsequently attracted broader international research interest as its distinctive anxiolytic-nootropic profile has become appreciated in the Western neuropharmacology literature.
The rational design basis of Selank reflects an insight into the neuropharmacological significance of tuftsin — a natural immunomodulatory tetrapeptide generated by enzymatic cleavage of the Fc region of IgG heavy chains — that extends beyond tuftsin’s canonical role as an immunostimulatory peptide activating macrophage and natural killer cell function. Research characterising the central nervous system effects of tuftsin documented anxiolytic and stress-reducing properties that pointed to central nervous system receptors or signalling mechanisms responsive to the tuftsin sequence — properties whose translational research utility was limited by tuftsin’s rapid proteolytic degradation in plasma and brain tissue. Selank’s design addressed this limitation by appending the Pro-Gly-Pro C-terminal extension — a sequence with known resistance to aminopeptidase degradation and additional pharmacological activity — to the tuftsin tetrapeptide core, producing a heptapeptide with substantially improved metabolic stability, preserved and enhanced anxiolytic activity, and a broader pharmacological profile encompassing nootropic and immunomodulatory effects that has made it one of the most distinctive centrally active research peptides developed from the Soviet and Russian neuropharmacology programme.
Selank’s mechanistic profile is multifaceted and continues to be an active area of research characterisation — with established or proposed mechanisms including positive modulation of GABA-A receptor function contributing to its anxiolytic effects, upregulation of brain-derived neurotrophic factor (BDNF) expression in hippocampus and other brain regions relevant to cognitive function and stress resilience, modulation of the serotonin metabolism including regulation of tryptophan hydroxylase and monoamine oxidase activity, inhibition of enkephalin-degrading enzymes that extend the biological half-life of endogenous opioid peptides in the brain, modulation of interleukin-6 and other cytokine expression relevant to neuroinflammatory biology, and interaction with the dopaminergic system in mesolimbic and mesocortical circuits relevant to mood and cognitive function. This mechanistic breadth — spanning GABAergic, serotonergic, dopaminergic, neurotrophic, opioidergic, and immunomodulatory systems — distinguishes Selank from single-target anxiolytics and has made the characterisation of its primary versus secondary pharmacological mechanisms an ongoing and productive area of research.
In controlled laboratory and pre-clinical settings, Selank is studied across a range of anxiolytic pharmacology, neurotrophic factor biology, cognitive enhancement, stress neurobiology, immunomodulation, and neuropeptide mechanism research applications:
Selank is studied as an anxiolytic research compound with a proposed mechanism involving positive modulation of GABA-A receptor function — examined through its effects on benzodiazepine binding site occupancy, GABA-A receptor subunit expression, and chloride conductance in GABAergic neurotransmission studies. Research has characterised Selank’s anxiolytic effects in standard pre-clinical anxiety paradigms including elevated plus maze, open field, light-dark box, and stress-induced hyperthermia tests — documenting dose-dependent reductions in anxiety-related behaviour comparable in magnitude to reference benzodiazepine anxiolytics but with a different side effect profile characterised by preserved cognitive function and motor coordination at anxiolytic doses. Studies have examined the GABAergic mechanism of Selank’s anxiolytic effects using GABA-A receptor antagonists and subunit-selective modulators as pharmacological probes — characterising whether Selank’s anxiolytic activity is blocked by flumazenil at the benzodiazepine binding site, and comparing the receptor subunit selectivity of Selank’s GABAergic modulation with classical benzodiazepines to characterise mechanistic similarities and differences. These anxiolytic pharmacology studies have positioned Selank as a research tool for studying peptide-mediated GABAergic modulation and comparing the anxiolytic biology of tuftsin-related peptides with classical small molecule GABAergic anxiolytics.
One of the most scientifically significant and distinctive aspects of Selank’s pharmacological profile is its capacity to upregulate BDNF expression — with research characterising increases in BDNF mRNA and protein levels in hippocampus, frontal cortex, and other brain regions following Selank administration. BDNF is the most abundantly expressed and functionally critical neurotrophin in the adult brain — regulating synaptic plasticity, neurogenesis, dendritic complexity, long-term potentiation, and the survival and maintenance of multiple neuronal populations — making its upregulation by Selank a research finding with implications for cognitive function, stress resilience, antidepressant biology, and neuroprotection that extend beyond Selank’s anxiolytic pharmacology. Research has characterised the dose-response relationship for Selank-induced BDNF upregulation, the brain regions showing the most pronounced BDNF increases, the signalling mechanisms through which Selank administration produces BDNF transcriptional upregulation including potential CREB activation and TrkB receptor pathway engagement, and whether Selank-induced BDNF increases are sustained during chronic administration or diminish with repeated dosing. These BDNF regulation studies have contributed to understanding of how short synthetic peptides can engage neurotrophic factor signalling pathways — positioning Selank as a research tool for studying peptide-mediated BDNF biology and the relationship between anxiety modulation and neurotrophic factor regulation.
Research has characterised Selank’s effects on serotonin metabolism — examining its influence on tryptophan hydroxylase activity and serotonin synthesis, monoamine oxidase activity and serotonin degradation, serotonin transporter expression and function, and the downstream consequences of altered serotonin tone in brain regions relevant to anxiety and mood regulation. Studies have documented changes in serotonin and its metabolite 5-HIAA levels in limbic and cortical brain regions following Selank administration — characterising the direction and magnitude of serotonin system changes and examining how these interact with the GABAergic and neurotrophic mechanisms that collectively produce Selank’s anxiolytic and antidepressant-like profile. Research has examined whether Selank’s serotonin system modulation involves direct interaction with serotonin receptors or transporters — or whether serotonin changes are secondary to upstream peptide receptor or enzyme effects — contributing to mechanistic understanding of how tuftsin-related peptides modulate monoamine neurotransmission. These serotonin research studies have contributed to understanding of Selank’s antidepressant-like effects and its potential relevance to research models of serotonin-related mood disorders.
The Pro-Gly-Pro C-terminal extension of Selank has been characterised as a substrate and inhibitor for enkephalin-degrading enzymes — including enkephalinase and other metallopeptidases responsible for rapid inactivation of endogenous opioid peptides in the brain — and research has examined Selank’s effects on enkephalin bioavailability and opioid peptide system biology. Studies have characterised how Selank’s inhibition of enkephalin degradation enzymes extends the biological half-life of endogenous Met-enkephalin and Leu-enkephalin in the brain — producing enhanced endogenous opioid signalling at mu and delta opioid receptors in pain, anxiety, and reward circuits. Research has examined the relationship between Selank-mediated enkephalin system modulation and its anxiolytic effects — investigating whether opioid receptor-mediated mechanisms contribute to the anxiolytic profile observed in behavioural studies and whether opioid receptor antagonists attenuate Selank-induced anxiolysis. These enkephalin system studies have contributed to understanding of the multimodal mechanism through which Selank simultaneously engages GABAergic, serotonergic, and opioidergic systems — and have positioned the Pro-Gly-Pro sequence as a pharmacologically active peptide fragment with enkephalinase inhibitory properties relevant to endogenous opioid peptide biology.
Selank’s nootropic properties — distinct from its anxiolytic effects and attributable to a combination of BDNF upregulation, serotonin system modulation, and potential direct effects on memory consolidation mechanisms — have been characterised in pre-clinical cognitive research paradigms. Research has documented improvements in learning and memory performance in rodent models using Morris water maze, passive and active avoidance, and novel object recognition paradigms — characterising Selank-induced improvements in memory acquisition, consolidation, and retrieval that occur without the sedative or motor-impairing effects that limit the cognitive utility of classical benzodiazepine anxiolytics at anxiolytic doses. Studies have examined the neural substrates of Selank’s nootropic effects — characterising hippocampal and prefrontal cortical changes in gene expression, synaptic plasticity markers, and neurotrophic factor levels that accompany cognitive improvement — and have investigated whether BDNF upregulation is causally required for Selank’s cognitive-enhancing effects through TrkB receptor blockade experiments. These cognitive enhancement studies have positioned Selank as a research tool for studying the relationship between anxiety modulation and cognitive function — and for examining how peptides that simultaneously reduce anxiety and upregulate BDNF produce cognitive enhancement profiles distinct from both anxiolytics and classical nootropics.
Selank has been studied in stress neurobiology research — examining its effects on HPA axis reactivity, corticosterone responses to acute and chronic stress, CRH expression in the paraventricular nucleus, and the neurobiological consequences of stress resilience produced by Selank treatment. Research has characterised Selank’s capacity to attenuate corticosterone elevation following acute stressors in rodent models — documenting HPA axis dampening effects consistent with its anxiolytic pharmacological profile — and has examined the brain regions and receptor mechanisms through which Selank modulates the stress response. Studies have examined Selank’s effects on stress-induced changes in gene expression in hippocampus and amygdala — characterising how Selank treatment alters the transcriptional consequences of acute and chronic stress exposure and whether BDNF upregulation contributes to Selank’s stress resilience-promoting effects. These stress neurobiology studies have contributed to understanding of how peptide anxiolytics with multimodal mechanisms produce stress resilience through integrated effects on GABAergic, HPA axis, and neurotrophic factor systems simultaneously.
Selank’s structural derivation from tuftsin — a well-characterised immunomodulatory peptide — confers immunomodulatory properties that have been studied in both peripheral immune and central neuroinflammatory research contexts. Research has characterised Selank’s effects on cytokine production — documenting modulation of interleukin-6, TNF-alpha, and interferon-gamma production in immune cell models and in brain tissue — and has examined how Selank’s immunomodulatory effects interact with its central anxiolytic and neurotrophic properties. Studies have examined Selank’s effects in neuroinflammation models — characterising its modulation of microglial activation, neuroinflammatory cytokine expression, and the relationship between anti-neuroinflammatory effects and cognitive and anxiolytic outcomes in models where neuroinflammation contributes to anxiety and cognitive impairment. These neuroinflammation and immunomodulatory biology studies have contributed to understanding of how Selank’s tuftsin-derived sequence confers immunomodulatory properties that may contribute to its central effects through modulation of the neuroimmune interface — positioning Selank as a research tool for studying the relationship between immune system modulation and central nervous system function in anxiety and stress biology.
Research has examined Selank’s effects on dopaminergic neurotransmission — characterising its influence on dopamine synthesis, dopamine transporter expression, dopamine receptor binding, and dopamine levels in mesolimbic and mesocortical circuits relevant to motivation, reward, and cognitive function. Studies have documented Selank-induced changes in dopamine metabolism in the nucleus accumbens and prefrontal cortex — regions whose dopaminergic tone is critical for working memory, executive function, and motivated behaviour — and have examined whether Selank’s nootropic effects on cognitive performance are associated with or causally dependent on altered dopaminergic signalling in these regions. Research has also examined the absence of significant dopaminergic reward or dependence-producing effects with Selank — characterising whether the compound produces conditioned place preference, self-administration, or withdrawal effects that would suggest abuse liability — contributing to understanding of the pharmacological basis for Selank’s separation of anxiolytic and nootropic effects from dependence and reward biology.
The combination of BDNF upregulation, anti-neuroinflammatory properties, and serotonergic system modulation produced by Selank has motivated research into its neuroprotective potential in neurodegeneration models. Studies have examined Selank’s effects in models of oxidative stress-induced neuronal damage, excitotoxicity, and neuroinflammation-associated neurodegeneration — characterising whether BDNF upregulation and anti-neuroinflammatory effects translate into measurable neuroprotective outcomes in vulnerable neuronal populations. Research has also examined Selank in models relevant to Alzheimer’s disease biology — studying its effects on amyloid biology, tau phosphorylation, and the cognitive deficits associated with cholinergic neurodegeneration — contributing to understanding of whether the neurotrophic and anti-inflammatory properties of Selank have relevance to neurodegenerative disease research beyond the anxiety and stress biology that represents its primary research focus.
Foundational research from Russian academic institutions established Selank’s anxiolytic efficacy across multiple pre-clinical anxiety paradigms — with studies characterising dose-dependent reductions in anxiety-related behaviour in elevated plus maze, open field, and conflict tests that were comparable in magnitude to diazepam reference doses at the anxiolytic endpoints measured. These behavioural pharmacology studies established Selank as a genuinely anxiolytic compound rather than a sedative — demonstrating that anxiolytic effects occurred at doses not producing the motor impairment, sedation, or amnesia that characterise benzodiazepine activity — and provided the foundational evidence for Selank’s distinct pharmacological profile relative to classical GABAergic anxiolytics.
Research has documented Selank-induced increases in BDNF expression in hippocampus and frontal cortex — characterising significant elevations in BDNF mRNA and protein levels following acute and repeated Selank administration that were not observed with benzodiazepine reference compounds at equivalent anxiolytic doses. These BDNF regulation studies established Selank’s neurotrophic mechanism as a pharmacologically distinctive feature separating it from classical anxiolytics — and provided the molecular basis for understanding why Selank produces cognitive-enhancing effects alongside anxiolysis, given BDNF’s established role in hippocampal synaptic plasticity, long-term potentiation, and memory consolidation.
Research has documented improvements in learning and memory performance in rodent cognitive paradigms following Selank administration — characterising enhanced acquisition and retention in passive avoidance, active avoidance, and maze paradigms that occurred without the motor impairment and sedation produced by benzodiazepines at equi-anxiolytic doses. These cognitive enhancement studies established Selank’s nootropic profile as a genuine and pharmacologically distinguishable component of its activity — demonstrating that the same treatment producing anxiolytic effects also improved cognitive performance, in direct contrast to classical benzodiazepines whose anxiolytic doses produce anterograde amnesia and impair cognitive performance.
Research has characterised Selank-induced changes in serotonin metabolism — documenting alterations in 5-HT and 5-HIAA levels in limbic brain regions and examining the enzymatic basis for these changes through tryptophan hydroxylase and monoamine oxidase activity measurements. These serotonin system studies characterised the serotonergic component of Selank’s pharmacological mechanism and provided evidence for a monoaminergic mechanism contributing to its antidepressant-like and anxiolytic effects alongside the GABAergic and neurotrophic mechanisms — establishing Selank’s multimodal mechanism as encompassing both GABA and serotonin system modulation.
Research has characterised the Pro-Gly-Pro component of Selank’s sequence as an inhibitor of enkephalin-degrading metallopeptidases — documenting reduced enzyme activity and elevated enkephalin levels in brain regions relevant to pain, anxiety, and reward following Selank administration. These enkephalin system studies established the opioidergic component of Selank’s mechanism and provided the biochemical basis for understanding how the Pro-Gly-Pro extension contributes pharmacological activity beyond simple metabolic stabilisation of the tuftsin core — demonstrating that the C-terminal extension is not pharmacologically inert but actively engages the enkephalin system to contribute to Selank’s overall neurobiological effects.
Research has documented Selank’s effects on cytokine production — characterising modulation of interleukin-6, interferon-gamma, and other cytokines in immune cell preparations and in brain tissue following Selank treatment. These immunomodulatory studies established that Selank retains the immunomodulatory biological activity of its tuftsin parent sequence while extending and broadening this activity through the C-terminal extension — contributing to understanding of how tuftsin-related peptides engage both central nervous system and immune system signalling and how these dual effects interact in the integrated biology of stress, anxiety, and immune function.
Research has documented Selank’s attenuation of HPA axis reactivity to acute stress — characterising reduced corticosterone responses to restraint stress and other acute stressors in Selank-treated animals alongside maintained baseline corticosterone levels consistent with anxiolytic rather than non-specifically immunosuppressive HPA modulation. These stress biology studies established the neuroendocrine basis for Selank’s stress resilience-promoting effects and contributed to understanding of how the combined GABAergic, serotonergic, and neurotrophic effects of Selank translate into attenuated HPA axis reactivity at the level of CRH and corticosterone secretion.
| Feature | Selank | Semax | Diazepam | Buspirone | Fluoxetine |
|---|---|---|---|---|---|
| Type | Synthetic heptapeptide — tuftsin analogue with Pro-Gly-Pro extension | Synthetic heptapeptide — ACTH(4-7) analogue with Pro-Gly-Pro extension | Benzodiazepine — small molecule GABA-A positive allosteric modulator | Azapirone — partial 5-HT1A agonist / D2 antagonist | SSRI — serotonin reuptake inhibitor |
| Primary Mechanism | GABAergic modulation / BDNF upregulation / serotonin metabolism modulation / enkephalinase inhibition / immunomodulation | BDNF and NGF upregulation / dopaminergic and serotonergic modulation / neuroprotection | GABA-A receptor positive allosteric modulation — benzodiazepine site | 5-HT1A partial agonism — reduces serotonergic tone in raphe / partial D2 antagonism | Serotonin transporter inhibition — raises synaptic 5-HT |
| Anxiolytic Effect | Yes — documented in multiple pre-clinical paradigms | Mild — primarily nootropic with secondary anxiolytic properties | Yes — potent, rapid onset | Yes — moderate, delayed onset | Yes — delayed onset, weeks |
| Nootropic / Cognitive Effect | Yes — memory enhancement, BDNF upregulation, no sedation | Yes — primary effect; cognitive enhancement, BDNF/NGF upregulation | No — impairs cognition at anxiolytic doses; anterograde amnesia | Neutral to mild improvement | Neutral to mild |
| BDNF Regulation | Upregulation — hippocampus and cortex | Upregulation — pronounced; primary mechanism | No significant effect | No significant direct effect | Upregulation — chronic treatment |
| Sedation Risk | Low — anxiolytic doses do not produce sedation | Low | High — dose-dependent sedation and motor impairment | Low | Low |
| Dependence / Withdrawal Risk | Not characterised as dependence-producing | Not characterised as dependence-producing | High — physical dependence and withdrawal syndrome | Low | Low — discontinuation syndrome |
| Immunomodulatory Effects | Yes — tuftsin-derived; cytokine modulation | Limited | Immunosuppressive at high doses | Minimal | Minimal |
| Research Origin | Russian Academy of Sciences — Institute of Molecular Genetics | Russian Academy of Sciences | Western pharmaceutical development | Western pharmaceutical development | Western pharmaceutical development |
| Research Profile | Extensively studied in Russian literature — growing international interest | Extensively studied in Russian literature — growing international interest | Extensively studied — reference GABAergic anxiolytic | Well-documented | Extensively studied — reference SSRI |
| Parameter | Detail |
|---|---|
| Name | Selank |
| Also Designated | TP-7 / Thr-Lys-Pro-Arg-Pro-Gly-Pro |
| Type | Synthetic Heptapeptide Anxiolytic and Nootropic Research Peptide — Research Grade |
| Structure | Thr-Lys-Pro-Arg-Pro-Gly-Pro — tuftsin (Thr-Lys-Pro-Arg) core with Pro-Gly-Pro C-terminal metabolic stabilisation and pharmacological extension |
| Molecular Weight | 751.86 Da |
| Mechanism | GABAergic modulation / BDNF upregulation in hippocampus and cortex / serotonin metabolism modulation / enkephalin-degrading enzyme inhibition / cytokine modulation / dopaminergic system effects |
| Key Research Distinction | Combined anxiolytic and nootropic profile without sedation or cognitive impairment — mechanistically distinct from benzodiazepines through multimodal peptidergic mechanism including BDNF upregulation |
| Primary Research Areas | Anxiolytic pharmacology / BDNF regulation / cognitive enhancement / stress neurobiology / serotonin system modulation / enkephalin biology / immunomodulation / HPA axis regulation |
| Structural Basis | Tuftsin tetrapeptide core for immunomodulatory and central nervous system activity + Pro-Gly-Pro extension for metabolic stability and enkephalinase inhibition |
| Metabolic Stability | Enhanced relative to tuftsin — Pro-Gly-Pro extension reduces aminopeptidase degradation |
| Purity | ≥99% HPLC & MS Verified |
| Form | Sterile Lyophilised Powder |
| Solubility | Sterile water or sterile saline — readily water soluble |
| Storage (Powder) | -20°C, protect from light and moisture |
| Storage (Reconstituted) | -80°C in aliquots — minimise freeze-thaw cycles |
| Manufacturing | GMP Manufactured |
| Intended Use | Research use only |
Selank is a hydrophilic heptapeptide with excellent aqueous solubility — reconstitution is straightforward and does not require organic solvents or acidified aqueous solutions at research-relevant concentrations. Add sterile water or sterile physiological saline slowly to the lyophilised powder and swirl gently until fully dissolved — Selank dissolves readily in aqueous solution without requiring bath sonication, elevated temperature, or pH adjustment. Neutral aqueous conditions are appropriate for Selank reconstitution as the peptide is chemically stable across the physiological pH range and does not contain structural elements such as disulfide bridges that would require specific redox conditions.
For intranasal administration paradigms — a route used in some rodent behavioural research given Selank’s clinical development as a nasal spray — prepare working solutions in sterile physiological saline at concentrations appropriate for the delivery volume, and administer immediately after preparation to maintain peptide concentration accuracy. For intraperitoneal or subcutaneous administration in in vivo behavioural studies, prepare fresh working solutions in sterile saline at the time of administration and maintain on ice during handling. For cell-based studies examining BDNF upregulation, cytokine modulation, or neuronal biology, dilute concentrated stock solutions into the appropriate cell culture media immediately before addition to cells — Selank is stable in aqueous solution at 4°C for several hours but should not be stored as dilute working solutions for extended periods. Prepare single-use aliquots immediately after reconstitution and store at -80°C — avoid repeated freeze-thaw cycles that can promote peptide degradation and reduce biological activity in sensitive cell-based and behavioural assays. Use low-binding polypropylene tubes throughout to minimise adsorptive losses at lower working concentrations.
Every order of Selank in Ireland includes:
✅ Batch-Specific Certificate of Analysis (CoA)
✅ HPLC Chromatogram
✅ Mass Spectrometry Confirmation
✅ Sterility & Endotoxin Testing Report
✅ Reconstitution Protocol — including intranasal and systemic administration guidance
✅ Technical Research Support
Yes — we supply research-grade Selank to researchers and institutions across Ireland with fast dispatch and full batch documentation. This compound is supplied strictly for laboratory research purposes only.
Tuftsin — Thr-Lys-Pro-Arg — is an endogenous immunomodulatory tetrapeptide generated by enzymatic cleavage of the Fc region of IgG heavy chains, originally characterised as an immunostimulatory peptide activating macrophage and natural killer cell phagocytosis and cytotoxic function before its central nervous system effects including anxiolytic and stress-modulating properties were characterised. Selank incorporates the complete tuftsin sequence as its N-terminal Thr-Lys-Pro-Arg core — preserving tuftsin’s immunomodulatory and central anxiolytic biology while addressing tuftsin’s primary pharmacological limitation: rapid proteolytic degradation in plasma and brain tissue by aminopeptidases and endopeptidases that cleave the tetrapeptide within minutes of administration, severely limiting its in vivo research utility. The Pro-Gly-Pro C-terminal extension appended to the tuftsin core in Selank serves two functions simultaneously — conferring metabolic stability through resistance to aminopeptidase attack at the C-terminus, and introducing additional pharmacological activity through Pro-Gly-Pro’s enkephalinase inhibitory properties that extend the biological half-life of endogenous enkephalins and contribute an opioidergic component to Selank’s mechanism absent from tuftsin itself. The result is a heptapeptide that retains and extends tuftsin’s central nervous system biology while adding novel pharmacological dimensions — making Selank pharmacologically richer than its tuftsin parent and a more tractable research tool for studying tuftsin-related central nervous system biology in in vivo models where metabolic stability is a prerequisite for reliable pharmacological activity.
Selank and benzodiazepines share the capacity to produce anxiolysis through mechanisms that involve the GABAergic system — but the nature of their GABAergic engagement and their additional pharmacological mechanisms differ substantially in ways that produce a distinctly different overall pharmacological profile. Benzodiazepines act as positive allosteric modulators at the benzodiazepine binding site of the GABA-A receptor — directly enhancing the receptor’s response to GABA by increasing the frequency of chloride channel opening, producing rapid, potent anxiolysis alongside sedation, muscle relaxation, anticonvulsant activity, and anterograde amnesia that are inseparable from the anxiolytic effect at the receptor level. Selank’s proposed GABAergic mechanism involves modulation of GABA-A receptor function through a mechanism that may not require direct benzodiazepine site occupancy — producing anxiolysis without the sedation, motor impairment, and cognitive disruption that accompany benzodiazepine receptor engagement at clinically relevant binding site occupancy. Beyond this GABAergic distinction, Selank’s anxiolytic pharmacology is multimodal — encompassing BDNF upregulation, serotonin metabolism modulation, enkephalinase inhibition, and immunomodulatory effects that collectively produce a different neurobiological state than benzodiazepine-mediated GABA-A potentiation alone. The practical consequence for research is that Selank allows separation of anxiolysis from cognitive impairment — enabling experimental designs examining anxiolytic effects while maintaining cognitive function as an independent measurable endpoint, a separation impossible with benzodiazepine reference compounds.
BDNF — brain-derived neurotrophic factor — is the most extensively studied and functionally critical neurotrophin in the adult brain, with established roles in hippocampal neurogenesis, synaptic plasticity and long-term potentiation, dendritic arborisation, memory consolidation, the antidepressant response, and stress resilience. BDNF upregulation is considered a key mechanism through which antidepressants produce their therapeutic effects — the neurotrophic hypothesis of depression posits that reduced BDNF signalling in hippocampus and prefrontal cortex contributes to the structural and functional brain changes accompanying major depression, and that BDNF restoration mediates the cognitive and mood improvements produced by effective antidepressant treatment. Selank’s documented capacity to upregulate BDNF expression in hippocampus and cortex — a property not shared by classical benzodiazepine anxiolytics — therefore carries multiple research implications: it provides a candidate mechanism for Selank’s nootropic cognitive-enhancing effects through enhanced synaptic plasticity; it suggests potential antidepressant-like properties mediated through the same neurotrophic mechanism implicated in antidepressant action; it points to potential neuroprotective effects in models of stress-induced hippocampal neuronal compromise; and it distinguishes Selank from purely symptomatic anxiolytics by suggesting a potential capacity to modify the neurotrophic substrates underlying anxiety and stress vulnerability. These BDNF biology implications make Selank a research tool not only for anxiolytic pharmacology but for the broader neurobiology of stress resilience, cognitive enhancement, and the neurotrophic underpinnings of mood and anxiety disorders.
The Pro-Gly-Pro C-terminal extension in Selank was incorporated into the design to serve primarily as a metabolic stabilisation sequence — exploiting the known resistance of proline-containing peptides to aminopeptidase degradation to protect the tuftsin core from the rapid N-to-C terminal exopeptidase cleavage that limits tuftsin’s in vivo half-life. However, subsequent research has established that Pro-Gly-Pro is not pharmacologically inert — characterising it as an inhibitor of enkephalin-degrading metallopeptidases including enkephalinase (neprilysin) and related neutral endopeptidases that normally rapidly degrade endogenous Met-enkephalin and Leu-enkephalin at synaptic sites throughout the brain. By inhibiting these enkephalin-degrading enzymes, the Pro-Gly-Pro component of Selank extends the synaptic residence time of endogenous enkephalins released during normal neural activity — effectively amplifying endogenous opioid neurotransmission in circuits where enkephalins are co-released with other neurotransmitters. This enkephalinase inhibitory activity contributes an endogenous opioid amplification component to Selank’s mechanism that is absent from the tuftsin tetrapeptide alone and represents a pharmacologically meaningful addition to the overall mechanism — contributing to Selank’s anxiolytic effects through delta opioid receptor-mediated anxiolysis and potentially to its analgesic and stress-modulating properties. The Pro-Gly-Pro component therefore exemplifies how a structural modification introduced for pharmacokinetic stabilisation can confer independent pharmacological activity that enriches the overall mechanism of the parent compound.
Selank and Semax are the two most extensively studied synthetic heptapeptides from the Russian neuropeptide research programme — both containing the Pro-Gly-Pro C-terminal extension that confers metabolic stability and enkephalinase inhibitory activity, and both upregulating BDNF in brain regions relevant to cognition and stress resilience, but with distinct primary pharmacological profiles that reflect their different N-terminal sequences. Semax — designed around the ACTH(4-7) sequence Met-Glu-His-Phe that provides its core biological activity — is primarily characterised as a nootropic and neuroprotective compound with pronounced cognitive-enhancing and neuroprotective effects through dopaminergic and serotonergic system modulation and strong BDNF and NGF upregulation, with anxiolytic effects that are secondary to its primary cognitive-enhancing profile. Selank — designed around the tuftsin sequence Thr-Lys-Pro-Arg — is primarily characterised as an anxiolytic with secondary nootropic properties through BDNF upregulation and serotonin system modulation, and with prominent immunomodulatory effects derived from its tuftsin core that Semax does not share. For research purposes, Selank is the preferred tool when anxiolytic pharmacology and the anxiety-cognition relationship are the primary research focus, while Semax is preferred when cognitive enhancement, neuroprotection, and dopaminergic biology are the primary endpoints — and both are used together in comparative research examining how ACTH-related versus tuftsin-related peptide sequences engage shared Pro-Gly-Pro-dependent mechanisms alongside their distinct primary pharmacological activities.
Rigorous Selank behavioural research requires several essential controls for mechanistic interpretation. Vehicle controls matched to the Selank reconstitution solvent — sterile saline administered at equivalent volume, route, and timing — must be included in every behavioural study. Reference anxiolytic controls — including diazepam or another benzodiazepine at a dose producing the target degree of anxiolysis — provide a reference point for calibrating Selank-induced anxiolytic effects and distinguishing anxiolytic from sedative activity. Motor function and coordination controls — rotarod, open field locomotor activity, and grip strength measurements — are essential for confirming that observed changes in anxiety paradigm performance reflect genuine anxiolytic effects rather than motor impairment confounds; the absence of rotarod impairment at Selank doses producing anxiolysis is a key pharmacological distinction from benzodiazepines. BDNF pathway controls — including TrkB receptor antagonist treatment to block BDNF signalling — are important for mechanistically attributing cognitive-enhancing effects to BDNF upregulation. For GABAergic mechanism studies, flumazenil pre-treatment to block benzodiazepine site occupancy before Selank administration tests whether Selank’s anxiolytic mechanism requires benzodiazepine site engagement. Dose-response characterisation across a range of doses in primary behavioural paradigms is important for establishing the dose-effect relationship and identifying the dose range where anxiolytic effects are separated from any sedative or motor effects.
≥99% purity is strongly recommended for anxiolytic pharmacology studies, BDNF regulation research, cognitive enhancement paradigms, serotonin and enkephalin system studies, HPA axis research, immunomodulatory biology, and all pre-clinical behavioural and mechanistic research where pharmacological specificity and reproducible biological activity are primary requirements. For behavioural research where modest between-group differences in anxiety paradigm performance or cognitive test scores are the primary endpoints, high purity ensures that observed effects are attributable to Selank’s defined pharmacological mechanisms rather than co-purified peptide fragments or impurities with independent central nervous system activity. Given Selank’s heptapeptide structure, degradation products including tuftsin (Thr-Lys-Pro-Arg) and Pro-Gly-Pro fragments could each have independent biological activity — making purity verification particularly important for research designs where the intact heptapeptide’s combined mechanism is the subject of study and fragment activity would confound interpretation. All Selank Ireland stock is independently verified to ≥99% purity by HPLC and mass spectrometry with identity confirmation.
Selank is supplied exclusively for legitimate scientific research purposes conducted within licensed laboratory environments. This product is not intended for human consumption, self-administration, or any therapeutic application. It must be handled by qualified researchers in compliance with applicable Irish and EU regulations and institutional ethics guidelines. By purchasing, you confirm that this compound will be used solely for approved in vitro or pre-clinical research purposes.
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