Semax: The Russian Nootropic Peptide for Focus, Memory, and Brain Recovery
Semax: The Russian Nootropic Peptide for Focus, Memory, and Brain Recovery
The Space-Program Peptide That Found Its Way Into Your Stack
In the late 1980s, researchers at the Institute of Molecular Genetics of the Russian Academy of Sciences in Moscow were looking for a molecule that could protect cosmonauts' brains during the neurological stress of spaceflight. What they developed was Semax — a synthetic heptapeptide based on a four-amino-acid fragment of ACTH, the pituitary hormone that drives cortisol production.
The problem they were solving wasn't cortisol enhancement. It was cognitive resilience under extreme physiological stress. And the insight that made Semax possible was the discovery that the ACTH molecule contains an embedded neuropeptide sequence — a region that signals directly to the brain's memory, attention, and plasticity systems, completely independent of the adrenal gland. By isolating and stabilizing that fragment, the Moscow team created a molecule that delivered ACTH's neuroprotective and pro-cognitive effects without the cortisol spike.
By 1996, Semax was registered as a pharmaceutical in Russia — one of the very few peptide-class molecules to achieve finished-pharmaceutical approval anywhere. It remains on the Russian List of Vital and Essential Drugs and is used clinically for stroke recovery, TBI, and optic nerve damage. It is not FDA-approved and is sold for research purposes only outside Russia.
This guide covers the complete science: structure, variants, mechanisms, cognitive and neuroprotective evidence, dosing protocols, and how Semax compares to its functional counterpart, Selank. Research purposes only. Not a substitute for professional medical care. Consult a physician before use.
What Is Semax?
Structure: ACTH(4-7) + Pro-Gly-Pro
Semax's full amino acid sequence is Met-Glu-His-Phe-Pro-Gly-Pro — a seven-residue chain. The first four residues (MEHF) correspond to the 4-7 fragment of adrenocorticotropic hormone (ACTH), the pituitary peptide that normally drives cortisol secretion from the adrenal cortex.
Here's the critical structural feature: ACTH(4-7) carries the neuropeptide signaling activity of ACTH — its effects on attention, learning, and stress resilience — without the adrenal-activating sequence. Full ACTH stimulates the adrenal cortex via MC2R. The 4-7 fragment does not engage MC2R. It's the cognitive signal, stripped of the cortisol consequence.
The Pro-Gly-Pro (PGP) C-terminal extension is where much of Semax's engineered utility lies. Bare ACTH(4-7) is extremely short-lived in vivo — degraded by aminopeptidases within minutes. The PGP tail dramatically slows this enzymatic degradation by conformationally shielding the C-terminus. The result: a peptide with the neuropeptide signaling of ACTH's 4-7 fragment and a meaningful half-life that makes it pharmacologically usable. Without PGP, the compound barely has time to do anything before it breaks down.
This same structural strategy — adding a PGP tail to extend half-life — was used later in Selank, the anxiolytic peptide developed by the same Russian research lineage.
Intranasal Delivery: Why the Nose Is the Right Route
Semax's primary delivery route is intranasal, and this isn't incidental — it's part of the design. The nasal mucosa sits adjacent to the olfactory epithelium and cribriform plate. Peptides absorbed here can travel along the olfactory nerve fibers directly into the CNS, largely bypassing the blood-brain barrier. This gives intranasal peptide administration a CNS bioavailability profile that's dramatically better than systemic injection for a molecule of this size.
The subjective result is fast onset — typically 15–20 minutes — and brain-direct delivery that systemic routes can't easily replicate for a polar heptapeptide.
NA-Semax and NA-Semax Amidate
Research-context Semax is available in three variants, and the differences are significant enough to affect dosing:
Standard Semax — The original registered pharmaceutical form. Half-life approximately 30 minutes in plasma, functional effect window 4–6 hours per dose.
N-Acetyl Semax (NA-Semax) — An acetyl group is attached to the N-terminus. This blocks aminopeptidase degradation from the N-terminal end, extending plasma half-life substantially and producing a functional effect window of 6–8 hours per dose. By equivalent effect, NA-Semax is estimated to be roughly 10x more potent by weight than standard Semax.
N-Acetyl Semax Amidate (NA-Semax Amidate) — The double-modified variant: N-terminal acetylation plus C-terminal amidation. The amide group blocks carboxypeptidase degradation from the other end, extending half-life further still. This is the most potent form by weight — estimated 2–3x more potent than NA-Semax alone — and produces the longest effect window. It also has the least published research, since the original clinical work used standard Semax.
For first-time users, standard Semax is the most conservative starting point. For ongoing protocols, NA-Semax is the practical workhorse. NA-Semax Amidate is for experienced users who've established baseline tolerance.
Mechanisms of Action
This is the core of what makes Semax interesting — not because it does one thing, but because it does several things simultaneously that happen to converge on the same outcome: better brain function. Here's the mechanism landscape, mechanism by mechanism.
BDNF Upregulation: The Headline
The central mechanism behind Semax's cognitive effects is brain-derived neurotrophic factor (BDNF) upregulation. BDNF is the principal neurotrophin governing synaptic plasticity, long-term potentiation, hippocampal neurogenesis, and the structural changes underlying learning and memory formation.
Russian research — including the work of Dolotov et al. (2006) — demonstrated that Semax administration produces measurable increases in BDNF and proBDNF expression specifically in the hippocampus and cerebral cortex within hours of intranasal dosing. The hippocampus is the brain's memory consolidation hub; the prefrontal cortex handles working memory and executive function. Raising BDNF in both areas simultaneously is, mechanistically, exactly what you want from a cognitive enhancer.
This is the "plasticity dividend" of Semax: not just more neurotransmitter activity, but a brain that is literally more capable of forming and strengthening connections. The effect isn't a temporary boost — it's a shift toward a more plastic, more learnable state.
NGF Modulation: The Second Neurotrophin
Semax also modulates nerve growth factor (NGF) expression in rodent models. NGF is the neurotrophin primarily associated with cholinergic neuron survival and maintenance of the basal forebrain neurons most closely linked to memory and Alzheimer's pathology. Increased NGF expression means better support for the neurons most critical to long-term memory function. This mechanism also provides a rationale for Semax's clinical interest in neurodegenerative contexts.
Dopaminergic and Serotonergic Systems: The Focus and Motivation Pathway
Semax modulates both dopaminergic and serotonergic neurotransmission. The critical distinction — and this is the distinction that matters for safety and dependence profile — is that Semax is not a dopamine receptor agonist. It doesn't directly occupy dopamine receptors the way amphetamines or methylphenidate do.
Instead, it modulates tone: the balance of synthesis, release, and reuptake dynamics across the dopaminergic and serotonergic systems. The functional outcome is restoration of monoaminergic balance under conditions of stress-induced or fatigue-induced dysregulation — not a supraphysiological dopamine spike followed by receptor downregulation and crash.
This is why Semax users report sustained, non-jittery focus rather than the stimulant pattern: sharp onset, performance plateau, hard crash. The dopaminergic modulation produces motivation and drive; the serotonergic component adds emotional stability. Neither gets exhausted by receptor occupancy.
Cholinergic System: Memory and Learning
Semax enhances acetylcholine (ACh) receptor sensitivity in brain regions associated with memory and learning. The cholinergic system — already supported by NGF through the neurotrophin pathway — gets an additional push from the receptor sensitivity side. Acetylcholine is the primary neurotransmitter of memory encoding in the hippocampus and the attention system in the prefrontal cortex. Enhancing receptor sensitivity in both areas in the context of elevated BDNF creates a convergent state optimized for learning and working memory throughput.
Melanocortin Receptor Partial Agonism: Without the HPA Cost
The ACTH lineage means Semax interacts with the melanocortin receptor system, particularly MC3R and MC4R expressed throughout the CNS. These receptors mediate attention, arousal, learning, and stress response. The structural elegance of Semax is that it activates CNS-relevant melanocortin receptors without touching MC2R — the receptor on the adrenal cortex responsible for cortisol secretion. No MC2R activation = no cortisol = no HPA axis activation.
This is ACTH-like neuropeptide signaling at the cognitive level, surgically divorced from the adrenal consequence. Pure signal, no cortisol cost.
Neuroprotection: Anti-Oxidative Stress and Anti-Apoptosis in Ischemia
In ischemia and oxidative-stress models, Semax has demonstrated anti-apoptotic effects — protecting neurons from programmed cell death under reduced oxygen, reduced glucose, or elevated oxidative damage conditions. The mechanisms include modulation of pro-inflammatory cytokines, mitochondrial function support, and direct neurotrophic effects via BDNF.
This is the mechanistic basis for the strongest clinical application in the Semax literature. Russian stroke research — including multi-center hospital studies and the registry data reviewed by Gusev and colleagues (1997) — found that Semax administered in the acute phase of ischemic stroke reduced neurological damage and accelerated functional recovery. The neuroprotection mechanism is the bridge between Semax's nootropic effects and its clinical medicine applications.
HIF-1α Pathway: Why It Works Under Hypoxic Stress
One of the more underappreciated mechanisms is Semax's interaction with hypoxia-inducible factor 1-alpha (HIF-1α), the master transcription factor that activates under low-oxygen conditions to drive adaptation — upregulating glycolysis, angiogenesis, and cellular survival pathways. Semax has been shown to upregulate HIF-1α activity, which provides a mechanistic explanation for its neuroprotective effects under ischemic conditions. When oxygen is scarce, cells have a narrow window to activate survival programs. Semax's activation of HIF-1α broadens that window.
This also provides a rationale for the biohacker interest in Semax for high-altitude training and other hypoxic stress contexts — areas where the HIF-1α pathway is central to performance.
Immune-CNS Axis: Neuroinflammation Reduction
Semax modulates the CNS immune axis, reducing neuroinflammatory cytokine expression and stabilizing mast cells in the CNS. Neuroinflammation is increasingly recognized as a major contributor to cognitive impairment in a wide range of contexts — from post-viral brain fog to traumatic brain injury to age-related cognitive decline. Semax's anti-neuroinflammatory action creates a cleaner, lower-inflammation neural environment. The BDNF upregulation and the neuroinflammation reduction work in concert: higher BDNF while simultaneously lowering the inflammatory noise that would otherwise reduce the utility of that BDNF.
Ready to build your cognitive stack? The Peptide Stacking Guide covers full cognitive protocols, sequencing logic, and how to combine Semax with Selank, BPC-157, and the rest of the toolkit — Peptide Stacking Guide ($14.99) →
Cognitive Benefits
Focus and Working Memory: The Central Use Case
The BDNF-and-cholinergic mechanism combination drives the two cognitive effects users most reliably report: sustained directed attention and working memory capacity. These aren't metaphorical — BDNF in the hippocampus and prefrontal cortex literally upregulates the molecular machinery of memory formation and synaptic plasticity. Cholinergic receptor sensitivity in the same regions amplifies the efficiency of that machinery.
The subjective effect isn't the stimulant pattern (sharp onset, peak, hard crash). It's more like a sustained baseline elevation — you can stay in a focused cognitive state longer, hold more working memory items without dropping them, and push through cognitively demanding work without the fatigue accumulation that normally fragments attention. Biohackers consistently describe it as the brain "running cleanly."
Verbal Memory and Learning Speed: Clinical Evidence
A Russian clinical trial by Kaplan and colleagues (1996) examined Semax in healthy subjects on standardized cognitive tests, finding improvements in verbal memory, learning speed, and attention measures. The effect sizes were meaningful rather than marginal, and the improvements were observed at the 400–600 mcg intranasal range that has since become the standard cognitive-enhancement dosing reference. These results are in Russian literature and haven't been independently replicated by Western groups — which is the honest limitation on the human evidence base.
ADHD-Adjacent Applications
The dopaminergic tone normalization mechanism creates genuine relevance for attention-related issues. The key distinction from stimulant ADHD medications: Semax does not operate through the adrenergic system. Amphetamines and methylphenidate work by driving dopamine and norepinephrine release and/or blocking reuptake — direct receptor-level catecholamine increase. Semax works by modulating tone and balance, not by driving receptor occupancy. No adrenal activation, no post-dose receptor downregulation, no crash.
This makes it mechanistically interesting for users whose attention issues are subclinical or who have not tolerated stimulants well. It is not a substitute for prescribed ADHD medication under physician supervision — this bears repeating because self-substituting stimulant medication with a research peptide without physician input is not a reasonable protocol. But for users without a clinical ADHD diagnosis who find conventional nootropics underwhelming, the mechanism is genuinely different and worth understanding.
Anxiety Reduction and Mood Stabilization
At lower doses (300 mcg), Semax shows mild anxiolytic effects that partially overlap with the Selank profile — though through a different mechanism. Where Selank is primarily GABAergic with enkephalin contributions, Semax's mild anxiety reduction appears to flow from serotonergic tone normalization and the stress-protective effects of the melanocortin system. It's a secondary effect, not the headline.
The mood stabilization effect is more consistent: users report emotional resilience under cognitive demand — the ability to maintain focus and equanimity under conditions that would normally produce frustration or distraction. This is the serotonergic contribution, and it's part of why the Semax + Selank combination works so well: Selank handles the acute anxiety floor while Semax provides the emotional stability needed for sustained high-output work.
Neuroprotection and Recovery
Stroke Recovery: The Strongest Clinical Signal
The largest, most clinically robust evidence base for Semax is in acute ischemic stroke recovery. Russian multi-center hospital studies, including the registry data from Gusev et al. (1997), evaluated Semax as an adjunct treatment in the acute phase of ischemic stroke — administered within hours to days of the event. Reported outcomes included faster neurological function recovery on standard scales, reduced infarct progression, and improved functional outcomes at 30 and 90 days post-event.
This is the clinical application that placed Semax on the Russian List of Vital and Essential Drugs. In Russian neurology hospitals, Semax is a standard component of acute stroke management — not an experimental compound, not a biohacker supplement, but routine clinical medicine. The neuroprotection mechanisms are the clear mechanism bridge: anti-apoptotic action during the secondary injury window, neurotrophic support via BDNF, and neuroinflammation modulation during the acute inflammatory phase after ischemia.
Important caveat for research-context readers: the Russian clinical data, while consistent and internally coherent, has not been reproduced in Western randomized controlled trials at FDA scale. This is the honest limitation.
Post-COVID Cognitive Issues (Brain Fog)
Post-COVID brain fog is characterized mechanistically by neuroinflammation and potential BDNF dysregulation in the contexts of chronic immune activation. Semax's anti-neuroinflammatory action — reducing inflammatory cytokine expression and mast cell activation in the CNS — combined with its BDNF upregulation creates a mechanistically coherent rationale for its application in post-viral cognitive impairment.
This is an area where the mechanism predicts utility, but controlled human trial data specific to post-COVID brain fog doesn't yet exist. The connection is mechanistically well-grounded but extrapolated — worth noting for researchers interested in this space while being clear that it's a mechanistic inference, not clinical data. As always, consult a physician before using any research compound to address symptoms from a medical condition.
Traumatic Brain Injury
Russian rehabilitation protocols have incorporated Semax for moderate TBI, with published data showing improvements in functional recovery, working memory, and attention measures compared to control groups. The mechanism — anti-apoptotic protection during the secondary injury cascade, BDNF-supported neuronal survival, neuroinflammation reduction — is the same as in stroke, applied to a different injury context. The preclinical data in rodent TBI models is consistent and supports the mechanism.
Neurodegeneration Protection
BDNF is one of the primary molecular mechanisms linking lifestyle factors — exercise, sleep, social connection, learning — to long-term brain health. Chronic BDNF deficiency is associated with accelerated cognitive aging and increased neurodegeneration risk. Semax's sustained BDNF upregulation in the hippocampus and cortex, combined with NGF modulation supporting cholinergic neuron survival, positions it as a neuroplasticity-maintenance tool across the aging timeline.
This is the longevity angle: not dramatic acute neuroprotection, but a consistent molecular environment that favors neuronal survival and synaptic maintenance over time. For this use case, see also Pinealon — the pineal peptide that addresses the circadian and sleep-quality dimensions of long-term neuroprotection that Semax doesn't touch.
Semax vs Selank
These two molecules come from the same Russian research lineage, target many of the same users, and are routinely confused or treated as interchangeable. They are not interchangeable. They're complementary — but that means understanding the difference first.
| Feature | Semax | Selank |
|---|---|---|
| Origin | ACTH(4-7) fragment + PGP | Tuftsin analogue + PGP |
| Primary mechanism | BDNF upregulation, melanocortin agonism, dopaminergic/serotonergic tone | GABA-A modulation, enkephalinase inhibition, BDNF |
| Primary effect | Cognitive amplification, focus, directed attention | Anxiolytic, stress reduction, mood stabilization |
| Delivery | Intranasal | Intranasal |
| Dosing frequency | 1–2× daily | 1–2× daily |
| Effect window (standard) | 4–6 hours | 6–8 hours |
| Best use case | Sustained cognitive work, memory, learning, neurological recovery | Anxiety, stress, calm focus under cognitive load |
| Anxiolytic strength | Mild (secondary) | Strong (primary) |
| Stimulating quality | Yes — activating, energizing | No — calming, anxiolytic |
The practical translation:
- Semax raises the signal. It amplifies cognitive output, working memory, and directed attention. It's activating — dosing late in the day can disrupt sleep. It's the tool you reach for when the goal is cognitive output.
- Selank dampens the noise floor. It reduces the chronic sympathetic tone and anxiety that fragment attention from underneath. It's calming without being sedating. It's the tool you reach for when the goal is not being blocked by anxiety or stress.
The stack case: Many advanced users run both. The pattern is typically Selank in the morning to establish a low-anxiety baseline, then Semax pre-work or pre-task for directed cognitive output. The mechanisms are non-overlapping at the primary level — GABAergic/enkephalin for Selank, melanocortin/BDNF for Semax — and the effects are genuinely additive. This is the two-molecule cognitive stack that the Russian literature, to the extent it addresses combination use, implicitly points toward. See the full Selank guide for the other half of this picture.
For a broader look at the entire cognitive peptide category — including Dihexa and Pinealon alongside Semax and Selank — the Cognitive Peptides Hub is the reference.
Dosing Protocols
These are research-context dosing ranges drawn from the Russian clinical literature and research community use. They are not medical recommendations. Consult a physician before use.
Standard Semax
- Dose: 300–600 mcg intranasal, 1–2× daily
- Cognitive stack protocol: 600 mcg pre-work or pre-training (morning)
- Neuroprotective protocol: 300 mcg daily, 10–14 day cycles
- Timing: Morning and/or early afternoon only — Semax is stimulating and will disrupt sleep if dosed in the evening
- Onset: 15–20 minutes intranasal
- Effect window: 4–6 hours per dose
NA-Semax
- Dose: 100–300 mcg intranasal, once daily
- Typical effective dose: 200 mcg morning
- Effect window: 6–8 hours per dose
- Note: Roughly 10x more potent by weight than standard Semax — reduce dose proportionally
NA-Semax Amidate
- Dose: 50–200 mcg intranasal, once daily
- Potency: Estimated 2–3x more potent than NA-Semax (so effective dose is substantially lower than standard Semax)
- Recommended for: Experienced users who have established baseline tolerance with standard or NA-Semax first
- Start conservative: Begin at 50–100 mcg and titrate up
Cycling
The Russian clinical standard is 2 weeks on, 1 week off for cognitive-enhancement use. This provides a cycling pattern that limits receptor adaptation. No clinically significant tolerance has been documented at therapeutic doses, but cycling is the prudent approach for a compound with limited long-term human RCT data.
For longer-term use, some protocols use 4-week-on/2-week-off cycles — matching the cycling pattern in the peptide cycling guide.
Contraindications
Never use Semax with MAOIs. Semax modulates serotonergic and dopaminergic neurotransmission; combining with monoamine oxidase inhibitors creates unpredictable additive effects on monoaminergic tone and carries serious risk.
Caution with: concurrent psychiatric medications (SSRIs, stimulants, antidepressants), pregnancy and lactation (unstudied), and active psychiatric diagnoses requiring medication management — all of these require physician oversight rather than self-directed use.
Safety and Side Effects
Semax's clinical safety profile is, by peptide research standards, unusually well-characterized — a consequence of its Russian pharmaceutical registration in 1996, which required a formal safety package before approval.
Commonly reported in clinical use:
- Nasal irritation — the most frequent adverse event. Mild, transient, typically resolves within the first few doses. Delivery-related, not systemic.
- Transient stimulation / sleep disruption — if dosed too late in the day. Avoid afternoon and evening dosing.
- Mild overstimulation at high doses — jitteriness or restlessness at the upper end of the dosing range, particularly with the more potent variants. Dose-responsive; reduce dose.
Not reported in the clinical record:
- No known physical dependence or withdrawal
- No hepatotoxicity or nephrotoxicity in studies that examined organ function
- No HPA axis activation — despite the ACTH lineage, Semax does not drive cortisol
- No addiction mechanism — Semax does not engage dopamine receptor agonism, the pharmacological substrate of addictive dependence
The honest caveat: There are no long-term randomized controlled trials in humans outside the Russian system. The Russian clinical data is internally consistent and has the weight of a registered pharmaceutical behind it, but independent Western replication at scale doesn't exist. This is the standard epistemic limitation that applies across the entire nootropic peptide category. For the broader safety framework, see the peptide side effects guide.
FAQ
Is Semax legal in the US?
Semax is not FDA-approved and is not a licensed pharmaceutical in the United States. It exists in a legal gray area: it is not a scheduled controlled substance and is not explicitly prohibited, but it cannot be legally marketed for human consumption. It is sold as a research chemical for laboratory and research use only. The practical reality is that gray-market vendors operate in this space; quality, purity, and dosing accuracy vary significantly. Not a medical recommendation of any kind — this is just the current regulatory landscape.
Does Semax show up on drug tests?
No standard sports or employment drug test screens for Semax. It is not on any major anti-doping organization's prohibited list (WADA, USADA) and is not tested for in routine workplace or law enforcement drug screening. That said, specialized research panels are technically capable of detecting it, and the regulatory landscape evolves. Do your own due diligence for your specific context.
Can I stack Semax with BPC-157?
Yes — this is a biologically coherent and commonly used combination. BPC-157 modulates the gut-brain axis and has its own emerging neurological literature, including effects on dopaminergic signaling in the CNS and tissue repair. Pairing Semax's central BDNF-and-neuroplasticity drive with BPC-157's broader neurotrophic and gut-axis effects creates a stack that addresses both upstream and downstream substrates of cognitive function. If you're new to both compounds, the Beginner's Guide is the right starting point before combining them.
What's the difference between Semax and NA-Semax Amidate?
Standard Semax is the original registered pharmaceutical — unmodified, shorter half-life (30 min plasma, 4–6 hr functional window), all the published research. NA-Semax Amidate has N-terminal acetylation and C-terminal amidation — both ends protected from enzymatic degradation — giving it the longest half-life, the longest effect window, and the highest potency per microgram (estimated 20–30x more potent by weight than standard Semax). If you're new to Semax, start with the standard form. NA-Semax Amidate is for users who've already established baseline tolerance and want maximum duration.
How long does Semax take to work?
Intranasal onset is typically 15–20 minutes. Most users notice effects within 30 minutes of dosing. The functional effect window is 4–6 hours for standard Semax, 6–8 hours for NA-Semax, and longer for NA-Semax Amidate. Cumulative neuroplasticity effects — the BDNF-mediated changes to synaptic plasticity and connectivity — may build over days to weeks of consistent use rather than from a single dose.
Conclusion
Most cognitive enhancers work by trade-off. Stimulants drive dopamine receptor occupancy and produce focus — but at the cost of crash, dependence potential, and narrowing of cognitive flexibility over time. Anxiolytics reduce arousal and produce calm — but at the cost of cognitive blunting. The classical racetam-family nootropics produce diffuse effects through partly understood mechanisms that few users find reliably perceptible.
Semax is unusual because it doesn't work by trade-off. By simultaneously upregulating BDNF in the hippocampus and cortex, activating melanocortin receptors without HPA axis involvement, normalizing dopaminergic and serotonergic tone rather than spiking receptor occupancy, and protecting neurons from apoptosis under oxidative stress — it raises the active output of the brain without the costs that conventional cognitive enhancers accumulate.
The Russian space agency needed a molecule that would protect the human brain under conditions of extreme physiological stress while preserving cognitive function. What they built, 40-plus years ago in a Moscow laboratory, is arguably the most mechanistically complete nootropic peptide in the current toolkit.
Paired with Selank — the anxiolytic half of the Russian cognitive peptide dyad — Semax forms the two-molecule cognitive stack that the biohacking community has been slowly converging on: Selank dampening the noise floor, Semax raising the signal. If you're approaching this space for the first time, the Beginner's Guide to Peptides is the right entry point before running anything. For the full cognitive nootropic picture — Semax, Selank, Dihexa, and Pinealon — the Cognitive Peptides Hub is the reference.
All research purposes only. Not FDA-approved. Not a substitute for medical care. Consult a physician.
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