Selank

Also identified as Thr-Lys-Pro-Arg-Pro-Gly-Pro

Tuftsin analogue

Sequence: Thr-Lys-Pro-Arg-Pro-Gly-Pro

Molecular weight: 751.9
Molecular formula: C33H57N11O9
CAS: 129954-34-3
Published studies reviewed: 12

FOR RESEARCH USE ONLY. NOT FOR HUMAN OR VETERINARY USE. NOT FOR HUMAN CONSUMPTION.

Compounds described on this site are supplied solely for laboratory research. They are not offered for human or veterinary use or for clinical use, and they are not intended to diagnose, mitigate, cure or prevent any disease.

Selank is the synthetic heptapeptide Thr-Lys-Pro-Arg-Pro-Gly-Pro, formed by extending the four residues of tuftsin with Pro-Gly-Pro. The twelve publications reviewed span enzyme and radioligand work, gene-expression studies in a human cell line and mouse spleen, an imaging study in healthy volunteers, and four Russian clinical studies. None of those clinical studies had a placebo arm, and three are recorded only as their English abstracts report them.

At a glance

Also identified as: Thr-Lys-Pro-Arg-Pro-Gly-Pro
Class: Tuftsin analogue
Target or mechanism: Enkephalin-degrading enzymes of human plasma and serum; [3H]GABA binding sites on brain cell plasma membranes
Evidence types represented: in vitro, animal, human
Published studies reviewed: 12
Last reviewed: 2026-09-21

Overview

Selank is a synthetic heptapeptide, Thr-Lys-Pro-Arg-Pro-Gly-Pro: the four residues of the immune peptide tuftsin extended by the tripeptide Pro-Gly-Pro.

Most of the published work on it comes from two Moscow institutes and much of it is in Russian-language journals, where PubMed often carries the abstract in English and nothing more. Everything recorded below is taken from an abstract this project pulled and read, except where a claim says it came from the full text.

The publications on this page are of five kinds: enzyme studies in human plasma and serum, a radioligand study on brain cell membranes, gene-expression studies in a human cell line and in mouse spleen, one imaging study in healthy volunteers, and four Russian clinical studies in people with psychiatric diagnoses, three of them comparisons against benzodiazepines.

Three of the four clinical studies are recorded as their English abstracts print them: none of those three describes how participants were allocated or whether anyone was blinded, and none prints a scale score, an effect size or a p-value for its clinical comparison. The fourth, a 70-person open-label study, was read in full and its figures are recorded, with the reasons to doubt its day-21 comparison stated beside them. None of the four has a placebo arm. Where a population is described as "the diagnoses named in the publication title", the title shown on the study card is the study's own wording of who was enrolled.

One thing is deliberately absent. The rat-brain transcriptome gene counts — the figures most often quoted for this peptide — are not recorded, because two publications report different counts in different brain regions and reconciling them is a prerequisite the owner set before either is published.

Mechanism under investigation

Selank

Enkephalin-degrading enzymes of human plasma and serum
[3H]GABA binding sites on brain cell plasma membranes

The publications recorded here report two separate lines of laboratory work: inhibition of the enzymes that degrade enkephalin in human plasma and serum, with IC50 values printed by each study, and modulation of [3H]GABA binding on isolated brain cell membranes. Neither line establishes a receptor this peptide binds as an agonist, and none of the human studies on this page was designed to establish a mechanism.

Scope of the published work

Areas investigated

Enkephalin-degrading enzyme activity
Carboxypeptidase specificity
GABA binding
Gene expression in immune tissue
Resting-state functional connectivity

Models used

Human plasma and serum in vitro
Rat brain cell membrane preparations
Human neuroblastoma IMR-32 cell culture
Mouse spleen
Imaging study in healthy volunteers
Clinical comparison studies against benzodiazepines
Human peripheral blood cell culture

Every human figure on this page was recorded in a controlled study, under supervision, using material prepared for that study, in a population selected by its entry criteria. It is not the research material PepGenex supplies and no result here transfers to it.

Limitations

Evidence represented on this page: in vitro, animal and human. The page reviews 12 published studies, and each figure is reported for the study that published it; results are not pooled across studies.

Common questions

What is Selank?

Selank is a synthetic heptapeptide, Thr-Lys-Pro-Arg-Pro-Gly-Pro: the four residues of the immune peptide tuftsin extended by the tripeptide Pro-Gly-Pro.

How does Selank work, according to the published research?

In radioligand binding on isolated brain cell plasma membranes, the peptide was reported to affect [3H]GABA binding as a positive allosteric modulator. Its joint action with certain benzodiazepines regulated [3H]GABA binding in a way the authors describe as not cumulative and different from either substance individually, and the peptide blocked the modulatory activity of diazepam and of olanzapine. (Vyunova et al., 2018, PMID 30255741)
Using Leu-enkephalin labelled with tritium at every residue, aminopeptidases, dipeptidylaminopeptidases and dipeptidylcarboxypeptidases were reported to account for approximately 80%, 2% and 10% of total enkephalin-degrading activity in human blood plasma, with a further pathway via carboxypeptidase accounting for approximately 6%. Bestatin predominantly inhibited aminopeptidases and carboxypeptidases, whereas Selank was reported to be more specific for carboxypeptidases and dicarboxypeptidases. (Zolotarev et al., 2004, PMID 15344652)
Reports that the heptapeptide dose-dependently inhibited enzymatic hydrolysis of plasma enkephalin, with an IC50 of 15 microM, and that it inhibited enkephalinases more strongly than the peptidase inhibitors bacitracin and puromycin. (Zozulya et al., 2001, PMID 11550013)

What has published research on Selank found, and what are its limits?

This page records 12 publications, reporting laboratory (in vitro) work in 6, animal work in 2, human work in 5. Each is listed with its identifier under References.

Human studies represented: Panikratova et al., 2020, PMID 32342318; Medvedev et al., 2015, PMID 26356395; Medvedev et al., 2014, PMID 25176261; Zozulia et al., 2008, PMID 18454096; Uchakina et al., 2008, PMID 18577961.

Evidence represented on this page: in vitro, animal and human.

The page reviews 12 published studies, and each figure is reported for the study that published it; results are not pooled across studies.

Is Selank approved by the U.S. FDA?

This page cites no FDA approval record for Selank; PepGenex Science states a U.S. regulatory status only where a sourced record exists.

PepGenex research materials are not FDA approved and are not for human or veterinary use.

What risks have published studies of Selank reported?

1 published human study on this page reports adverse events or safety measurements. Each is listed with its publication in the adverse-events section of this page.

Trial events do not establish a complete safety profile.

What adverse events have been reported in published studies of Selank?

Adverse events and safety measurements as reported by the published human studies on this page. Each entry is attributed to its publication.

Medvedev et al., 2015, PMID 26356395

Design and population: In an open-label, naturalistic study, 70 participants were randomly allocated to phenazepam alone (30 participants) or Selank added to phenazepam (40 participants) for 14 days; 20 of the 40 then continued Selank alone to day 21. Outcomes were assessed clinically and with the HADS (which the paper labels 'HDRS'; its methods define the hospital self-rating scale, not the Hamilton scale), the CGI and the Spielberger inventory; tolerability with the UKU scale; cognition with the Stroop and verbal fluency tests; and quality of life with the SF-36. Allocation and duration are from the full text, and no one was blinded. 70 people with diagnoses in ICD-10 categories F40.2–9, F41.1–9 and F45.0–2, described in the abstract as the disorders named in the title together with hypochondriac and somatoform disorders.
Events reported: With Selank added, the level of the adverse effects of phenazepam was reported to be lower — attention and memory impairment, asthenia, sedation, increased sleep duration, sexual disturbances, emotional indifference and orthostatism — both during the course and after phenazepam was withdrawn, and quality of life was reported to improve. No frequencies, UKU scores or statistics are printed.

Trial events do not establish a complete safety profile.

Published research

Grouped by the kind of study. Select one to narrow what is shown below.

Laboratory (in vitro)(5)

Laboratory (in vitro)

Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity.

Vyunova TV, Andreeva L, Shevchenko K, Myasoedov N, Protein and Peptide Letters, 2018;25(10):914-923

published

In radioligand binding on isolated brain cell plasma membranes, the peptide was reported to affect [3H]GABA binding as a positive allosteric modulator. Its joint action with certain benzodiazepines regulated [3H]GABA binding in a way the authors describe as not cumulative and different from either substance individually, and the peptide blocked the modulatory activity of diazepam and of olanzapine.
The authors state their conclusion as a hypothesis they tested and showed: that one molecular mechanism of the peptide can be associated with subtype-selective, concentration-dependent allosteric modulation of GABA receptors. They also note that the peptide's and the benzodiazepines' binding sites are apparently not the same, but may partially overlap.

Limitations

The two GABA-related records disagree in an informative way. A radioligand study on membrane preparations reports allosteric modulation of GABA binding; a study in a human neuroblastoma cell line reports no change at all in the mRNA levels of 84 GABAergic and neurotransmission genes under the peptide alone. Binding and transcription are different measurements, so neither refutes the other — but a page that showed only the first would read as settled, and it is not.

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Laboratory (in vitro)

GABA, Selank, and Olanzapine Affect the Expression of Genes Involved in GABAergic Neurotransmission in IMR-32 Cells.

Filatova E, Kasian A, Kolomin T, et al., Frontiers in Pharmacology, 2017;8:89

published

In cultured human neuroblastoma IMR-32 cells, no changes were found in the mRNA levels of the 84 genes studied under the effect of Selank on its own.
Combined with GABA, the peptide led to nearly complete suppression of the expression changes that GABA produced on its own; combined with olanzapine, more genes changed expression than with olanzapine alone. The authors read this as no direct effect on the mRNA levels of these genes in this cell line, with partial support for the hypothesis that the peptide affects the interaction of GABA with GABA-A receptors.

Limitations

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Laboratory (in vitro)

[Leu-enkephalin homogeneously labeled with tritium in studying the Selank inhibiting effect on the enkephalin-degrading enzymes of human plasma].

Zolotarev IuA, Sokolov OIu, Kost NV, et al., Bioorganicheskaia Khimiia, 2004;30(3):234-240

published

Using Leu-enkephalin labelled with tritium at every residue, aminopeptidases, dipeptidylaminopeptidases and dipeptidylcarboxypeptidases were reported to account for approximately 80%, 2% and 10% of total enkephalin-degrading activity in human blood plasma, with a further pathway via carboxypeptidase accounting for approximately 6%. Bestatin predominantly inhibited aminopeptidases and carboxypeptidases, whereas Selank was reported to be more specific for carboxypeptidases and dicarboxypeptidases.

Context

The enzyme work is the most consistently reported line on this page: three separate publications, two of them in human plasma or serum, agreeing that the peptide inhibits the enzymes that degrade enkephalin and printing IC50 values in the tens of micromolar. It is laboratory enzymology in isolated fluid, not a finding about anything happening in a person, and the two Russian-language papers were read as English abstracts of Russian articles.

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Laboratory (in vitro)

The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity.

Zozulya AA, Kost NV, Sokolov OYu, et al., Bulletin of Experimental Biology and Medicine, 2001;131(4):315-317

published

Reports that the heptapeptide dose-dependently inhibited enzymatic hydrolysis of plasma enkephalin, with an IC50 of 15 microM, and that it inhibited enkephalinases more strongly than the peptidase inhibitors bacitracin and puromycin.

Context

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Laboratory (in vitro)

[Semax and selank inhibit the enkephalin-degrading enzymes from human serum].

Kost NV, Sokolov OIu, Gabaeva MV, et al., Bioorganicheskaia Khimiia, 2001;27(3):180-183

published

In human serum, the inhibitory effect on enkephalin-degrading enzymes was dose-dependent, with an IC50 of 20 microM for Selank and 10 microM for Semax, both described as more pronounced than puromycin (IC50 10 mM) and bacitracin.
The pentapeptide fragments of both heptapeptides also showed an inhibitory effect, while their tri-, tetra- and hexapeptide fragments did not.

Context

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Preclinical (animal)(2)

Preclinical (animal)

The temporary dynamics of inflammation-related genes expression under tuftsin analog Selank action.

Kolomin T, Morozova M, Volkova A, et al., Molecular Immunology, 2014;58(1):50-55

published

C3 mRNA level in mouse spleen

Preclinical · 30 minutes · Mice

Arm	Reported
Selank, single dose	3-fold decrease

Over the same time course, Casp1 mRNA changed in a pattern the authors describe as wave-like, Il2rg mRNA changed significantly at early time points, and Xcr1 mRNA was reduced at 90 minutes. The dipeptide fragment Gly-Pro produced similar profiles for most of these genes.

Limitations

The rat-brain transcriptome figures that circulate for this peptide are not on this page. Two publications report different counts of genes changed, in different brain regions, by different methods, and the counts are held until that is reconciled. The mouse spleen records below are a separate, targeted 84-gene panel and are not those figures.

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Preclinical (animal)

Expression of inflammation-related genes in mouse spleen under tuftsin analog Selank.

Kolomin T, Shadrina M, Andreeva L, Slominsky P, Limborska S, Myasoedov N, Regulatory Peptides, 2011;170(1-3):18-23

published

In mouse spleen, 6 and 24 hours after a single dose, significant changes were reported in the expression of 34 of the 84 inflammation-related genes measured by real-time PCR, for the heptapeptide and for two of its fragments.
The Bcl6 gene showed significant changes in expression in response to each of the peptides tested, and changes were also observed for Bcl6 target and corepressor genes.

Limitations

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Human study (phase not stated)(5)

Human study (phase not stated)n = 52

Functional Connectomic Approach to Studying Selank and Semax Effects.

Panikratova YR, Lebedeva IS, Sokolov OY, et al., Doklady Biological Sciences, 2020;490(1):9-11

published

Resting-state functional MRI was carried out three times in each participant — before, and 5 and 20 minutes after Selank, Semax or placebo — to assess whole-brain functional connectivity of predefined regions of interest, which included the amygdala and the dorsolateral prefrontal cortex in each hemisphere.

52 healthy participants were studied. The abstract states no further entry criteria.

Between-group and between-condition differences were reported in functional connectivity between the right amygdala and a region spanning the fusiform, inferior and middle temporal and parahippocampal gyri of the right hemisphere. The authors describe general and specific effects of the two peptides on that connectivity. The abstract prints no numeric values, no effect sizes and no p-values.

Limitations

The one study in healthy volunteers reports an imaging signal with no numbers attached: its abstract states that connectivity differences were found and prints no value, no effect size and no p-value.

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Human study (phase not stated)n = 70

Medvedev et al., 2015 (title withheld on this site; see the publication record)

Medvedev VE, Tereshchenko ON, Kost NV, et al., Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 2015;115(6):33-40

published

In an open-label, naturalistic study, 70 participants were randomly allocated to phenazepam alone (30 participants) or Selank added to phenazepam (40 participants) for 14 days; 20 of the 40 then continued Selank alone to day 21. Outcomes were assessed clinically and with the HADS (which the paper labels 'HDRS'; its methods define the hospital self-rating scale, not the Hamilton scale), the CGI and the Spielberger inventory; tolerability with the UKU scale; cognition with the Stroop and verbal fluency tests; and quality of life with the SF-36. Allocation and duration are from the full text, and no one was blinded.

70 people with diagnoses in ICD-10 categories F40.2–9, F41.1–9 and F45.0–2, described in the abstract as the disorders named in the title together with hypochondriac and somatoform disorders.

On the HADS (labelled 'HDRS' in the paper), the positive effect of phenazepam was reported to be reached earlier when Selank was added. The abstract prints no scores, timepoints or statistics.
The paper defines a responder as a participant whose HADS total score (labelled 'HDRS') fell by 50% or more by day 14. At day 14, 23% of the phenazepam-alone group and 40% of the Selank-plus-phenazepam group met that definition — a difference that was not statistically significant (χ² = 2.6, p = 0.14).
After day 14, 20 participants from the Selank-plus-phenazepam group continued Selank alone for 7 more days while everyone else stopped. The paper says this continuation was to study tolerability and withdrawal, and does not say how the 20 were chosen. At day 21, 75% of those 20 met the responder definition, against 30% of the phenazepam-alone group after phenazepam was stopped (χ² = 9.7, p = 0.0018) and 25% of the Selank-plus-phenazepam participants who stopped at day 14 (χ² = 10, p = 0.0016). The comparison is open-label.
At day 21, the mean HADS total score (labelled 'HDRS') of the 20 participants who continued Selank alone was 30% lower than in the Selank-plus-phenazepam participants who stopped at day 14 (p < 0.05) and 40% lower than in the phenazepam-alone group after phenazepam was stopped (p < 0.01). The paper prints these as percentage differences with no absolute scores in the text, and does not say how the 20 were chosen. The comparison is open-label.
With Selank added, the level of the adverse effects of phenazepam was reported to be lower — attention and memory impairment, asthenia, sedation, increased sleep duration, sexual disturbances, emotional indifference and orthostatism — both during the course and after phenazepam was withdrawn, and quality of life was reported to improve. No frequencies, UKU scores or statistics are printed.

Limitations

The four clinical publications are the weakest records on this page for their size. All four are Russian-language articles in one journal, from one research network whose authors recur across all four. Three were read as English abstracts only: none of those describes how participants were allocated or whether anyone was blinded, none states the dose or route, and none prints a scale score, an effect size or a p-value. The fourth (the 70-person add-on study) was read in full: it was open-label with random allocation, and its responder and day-21 mean-score figures are recorded above — including a day-14 difference that was not significant and a day-21 comparison in a 20-person continuation group whose selection the paper does not describe. None of the four has a placebo arm, and one names a comparator in its title and reports no result for it. These are claims the authors made, and only one of them can be weighed from its own numbers.

Limitations

The day-21 figures compare people who were still taking a drug with people who had stopped one a week earlier. Both comparison groups had just stopped phenazepam, a benzodiazepine, at day 14, and symptoms commonly return or rebound for a period after a benzodiazepine is stopped. The 20 who continued were still taking Selank. So part or all of the day-21 difference may reflect the comparison groups coming off a benzodiazepine rather than anything Selank did; the paper does not separate the two. This caveat is this page's reading of the design, not something the paper states.

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Human study (phase not stated)n = 60

Medvedev et al., 2014 (title withheld on this site; see the publication record)

Medvedev VE, Tereshchenko ON, Israelian AIu, et al., Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 2014;114(7):17-22

published

A comparison of Selank with the benzodiazepine phenazepam in 60 people with diagnoses in ICD-10 categories F40.2–9, F41.1–9 and F45.0–1, which the abstract groups as the disorders named in the title together with somatoform disorders. The abstract does not give the split between arms, the allocation method, blinding, dose, route or duration.

The authors report pronounced anxiolytic and mild nootropic effects of Selank, an anxiolytic effect that lasted for a week after the last dose, and a positive effect on quality of life. The abstract reports no result for the phenazepam arm and no tolerability data, although both are named in the title, and prints no scores or statistics.

Limitations

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Human study (phase not stated)n = 62

Zozulia et al., 2008 (title withheld on this site; see the publication record)

Zozulia AA, Neznamov GG, Siuniakov TS, et al., Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 2008;108(4):38-48

published

Selank was compared with the benzodiazepine medazepam: 30 participants received Selank and 32 medazepam. Clinical state was assessed with the Hamilton and Zung scales and the Clinical Global Impression (CGI) scale, and enkephalin activity in blood serum was also measured. The abstract does not state how participants were allocated, whether anyone was blinded, or the dose, route or duration.

62 people with the two diagnoses named in the publication title were studied. The abstract gives no age range, sex split or further entry criteria.

The authors report that the anxiolytic effects of Selank and medazepam were similar, and that Selank also showed antiasthenic and psychostimulant effects. The abstract prints no scale scores, no between-group statistics and no p-values.
Participants had a decreased serum Leu-enkephalin half-life (τ1/2), which correlated with disease duration and with symptom severity; the abstract does not name the reference group it was lower than. The half-life increased during the course of Selank, mostly in participants with the first diagnosis named in the title, and its positive correlation with measured symptom level became stronger. No values are printed.

Limitations

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Laboratory (in vitro)Human study (phase not stated)

Uchakina et al., 2008 (title withheld on this site; see the publication record)

Uchakina ON, Uchakin PN, Miasoedov NF, et al., Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 2008;108(5):71-75

published

In peripheral blood cell culture, Selank at 10⁻⁷ M was reported to completely suppress IL-6 gene expression in cells from donors diagnosed with depression but not in cells from healthy controls, while IL-6 concentration in the culture from the diagnosed donors increased significantly (p < 0.05). The abstract gives no number of donors.
Changes in the Th1/Th2 cytokine balance were found in the serum of people with the diagnoses named in the publication title who received Selank for 14 days, and the dynamics of these changes showed a significant inverse correlation. The abstract gives no sample size, no comparison group and no cytokine values.

Limitations

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Compared with related compounds

Classification, structure, recorded targets, evidence types and FDA status only, each read from the two compounds' own pages. These comparisons do not compare study results.

Selank and Semax

Synthetic heptapeptide analogues of natural peptide fragments: tuftsin and ACTH(4-10).

	Selank	Semax
Classification	Tuftsin analogue	Synthetic ACTH(4-10) analogue
Structure	Sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro; formula C33H57N11O9	Sequence Met-Glu-His-Phe-Pro-Gly-Pro; formula C37H51N9O10S
Targets recorded	Enkephalin-degrading enzymes of human plasma and serum; [3H]GABA binding sites on brain cell plasma membranes	BDNF/trkB system (rat hippocampus)
Evidence types represented	in vitro, animal, human	in vitro, animal
Status with the U.S. FDA	Not shown (no Drugs@FDA application record verified for this page)	Not shown (no Drugs@FDA application record verified for this page)

References

Published studies reviewed (12)

The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity. — Zozulya AA, Kost NV, Sokolov OYu, et al., Bulletin of Experimental Biology and Medicine, 2001;131(4):315-317
DOI 10.1023/a:1017979514274 · PMID 11550013
View publication →
[Semax and selank inhibit the enkephalin-degrading enzymes from human serum]. — Kost NV, Sokolov OIu, Gabaeva MV, et al., Bioorganicheskaia Khimiia, 2001;27(3):180-183
DOI 10.1023/a:1011373002885 · PMID 11443939
View publication →
[Leu-enkephalin homogeneously labeled with tritium in studying the Selank inhibiting effect on the enkephalin-degrading enzymes of human plasma]. — Zolotarev IuA, Sokolov OIu, Kost NV, et al., Bioorganicheskaia Khimiia, 2004;30(3):234-240
DOI 10.1023/b:rubi.0000030126.09208.c3 · PMID 15344652
View publication →
Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. — Vyunova TV, Andreeva L, Shevchenko K, Myasoedov N, Protein and Peptide Letters, 2018;25(10):914-923
DOI 10.2174/0929866525666180925144642 · PMID 30255741
View publication →
GABA, Selank, and Olanzapine Affect the Expression of Genes Involved in GABAergic Neurotransmission in IMR-32 Cells. — Filatova E, Kasian A, Kolomin T, et al., Frontiers in Pharmacology, 2017;8:89
DOI 10.3389/fphar.2017.00089 · PMID 28293190 · PMC5328971
View publication →
Expression of inflammation-related genes in mouse spleen under tuftsin analog Selank. — Kolomin T, Shadrina M, Andreeva L, Slominsky P, Limborska S, Myasoedov N, Regulatory Peptides, 2011;170(1-3):18-23
DOI 10.1016/j.regpep.2011.05.001 · PMID 21609736
View publication →
The temporary dynamics of inflammation-related genes expression under tuftsin analog Selank action. — Kolomin T, Morozova M, Volkova A, et al., Molecular Immunology, 2014;58(1):50-55
DOI 10.1016/j.molimm.2013.11.002 · PMID 24291245
View publication →
Functional Connectomic Approach to Studying Selank and Semax Effects. — Panikratova YR, Lebedeva IS, Sokolov OY, et al., Doklady Biological Sciences, 2020;490(1):9-11
DOI 10.1134/S001249662001007X · PMID 32342318
View publication →
Zozulia et al., 2008 (title withheld on this site; see the publication record) — Zozulia AA, Neznamov GG, Siuniakov TS, et al., Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 2008;108(4):38-48
PMID 18454096
View publication →
Medvedev et al., 2014 (title withheld on this site; see the publication record) — Medvedev VE, Tereshchenko ON, Israelian AIu, et al., Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 2014;114(7):17-22
PMID 25176261
View publication →
Medvedev et al., 2015 (title withheld on this site; see the publication record) — Medvedev VE, Tereshchenko ON, Kost NV, et al., Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 2015;115(6):33-40
DOI 10.17116/jnevro20151156133-40 · PMID 26356395
View publication →
Uchakina et al., 2008 (title withheld on this site; see the publication record) — Uchakina ON, Uchakin PN, Miasoedov NF, et al., Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 2008;108(5):71-75
PMID 18577961
View publication →

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