Semax — Research Overview
Chemical Name: Met-Glu-His-Phe-Pro-Gly-Pro (methionine-glutamic acid-histidine-phenylalanine-proline-glycine-proline) Single-Letter Sequence: MEHFPGP Also Known As: Semax, ACTH(4-10) analog, synthetic ACTH(4-7)PGP; the name “Semax” derives from the Russian abbreviation for “seven amino acids” (СЕМь АминоКиСлот) Structure: Synthetic heptapeptide (7 amino acids) composed of the naturally occurring ACTH(4-7) fragment (Met-Glu-His-Phe) extended by the C-terminal tripeptide Pro-Gly-Pro for metabolic stability Parent Sequence: Adrenocorticotropic hormone (ACTH, corticotropin) fragment 4-10. ACTH is a pituitary hormone that stimulates cortisol production from the adrenal cortex. The ACTH(4-10) fragment — and shorter derivatives like ACTH(4-7) — retain the behavioral and nootropic effects of ACTH without its hormonal (adrenal-stimulating) activity. Semax preserves the neurotropic activity of the native melanocortin fragment while being completely free of hormonal activity. Development: Institute of Molecular Genetics, Russian Academy of Sciences, in collaboration with the V.V. Zakusov Research Institute of Pharmacology, under the direction of Nikolay Myasoedov. First described in scientific literature in 1991. Russian Regulatory Status: Registered as a prescription pharmaceutical in Russia for treatment of stroke, cerebrovascular insufficiency, and optic nerve disorders. Listed on the Russian government’s List of Vital and Essential Drugs since December 2011. Available as a 0.1% nasal spray. FDA/EMA Status: Not approved. No Western Phase 1-3 clinical trial registration as of this compilation. Sibling Compound: Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) — also a heptapeptide from the same Institute, also ending in Pro-Gly-Pro stabilization sequence. Selank is derived from tuftsin (IgG fragment) and has a primary anxiolytic profile. Semax is derived from ACTH(4-7) and has a primary neuroprotective and nootropic profile. Both share enkephalinase inhibition activity and were developed by the same research program. WADA Status: Not specifically listed on the WADA prohibited list as of this compilation. Category: ACTH(4-10) synthetic analog / melanocortin-system neuropeptide / BDNF/NGF upregulator / nootropic / neuroprotective research peptide / stroke treatment (Russian clinical use)
Research Use Only — Disclaimer
The scientific literature on this page is provided strictly for educational and informational purposes. All Rogue Compounds products are intended for in-vitro laboratory research use only and are not approved by the FDA for human or animal consumption. The studies referenced below are independent third-party peer-reviewed publications. Rogue Compounds makes no claims that any product diagnoses, treats, cures, or prevents any disease or condition. Researchers are responsible for compliance with all applicable local, state, and federal regulations.
What Is Semax?
Semax is a synthetic heptapeptide developed at the Institute of Molecular Genetics of the Russian Academy of Sciences as a metabolically stabilized, hormonally inert analog of the ACTH(4-10) fragment of adrenocorticotropic hormone. Its development was rooted in the decades-long research tradition characterizing the behavioral and neurotropic effects of ACTH and its fragments — a tradition that established that the melanocortin system influences learning, memory, and stress adaptation through mechanisms entirely independent of the hormonal (cortisol-stimulating) pathway associated with full-length ACTH.
The key structural insight underlying Semax’s development was that the ACTH(4-7) fragment (Met-Glu-His-Phe) retains essentially all of ACTH’s neurotropic activity while being completely devoid of its adrenal-stimulating hormonal effects — making it safe to administer at doses that would produce unacceptable hormonal effects with full ACTH. The addition of the Pro-Gly-Pro tripeptide to the C-terminus of ACTH(4-7) dramatically improved metabolic stability, extending the peptide’s biological activity from minutes to hours. The resulting heptapeptide MEHFPGP — Semax — combines the neurotropic pharmacophore of the ACTH N-terminal fragment with the stability enhancement required for practical therapeutic and research use.
Semax’s primary research and clinical significance centers on three interconnected biological activities: neuroprotection in ischemic and hypoxic injury contexts, nootropic effects on learning and memory through BDNF/TrkB axis upregulation, and monoamine neurotransmitter system modulation affecting serotonin, dopamine, and noradrenaline tone. These three activities are mechanistically connected through the BDNF/neurotrophin upregulation mechanism — BDNF supports synaptic plasticity (explaining cognitive enhancement), promotes neuronal survival under stress (explaining neuroprotection), and modulates dopamine and serotonin release and signaling (explaining monoamine effects). Semax’s clinical use in Russia for stroke treatment is directly grounded in these neuroprotective mechanisms.
ACTH and the Melanocortin Foundation
To understand Semax, the ACTH/melanocortin system must be understood in its neurotropic rather than hormonal context.
Adrenocorticotropic hormone (ACTH) is a 39-amino acid peptide produced by the anterior pituitary gland from the proopiomelanocortin (POMC) precursor — the same precursor that generates alpha-MSH, beta-MSH, gamma-MSH, and other melanocortin peptides. In its classical endocrine role, full-length ACTH stimulates cortisol biosynthesis from the adrenal cortex through MC2R activation.
Independent of this hormonal action, extensive research since the 1960s — pioneered by David de Wied in the Netherlands — established that ACTH fragments, particularly the ACTH(4-10) heptapeptide, profoundly influence learning, memory, and adaptive behavior in rodents. These behavioral effects are mediated through brain melanocortin receptors (MC3R, MC4R, MC5R) and do not require adrenal glands or cortisol production — they are direct central nervous system effects of the peptide fragment. The ACTH(4-10) fragment, while retaining these neurotropic properties, lacks the adrenal-stimulating activity of full-length ACTH.
This separation of neurotropic activity from hormonal activity in ACTH fragments was the foundational insight that made Semax’s development rationally feasible — a peptide that could be administered to produce CNS neurotropic effects without the endocrine consequences that would accompany ACTH therapy.
Mechanism of Action
BDNF and TrkB axis upregulation — the master neuroprotective and nootropic mechanism: The most extensively characterized molecular mechanism of Semax is its capacity to rapidly elevate brain-derived neurotrophic factor (BDNF) levels and the expression of its high-affinity receptor TrkB (tropomyosin receptor kinase B) in the hippocampus and other brain regions. A single intranasal application of Semax at 50 micrograms/kg produced a 1.4-fold increase in BDNF protein levels, a 1.6-fold increase in TrkB tyrosine phosphorylation (indicating activated signaling), and a 3-fold and 2-fold increase in BDNF and TrkB mRNA levels, respectively, in the rat hippocampus. Semax-treated animals showed significantly improved conditioned avoidance reactions — directly linking the BDNF/TrkB molecular changes to cognitive performance outcomes.
This BDNF/TrkB upregulation mechanism is central to all three of Semax’s primary activities. BDNF is essential for long-term potentiation, synaptic plasticity, and the structural changes underlying memory formation — explaining cognitive enhancement. BDNF promotes neuronal survival and activates anti-apoptotic signaling pathways — explaining neuroprotection. BDNF modulates dopamine and serotonin release from presynaptic terminals — explaining monoamine effects. The neurotrophin upregulation by Semax is therefore a mechanistic master switch that coordinates multiple downstream effects rather than a single isolated action.
Nerve growth factor (NGF) gene expression is also rapidly upregulated by Semax alongside BDNF — a rapid gene- and region-specific neurotrophin expression response observed in rat hippocampus and frontal cortex after intranasal administration. This combined BDNF and NGF upregulation provides a broader trophic support than BDNF alone.
Melanocortin receptor interactions — proposed but incompletely characterized: The exact receptor mechanism through which Semax initiates its cellular effects remains incompletely characterized. Evidence suggests Semax competitively antagonizes alpha-MSH at MC4R and MC5R, indicating it may act as an antagonist or partial agonist at these receptors — a mechanistically unusual profile given that other ACTH fragments typically act as agonists. Specific high-affinity binding sites for radiolabeled Semax have been identified in rat brain membranes (particularly basal forebrain), with dissociation constant KD of 2.4 nM and requirement for calcium ions — suggesting a specific and saturable receptor-like binding site. Whether this binding site corresponds to a known melanocortin receptor or represents a distinct site remains under investigation.
Serotonin and dopamine system modulation: Semax significantly elevated serotonin metabolism (measured as 5-HIAA, the primary serotonin metabolite) in the rat striatum — increasing extracellular 5-HIAA up to 180% of baseline within 1-4 hours of administration. This serotonergic activation contributes to antidepressant-like and anxiolytic-like effects observed in behavioral studies. Semax also potentiated dopamine release induced by D-amphetamine — suggesting a facilitatory modulatory role in dopaminergic transmission relevant to attention, motivation, and the cognitive enhancement associated with catecholamine signaling.
Enkephalinase inhibition — shared with Selank: Like Selank, Semax inhibits enzymes responsible for degradation of endogenous enkephalins, prolonging the duration of enkephalin signaling. Both compounds were shown to inhibit enkephalin-degrading enzymes from human serum with an IC50 of approximately 10 μM. This enkephalinase inhibitory activity contributes to the anxiolytic-like effects of Semax observed in behavioral studies and represents an additional convergence point between the mechanistic profiles of the two sibling neuropeptides.
Neuroprotection in ischemia — neurotrophin, VEGF, and immune gene expression: In cerebral ischemia models (permanent middle cerebral artery occlusion, pMCAO), Semax activates a coordinated transcriptional response involving neurotrophins (BDNF, NGF, neurotrophin-3), their high-affinity receptors (TrkA, TrkB, TrkC), and vascular endothelial growth factor (VEGF) gene family members. VEGF-B and VEGF-D are particularly affected, with Semax’s effects on these genes opposing the ischemia-induced changes — suggesting that Semax pharmacologically counteracts the dysregulation of these angiogenic and neuroprotective factors caused by the ischemic insult. Genome-wide transcriptional analysis additionally revealed that Semax enhances expression of immune-related genes in ischemic brain — including cytokines and immunoglobulins involved in anti-inflammatory post-ischemic responses — revealing an immunomodulatory dimension to neuroprotection not previously recognized.
Calcium signaling in hippocampal neurons: Application of Semax at 1 μM significantly increased the frequency of spontaneous intracellular calcium fluctuations in pyramidal layer cells of the hippocampal CA1 field — a measure of neuronal excitability and network activity. This calcium signaling effect in hippocampal pyramidal neurons is consistent with the BDNF-mediated enhancement of synaptic activity and long-term potentiation. Importantly, Semax did not affect proton-stimulated calcium entry in cerebellar granule cells through acid-sensing ion channels — establishing that the primary neuroprotective mechanism is unlikely to involve ASIC channel modulation in cerebellar neurons.
Anti-inflammatory immunomodulation in stroke: Clinical research in acute ischemic stroke patients demonstrated that Semax shifts the post-ischemic neuroinflammatory balance — increasing anti-inflammatory factors (interleukin-10) and modulating tumor necrosis factor-alpha while reducing pro-inflammatory mediators including interleukin-8 and C-reactive protein. This shift of neuromediatory balance toward anti-inflammatory agents provides a mechanism for reducing secondary inflammatory damage in the ischemic penumbra — the zone of potentially salvageable brain tissue surrounding the core infarct.
Published Research
Study 1 — Foundational Molecular Mechanism: BDNF and TrkB Regulation in the Hippocampus
Authors: Dolotov OV, Karpenko EA, Inozemtseva LS, Seredenina TS, Levitskaya NG, Rozyczka J, Dubynina EV, Novosadova EV, Andreeva LA, Alfeeva LY, Kamensky AA, Grivennikov IA, Myasoedov NF, Engele J Year: 2006 Journal: Brain Research PMID: 16996037 Full text: https://pubmed.ncbi.nlm.nih.gov/16996037/
This study was the primary characterization of Semax’s BDNF/TrkB molecular mechanism — the first demonstration that intranasal Semax directly upregulates both BDNF protein levels and TrkB receptor expression and activation in the rat hippocampus, and that these molecular changes are associated with cognitive improvement.
A single intranasal application of Semax at 50 micrograms/kg produced a maximal 1.4-fold increase in BDNF protein levels in rat hippocampus, a 1.6-fold increase in TrkB tyrosine phosphorylation, a 3-fold increase in exon III BDNF mRNA, and a 2-fold increase in TrkB mRNA.
Semax-treated animals showed a distinct increase in the number of conditioned avoidance reactions — cognitive performance improvement directly correlated with the BDNF/TrkB molecular changes, establishing the mechanistic link from neurotrophin upregulation to behavioral cognitive enhancement.
The authors concluded that Semax affects cognitive brain functions by modulating the expression and activation of the hippocampal BDNF/TrkB system — the first direct molecular mechanistic explanation for Semax’s established nootropic and cognitive-enhancing effects.
Study 2 — Monoamine System: Semax Activates Serotonergic and Dopaminergic Brain Systems
Authors: Eremin KO, Kudrin VS, Saransaari P, Oja SS, Grivennikov IA, Myasoedov NF, Rayevsky KS Year: 2005 Journal: Neurochemical Research PMID: 16362768 Full text: https://link.springer.com/article/10.1007/s11064-005-8826-8
This study directly characterized Semax’s effects on serotonin and dopamine neurotransmitter systems in rodent brain using microdialysis and tissue assay measurements.
Semax administration at 0.15 mg/kg significantly increased 5-HIAA (the primary serotonin metabolite) by 25% in striatal tissue 2 hours after administration. Extracellular striatal 5-HIAA gradually increased up to 180% of baseline within 1-4 hours — establishing robust and sustained serotonergic activation.
Semax alone did not alter tissue or extracellular dopamine concentrations — but when Semax was administered 20 minutes prior to D-amphetamine, it dramatically enhanced amphetamine’s effects on both extracellular striatal dopamine levels and locomotor activity. This potentiation of amphetamine-induced dopamine release suggests that Semax modulates the dopaminergic system’s responsiveness to activation rather than directly driving dopamine release.
The results established Semax as a positive modulator of both the striatal serotonergic system and the dopaminergic system’s responsiveness — providing neurochemical explanations for the antidepressant-like, anxiolytic-like, and motivational/attentional effects observed in behavioral studies, and for the proposed application of Semax in ADHD (where dopaminergic enhancement is therapeutically relevant).
Study 3 — Neurotrophin Upregulation in Stroke: Semax and PGP Activate BDNF, NGF, and TrkB After Cerebral Ischemia
Authors: Dmitrieva VG, Povarova OV, Skvortsova VI, Limborska SA, Myasoedov NF, Dergunova LV Year: 2010 Journal: Cellular and Molecular Neurobiology Full text referenced via: PMC11498467
This study characterized Semax’s neurotrophin gene expression effects in the ischemic context — demonstrating that the BDNF/TrkB upregulation mechanism active in intact brain is also operative and therapeutically relevant during acute ischemic injury.
Both Semax and its C-terminal tripeptide Pro-Gly-Pro activated transcription of BDNF, NGF, TrkA, TrkB, and TrkC in the cortex of rats subjected to permanent middle cerebral artery occlusion (pMCAO).
Semax enhanced transcription of BDNF, TrkC, and TrkA at 3 hours after occlusion, Nt-3 and NGF at 24 hours, and NGF at 72 hours — a temporally staged neurotrophin induction that spans the critical acute phase of ischemic injury during which penumbral neurons remain viable and potentially salvageable.
The profiles of neurotrophin gene activation under Semax and PGP treatment partially overlapped but were not identical — with PGP additionally enhancing neurotrophin receptor gene transcription at 24 hours in a manner not observed with Semax alone. Both Semax and its C-terminal fragment contribute to neuroprotective neurotrophin induction, providing insight into which structural components of Semax are responsible for which aspects of its biological activity.
Study 4 — Genome-Wide Analysis: Semax’s Immune and Vascular Gene Effects in Focal Ischemia
Authors: Medvedeva EV, Dmitrieva VG, Povarova OV, Limborska SA, Skvortsova VI, Myasoedov NF, Dergunova LV Year: 2014 Journal: BMC Genomics Full text: https://link.springer.com/article/10.1186/1471-2164-15-228
This genome-wide transcriptional analysis was the most comprehensive molecular characterization of Semax’s effects in brain ischemia — moving beyond targeted neurotrophin studies to characterize Semax’s effects across the entire transcriptome of ischemic brain cortex.
Semax’s gene expression effects were categorized into four broad subgroups: general biological processes, brain cell function, immune system, and vascular processes — establishing that Semax’s neuroprotective effects extend far beyond the neurotrophin axis that had been the primary focus of earlier mechanistic research.
Three hours after pMCAO, Semax influenced expression of genes affecting immune cell activity — 24 hours after pMCAO, the scope of immune system gene regulation by Semax increased considerably, with elevated transcripts encoding transmembrane receptors, cytokines, and immunoglobulins. This revealed a previously uncharacterized immunomodulatory dimension to Semax’s neuroprotective mechanism.
Semax’s effects on chemokine-encoding genes were notable — chemokines function as unique neuromediators that coordinate the interface between neurons and their microenvironment, including the inflammatory response that drives secondary injury in the ischemic penumbra.
The authors concluded that the neuroprotective and nootropic properties of Semax had been previously associated only with events directly relevant to nervous tissues, and that this genome-wide study revealed the additional action of Semax on the immune system for the first time — significantly expanding the mechanistic understanding of how Semax achieves neuroprotection in acute stroke.
Study 5 — Clinical Evidence: Semax Increases BDNF and Improves Motor Recovery in Ischemic Stroke Patients
Authors: Gusev EI, Martynov MYu, Kostenko EV, Petrova LV, Bobyreva SN (Pirogov Russian National Research Medical University) Year: 2018 Journal: Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova PMID: 29798983
This clinical study in 110 ischemic stroke patients directly evaluated Semax’s effects on plasma BDNF levels, motor performance, and functional outcome — providing the most directly human-relevant evidence connecting Semax’s neurotrophin mechanism to clinical outcomes.
110 patients after ischemic stroke were divided into early (89 days mean) and late (214 days mean) rehabilitation groups, each subdivided into Semax-receiving and non-Semax subgroups. The standard Semax regimen was 2 courses of 6,000 micrograms per day for 10 days each, with a 20-day interval.
Administration of Semax, regardless of the timing of rehabilitation, increased plasma BDNF levels which remained elevated throughout the entire study period — directly demonstrating that Semax’s BDNF-upregulating mechanism, characterized extensively in animal studies, is pharmacologically active in human stroke patients.
In Semax-negative subgroups, high BDNF plasma levels were positively correlated with early rehabilitation — confirming that endogenous BDNF elevation from exercise and rehabilitation independently supports recovery. Semax pharmacologically replicated and sustained this BDNF elevation.
Semax administration and high BDNF levels accelerated the improvement and ameliorated the final outcome of Barthel Index scores (the standard functional outcome measure in stroke rehabilitation). A positive correlation was observed between BDNF plasma levels and Barthel scores, as well as between early rehabilitation and motor performance improvement.
The authors concluded that early rehabilitation and Semax administration increase BDNF plasma levels, speed functional recovery, and improve motor performance in post-stroke patients — directly linking the neurotrophin mechanism to clinical functional outcomes in humans.
Study 6 — Acute Stroke Treatment: Early Clinical Evidence
Authors: Gusev EI, Skvortsova VI, Myasoedov NF et al. Year: 1997 (original); reviewed extensively in subsequent publications PMID: 11517472 (later study), referenced via multiple clinical publications
This early clinical study evaluated Semax in 30 patients in the acute phase of hemispheric ischemic stroke, compared with 80 control patients treated with conventional therapy — establishing the foundational clinical evidence for Semax’s utility in acute stroke treatment.
Semax in combined intensive therapy of acute ischemic stroke influenced the rate of restoration of damaged neurological functions — specifically increasing the regression of general cerebral and focal symptoms, especially motor disorders.
EEG monitoring and somatosensory evoked potential analysis documented electrophysiological correlates of neurological improvement in Semax-treated patients, providing objective neurophysiological evidence beyond clinical rating scales alone.
Mechanistic studies in the same patient population documented the immunobiochemical basis of neuroprotection — shifting the neuroinflammatory balance toward anti-inflammatory mediators including elevated IL-10 and modulation of TNF-alpha while reducing pro-inflammatory IL-8 and C-reactive protein levels. This anti-inflammatory shift in post-ischemic brain represents a pharmacological reduction of secondary inflammatory injury.
Semax showed angioprotective, antihypoxic, and neurotrophic activity in the experimental doses studied — the convergence of these three independent neuroprotective mechanisms (vascular protection, hypoxia resistance, and neurotrophin support) providing mechanistic coherence for the clinical benefit observed.
Semax vs Selank — Completing the Sibling Comparison
Semax and Selank represent complementary research tools from the same laboratory program, with meaningfully different primary pharmacological profiles that should not be conflated.
Both compounds are synthetic heptapeptides ending in the Pro-Gly-Pro C-terminal stabilization sequence. Both inhibit enkephalin-degrading enzymes. Both were developed by the Myasoedov laboratory at the Institute of Molecular Genetics. Both are registered pharmaceuticals in Russia.
Semax (ACTH 4-7 derived, MEHFPGP) has its primary research significance in neuroprotection and nootropic cognitive enhancement — registered for acute stroke, cerebrovascular insufficiency, and optic nerve disorders. Its defining mechanism is BDNF/NGF upregulation, with strong ischemia neuroprotection data and human clinical evidence in stroke populations.
Selank (tuftsin derived, TKPRPGP) has its primary research significance in anxiety and stress modulation — registered for generalized anxiety disorder and neurasthenia. Its defining mechanism is GABAergic modulation and enkephalinase inhibition producing benzodiazepine-comparable anxiolysis without adverse effects, with clinical data from anxiety disorder patient populations.
For research designs targeting neuroprotection, cognitive enhancement, stroke-relevant neurotrophin biology, or monoamine neurotransmitter modulation — Semax is the appropriate tool. For research designs targeting anxiety mechanisms, GABAergic modulation without sedation, or immunomodulatory anxiolysis — Selank is the appropriate tool. The two compounds are complementary, not interchangeable.
Semax and Optic Nerve Disease
A notable and distinctive clinical application area for Semax is optic nerve pathology. Russian clinical research documented the therapeutic effect of Semax (0.1% nasal drops) in optic nerve atrophy — including atrophy of inflammatory or toxic-allergic etiology. The mechanistic basis is consistent with Semax’s neuroprotective mechanism in stroke: BDNF upregulation promotes retinal ganglion cell survival, NGF supports optic nerve fiber maintenance, and improved trophic supply to the optic nerve through vascular and neurotrophin mechanisms parallels the ischemia neuroprotection pathway. Given that glaucomatous optic neuropathy shares pathological mechanisms with chronic cerebral ischemia (including retinal ganglion cell loss through ischemic and excitotoxic mechanisms), the rationale for Semax in optic disease is mechanistically grounded in the same neurotrophic and vascular biology characterizing its stroke application.
Honest Assessment of Research Limitations
Semax’s evidence base carries important honest limitations that are consistent with those described for Selank.
The primary research program is concentrated in Russia with the originating Myasoedov laboratory and clinical collaborators. Independent external replication by researchers not affiliated with this program is limited, though the molecular mechanistic findings (BDNF upregulation, monoamine effects) have been confirmed in some cases by independent groups.
The clinical stroke and cerebrovascular evidence, while published and meaningful, predates modern rigorous trial design standards in many cases — early studies lacked appropriate blinding in some cases and had relatively small sample sizes by current standards. The 2018 Gusev et al. study in 110 stroke patients represents more recent and better-designed clinical evidence but still within the Russian research system rather than through Western regulatory agency trial programs.
The mechanism of action at the receptor level remains incompletely resolved. Semax does not act through a clearly identified single receptor the way conventional pharmacological agents do — the BDNF/neurotrophin upregulation appears mechanistically primary, but how Semax initiates this upregulation at the molecular level (through which receptor, signaling cascade, or chromatin regulatory mechanism) remains an active research question.
No FDA or EMA approval exists, and no Western registration trial program has been initiated as of this compilation. Researchers outside Russia and Eastern Europe should treat Semax as a pharmacologically compelling but insufficiently externally validated neuroprotective research compound with a promising preclinical and Russian clinical evidence base.
Current Research Status
Semax is registered in Russia as a 0.1% nasal spray for treatment of stroke, cerebrovascular insufficiency, and optic nerve disorders. Listed on Russia’s List of Vital and Essential Drugs since 2011. Research continues on mechanisms of BDNF upregulation, expanded neurological applications including Parkinson’s disease models and ADHD, and potential applications in peripheral nerve injury. No FDA or EMA approval exists.
Reconstitution Note
Semax is supplied as lyophilized powder. Bacteriostatic water is the standard reconstitution solvent. The registered Russian pharmaceutical formulation is a 0.1% nasal spray. Semax dissolves readily in aqueous solution. Protect from light. Always confirm the recommended solvent against the specific lot datasheet before reconstitution.
In-Use Period and Storage
Before Reconstitution — Lyophilized Powder
Rogue Compounds stores all products refrigerated prior to shipping to maintain compound integrity from production through to delivery. Upon receipt researchers should store vials at 2 to 8 degrees Celsius immediately. Keep vials sealed, dry, and away from direct light until ready for use. Do not freeze. Repeated freeze-thaw cycling has been documented in peer-reviewed pharmaceutical formulation literature to accelerate structural degradation even in dry powder form, potentially compromising molecular integrity and experimental reproducibility.
Why We Refrigerate Instead of Freeze
Freezing and thawing introduces mechanical and osmotic stress at the molecular level. Published pharmaceutical research identifies freeze-thaw cycling as a significant risk factor for loss of structural integrity in peptides and protein-based compounds. To protect compound quality at every stage of handling and fulfillment, Rogue Compounds maintains refrigerated rather than frozen cold chain storage throughout the entire process.
After Reconstitution — Liquid Solution
Store reconstituted solutions refrigerated at 2 to 8 degrees Celsius immediately after preparation. Protect from light. Avoid repeated freeze-thaw cycles. Use within the timeframe recommended for the individual compound. Label each aliquot with the compound name, concentration, date of reconstitution, and diluent used. Discard any solution that shows visible particulate matter, discoloration, or signs of contamination.
Note: Storage and in-use recommendations on this page are provided as general laboratory guidance based on standard peptide handling practices documented in peer-reviewed pharmaceutical literature. Researchers should always refer to the individual compound’s published research literature and datasheet for any specific requirements. All products sold by Rogue Compounds are intended strictly for in-vitro laboratory research use only.
Available from Rogue Compounds
View the Semax product page: https://roguecompounds.com/product/semax/