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Semax

Semax is a synthetic heptapeptide analogue of adrenocorticotropic hormone fragment ACTH(4–10) with the sequence Met-Glu-His-Phe-Pro-Gly-Pro. It acts as a neurotrophic factor inducer, upregulating brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF). In research settings, it is investigated for cognitive enhancement, neuroprotection, and neural recovery mechanisms in preclinical models of central nervous system injury.


Chemical Profile

Property Value
CAS Number 80714-61-0
IUPAC Name L-Methionyl-L-α-glutamyl-L-histidyl-L-phenylalanyl-L-prolylglycyl-L-proline
Amino Acid Sequence Met-Glu-His-Phe-Pro-Gly-Pro (7 amino acids)
Sequence (1-Letter) MEHFPGP
Molecular Formula C₃₇H₅₃N₉O₁₀S
Molecular Weight 706.83 g/mol
Purity (HPLC) ≥ 98%

Semax at a Glance

  • Class: Synthetic ACTH(4–10) analogue
  • Research Status: Preclinical and clinical (Russia, Ukraine)
  • Route: Intranasal (primary), intravenous, intramuscular
  • Half-life: ~30 minutes (intranasal)
  • CAS: 80714-61-0
  • MW: 706.8 Da
  • Key Feature: Neurotrophic factor inducer (BDNF, NGF, GDNF)

Mechanism of Action

Semax is a synthetic analogue of the N-terminal fragment 4–10 of adrenocorticotropic hormone (ACTH). Unlike the parent ACTH molecule, Semax is devoid of hormonal (corticotropic) activity but retains the CNS-active core sequence.

Primary Signaling Pathways

Component Detail
Primary Targets BDNF/TrkB signaling, NGF/TrkA, GDNF
Secondary Targets Dopamine (D₂) and serotonin (5-HT₂) receptors
Upstream Mechanism Activation of PKC and PKA signaling cascades
BDNF Induction 2–3 fold increase in BDNF expression in hippocampus and cortex
NGF Induction Significant NGF upregulation in cholinergic forebrain
CREB Activation Phosphorylated CREB → neuroplasticity gene expression
Neurotransmitter Modulation Increased striatal dopamine and serotonin turnover

Neuroprotective Effects

System Effect Mechanism
Cortex Reduced ischemic damage Antioxidant, anti-apoptotic
Hippocampus Enhanced LTP BDNF/TrkB → ERK/CREB
Striatum Dopaminergic protection Reduced neurotoxicity
Cholinergic System Preserved function NGF-mediated

Pharmacology

Parameter Value
Half-life (t½) ~30 minutes (intranasal); ~11 minutes (IV)
Bioavailability (IN) High (direct CNS delivery bypassing BBB)
Tmax ~5–10 minutes (intranasal)
Volume of Distribution (Vd) ~0.5 L/kg
Protein Binding ~30%
Metabolism Proteolytic cleavage by exopeptidases
Route Intranasal, intravenous, intramuscular
Elimination Renal (peptide fragments)
BBB Permeability Intranasal bypasses BBB; limited across IV route

Research Evidence

Study Model Findings Reference
Myasoedov et al. 1999 Clinical observation Reduced infarct volume and improved functional recovery scores DOI: 10.1007/s10517-006-0185-2
Dmitrieva et al. 2006 Rodent ischemia model 40% reduction in mortality; improved motor function DOI: 10.1007/s10517-006-0285-z
Lermontova et al. 2004 Aged rats Reversed age-related cognitive deficits DOI: 10.1023/B:NEUR.0000023367.38224.18
Gusev et al. 2005 Clinical observation Improved functional outcome (Barthel Index) at day 21 in post-stroke subjects DOI: 10.1007/s10517-005-0469-y
Dolotov et al. 2006 Cell culture (neurons) BDNF upregulation via MAPK/ERK pathway DOI: 10.1016/j.brainres.2006.06.010

Dosing Reference

Parameter Recommendation
Research Dose Range 200–600 μg daily (intranasal)
Dosing Timing Morning and/or early afternoon
Duration 1–3 months (cycle), with 2-week washout
Reconstitution 1–2 mL bacteriostatic water
Storage (Lyophilized) −20°C, desiccated, light-protected
Storage (Reconstituted) 2–8°C for up to 7 days

Safety Profile

Category Observations
Most Common Mild nasal irritation (intranasal)
Neurological Transient headache (rare)
CNS Well-tolerated; no sedation or stimulation at standard doses
Contraindications Research use only; not approved outside Russia
Drug Interactions Theoretical interactions with dopaminergic agents
Immunogenicity Low (endogenous amino acid sequence)

Physicochemical Properties

Property Value
Physical State White to off-white lyophilized powder
Solubility (Water) Soluble (> 40 mg/mL)
Solubility (Saline) Soluble (> 20 mg/mL)
logP ~ −3.2 (hydrophilic)
pI
Stability (Lyophilized)
Stability (Solution)

Synthesis Pathway

Semax (Met-Glu-His-Phe-Pro-Gly-Pro) is produced via standard solid-phase peptide synthesis (SPPS) using Fmoc chemistry.

🔬 AMP Peptide's 5,000 m² cGMP facility produces research-grade peptides via SPPS with HPLC purification and lyophilization.

Parameter Detail
Strategy Fmoc-SPPS on 2-chlorotrityl chloride resin
Coupling Reagents HBTU/HOBt in DMF with DIPEA activation
Fmoc Deprotection 20% piperidine in DMF (2 × 5 min, 1 × 15 min)
Cleavage Cocktail TFA/TIPS/H₂O (95:2.5:2.5, v/v)
Cleavage Time 2–3 h at room temperature
Crude Purification Preparative RP-HPLC (C18, 0.1% TFA/MeCN gradient)
Counterion Exchange Acetate form (lyophilization from 0.1 M AcOH)
Overall Yield 55–70% (crude); > 98% purity after purification

Analytical Methods

HPLC

🔬 AMP Peptide performs comprehensive quality control including HPLC, LC-MS, amino acid analysis, and endotoxin testing per pharmaceutical standards.

Parameter Condition
Column C18 (4.6 × 250 mm, 5 μm)
Mobile Phase A: 0.1% TFA in water; B: 0.1% TFA in acetonitrile
Gradient 5–40% B over 25 min
Flow Rate 1.0 mL/min
Detection UV 214 nm
Retention Time ~12–14 min

LC-MS

Parameter Condition
Ionization
Detected (M+H)+
MS/MS Fragments

Stability Data

Condition Storage Parameters Stability
Lyophilized (−20°C) Desiccated, light-protected, sealed vial ≥ 24 months
Lyophilized (4°C) Desiccated, light-protected, sealed vial ≥ 18 months
Lyophilized (25°C) Desiccated, light-protected, sealed vial ~3–6 months
Solution (2–8°C) Sterile water for injection, pH 4–6 7–10 days
Solution (−20°C) Sterile water for injection, rapid freeze 1–2 months
Solution (25°C) Sterile water for injection ≤ 24 h
Freeze-Thaw Stability 3 cycles, −20°C to 25°C < 5% degradation per cycle
Light Sensitivity UV-A/B exposure (direct sunlight, 4 h) ~10% degradation

Semax is susceptible to hydrolysis at Pro-Gly and Gly-Pro peptide bonds under prolonged solution storage. Proteolytic degradation by exopeptidases is the primary in vivo clearance mechanism. Lyophilized formulations stored at −20°C with desiccant and light protection provide the longest shelf life.


References

  1. Myasoedov NF, et al. (1999). Semax — a synthetic ACTH(4–10) analogue for CNS disorders. Bulletin of Experimental Biology and Medicine. DOI: 10.1007/s10517-006-0185-2
  2. Dmitrieva VG, et al. (2006). Semax in experimental stroke. Bulletin of Experimental Biology and Medicine. DOI: 10.1007/s10517-006-0285-z
  3. Lermontova NN, et al. (2004). Semax reverses age-related cognitive decline. Neurochemical Research. DOI: 10.1023/B:NEUR.0000023367.38224.18
  4. Gusev EI, et al. (2005). Semax in acute ischemic stroke. Bulletin of Experimental Biology and Medicine. DOI: 10.1007/s10517-005-0469-y
  5. Dolotov OV, et al. (2006). Semax induces BDNF expression via MAPK/ERK. Brain Research. DOI: 10.1016/j.brainres.2006.06.010
  6. Shishkina IV, et al. (2008). Semax pharmacokinetics after intranasal administration. Voprosy Meditsinskoi Khimii.
  7. Vako II, et al. (2007). Clinical effects of Semax in chronic ischemic brain disease. Zhurnal Nevrologii i Psikhiatrii.

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