Description

Semax — Advanced Biochemical Mechanism Profile

(Synthetic ACTH(4-10) analog; neuropeptide research compound)

Semax is a heptapeptide fragment derived from ACTH(4-10) engineered to retain neuromodulatory and neurotrophic signaling properties without interacting with classical melanocortin receptors in the same manner as ACTH.
In neuronal and glial research models, Semax has been shown to modulate BDNF expression, dopaminergic signaling, and oxidative-stress pathways through transcriptional and second-messenger regulation.

✅ 1. Primary Molecular Interactions (In-Vitro Evidence)

A. Neurotrophin Pathway Modulation

Studies demonstrate that Semax upregulates:

• BDNF

• GDNF

• NGF-related receptor signaling

This appears to involve:

• cAMP → PKA → CREB phosphorylation

• ERK1/2 activation

• Increased transcription of neuroplasticity-associated genes

B. Dopaminergic Regulation

Semax influences dopamine turnover and transport by modulating:

• Tyrosine hydroxylase (TH)

• Dopamine transporter (DAT, SLC6A3)

• Monoamine oxidase (MAOA)

Resulting effects observed in neuronal cultures:

• ↑ Dopaminergic synaptic signaling

• Altered release and reuptake dynamics

C. Antioxidant & Anti-Inflammatory Gene Expression

Semax has been shown to reduce expression of inflammatory mediators and enhance antioxidant coding genes via:

• NF-κB pathway inhibition

• Upregulation of Nrf2-associated genes

• Improvement of endogenous antioxidant enzyme transcription

✅ 2. Intracellular Signaling Pathways

A. ERK/MAPK Cascade

• Semax stimulates Ras → Raf → MEK → ERK1/2

• ERK1/2 translocates to the nucleus

• Triggers transcription of immediate early genes and neurotrophic factors

ERK-responsive genes commonly monitored:

• FOS

• JUN

• EGR1

• BDNF

B. cAMP → PKA → CREB

• Semax elevates cAMP in neuronal cells

• Activates PKA

• Phosphorylates CREB

• CREB regulates promoters for:

  • BDNF

  • NR4A1

  • Synaptic plasticity genes

C. Anti-oxidant / Cytokine Pathways

• ↓ TNF-α, IL-6, IL-1β

• ↑ SOD2, CAT, GPX1

• Linked to NF-κB inhibition and Nrf2 upregulation

✅ 3. Second Messengers & Enzymatic Outputs

✅ 4. Representative Gene Targets

✅ Mechanistic Summary

• Synthetic ACTH(4-10) analog

• Modulates cAMP/PKA/CREB and ERK1/2 pathways

• Upregulates BDNF, GDNF, and synaptic-plasticity genes

• Influences dopaminergic turnover and transporter expression

• Regulates oxidative-stress and cytokine gene transcription

Research-Only Classification

Semax is provided solely for controlled in-vitro laboratory research.
Not approved for human or animal administration, therapeutic use, or biological application outside research settings.