Cerluten

Cerluten is a natural peptide bioregulator derived from the cerebral cortex of young animals. It is designed to restore optimal gene expression and cellular function in brain tissue. Its benefits include improved cognition, reduced neuroinflammation, and enhanced neuronal repair in both aging and pathological states. Cerluten belongs to the Khavinson class of cytomedins—short peptides with high tissue specificity. It targets neurons and astroglial cells within the cerebral cortex, supporting protein synthesis, anti-apoptotic signaling, and regulation of inflammatory cascades. It is relevant for conditions like Alzheimer’s, post-stroke recovery, and cognitive aging.

- Experiencing age-related cognitive decline or neurodegenerative conditions

- Seeking to enhance memory, focus, and mental clarity

- Recovering from neurological injuries or strokes

- Supporting overall CNS health

- Mitigating chronic-stress effects on brain function

Mechanism of Action

How this peptide works in the body

DNA Binding and Epigenetic Regulation

Cerluten contains ultra-short peptide fragments capable of entering the nucleus and binding to specific sequences within promoter regions of neural genes. This interaction appears to occur through hydrogen bonding and minor groove fitting, particularly at AT- and GC-rich motifs. Once bound, these peptides recruit chromatin-modifying enzymes such as histone acetyltransferases (HATs), leading to acetylation of histones H3 and H4. This epigenetic modification relaxes nucleosome structure, increasing transcriptional accessibility. Additionally, Cerluten appears to inhibit DNA methyltransferases (DNMTs), reducing methylation of neurogenesis-associated genes and enhancing their expression in neurons and astrocytes.

Transcription Factor Modulation

Cerluten influences second messenger systems (e.g., cAMP) that activate protein kinase A (PKA), leading to phosphorylation of CREB (cAMP response element-binding protein). Phosphorylated CREB binds DNA at CRE (cAMP response element) sites and enhances transcription of genes like BDNF (brain-derived neurotrophic factor) and NGF (nerve growth factor), which promote synaptic plasticity and neuron survival. Simultaneously, the peptide downregulates the expression of stress-associated transcription factors such as p53 and FOXO3a, reducing caspase activation and suppressing programmed cell death.

Neuroinflammation and Cytokine Modulation

In glial cells and microglia, Cerluten downregulates the toll-like receptor 4 (TLR4) pathway, thereby reducing activation of the NF-κB transcription factor. This leads to decreased transcription of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α. The suppression of NF-κB also stabilizes the blood-brain barrier and reduces leukocyte infiltration. Additionally, Cerluten promotes upregulation of TGF-β and IL-10, shifting the microglial phenotype from M1 (pro-inflammatory) to M2 (neuroprotective), helping to prevent chronic neuroinflammation and glial scarring.

Neurotransmitter Regulation

Cerluten enhances synthesis of acetylcholine by upregulating the expression of choline acetyltransferase (ChAT) in cholinergic neurons. It also influences dopamine synthesis by supporting tyrosine hydroxylase (TH) transcription and reduces breakdown via mild inhibition of monoamine oxidase-A (MAO-A). These effects lead to improved synaptic neurotransmitter levels in the prefrontal cortex and hippocampus, improving cognition, executive function, and mood regulation.

Synaptic Plasticity and Axonal Integrity

Cerluten promotes structural synaptic remodeling by increasing the expression of GAP-43 (growth-associated protein 43) and synapsin I. GAP-43 facilitates axonal sprouting and regeneration, while synapsin I regulates synaptic vesicle availability and release. These molecular changes enhance long-term potentiation (LTP), the cellular basis of learning and memory. Furthermore, Cerluten appears to stimulate the PI3K/Akt pathway, which is essential for neurite outgrowth and axonal transport restoration following CNS injury.

Cellular Senescence and Longevity Signaling

Cerluten reduces expression of cell cycle arrest proteins such as p16^INK4a and p21^CIP1, which are typically elevated in senescent neurons. It simultaneously increases expression of sirtuins, particularly SIRT1 and SIRT6. These NAD⁺-dependent deacetylases modulate chromatin compaction, improve genomic stability, and enhance DNA repair through base excision repair (BER) pathways. This anti-senescence effect preserves neuron viability and function during aging or oxidative stress.

Mitochondrial Function and Antioxidant Pathways

Cerluten activates PGC-1α, the master regulator of mitochondrial biogenesis, via AMPK and SIRT1 signaling. This leads to increased production of mitochondria and improved oxidative phosphorylation (OXPHOS) efficiency. Additionally, Cerluten enhances expression of antioxidant genes such as SOD2 (superoxide dismutase), GPx (glutathione peroxidase), and HO-1 (heme oxygenase-1) via Nrf2 activation. This results in decreased mitochondrial ROS production and protection of mitochondrial DNA from oxidative damage, maintaining ATP output in neurons under metabolic stress.