NEURO REGENERATION 1 - 10ml+100ml

ADVANCED DELIVERY SYSTEM - CELL PENETRATING PEPTIDE TECHNOLOGY

This product utilizes advanced delivery technology incorporating calibrated cell-penetrating peptide (CPP) systems. The formulation is engineered to support efficient and targeted intracellular delivery of active ingredients, contributing to enhanced transport performance and bioavailability under controlled laboratory conditions.

SPECIFICATIONS

Product Code: NR1030L

COLIVELIN - 100 mg

Sequence: H-Ser-Ala-Leu-Leu-Arg-Ser-Ile-Pro-Ala-Pro-Ala-Gly-Ala-Ser-Arg-Leu-Leu-Leu-Leu-Thr-Gly-Glu-Ile-Asp-Leu-Pro-OH

Molecular Formula: C119H206N32O35

Molecular Weight: 2645.13 g/mol

CAS: 867021-83-8

Purity: Technical / Research Grade ≥98%

CORTAGEN - 100 mg

Sequence: L-Ala-L-Glu-L-Asp-L-Pro

Molecular Formula: C17H26N4O9

Molecular Weight: 430.41 g/mol

CAS: 335591-03-2

Purity: Technical / Research Grade ≥98%

HUMANIN G - 10 mg

HNG (Humanin-G) is an analog of Humanin, generated by S14G (serine-14-glycine)

Sequence: H-Met-Ala-Pro-Arg-Gly-Phe-Ser-Cys-Leu-Leu-Leu-Leu-Thr-Gly-Glu-Ile-Asp-Leu-Pro-Val-Lys-Arg-Arg-Ala-OH

Molecular Formula: C118H202N34O31S2

Molecular Weight: 2657,3 g/mol

CAS: 330936-70-4

Purity: Technical / Research Grade ≥98%

General Properties 

Other details: No TFA Salt

Form: Liquid Solution

Color: Clear / Slightly opalescent

Total Content: 210 mg in 10 mL (21 mg/mL total peptide concentration)

Concentration per mL:  Colivelin: 10 mg; Cortagen: 10 mg; Humanin G: 1 mg

Approximate Sprays per Bottle: ~82

Approximate Peptide per Spray: Colivelin ~ 1.22 mg + Cortagen ~ 1.22 mg + Humanin G ~ 0.12 mg  per spray 

Vehicle / Carrier System: Proprietary carrier system

Storage Temperature: 4°C (Do not freeze)

Source: Synthetic

Safety classification: Standard handling

J-147 - 450 mg

2,2,2-Trifluoroacetic acid 1-(2,4-Dimethylphenyl)-2-[(3-methoxyphenyl)methylene]hydrazide

Molecular Formula: C18H17F3N2O2

Molecular Weight: 350.33 g/mol

CAS: 1146963-51-0

Purity: Technical / Research Grade ≥99%

NSI-189 PHOSPHATE - 1200 mg

(2-((3-Methylbutyl)amino)-3-pyridinyl)(4-(phenylmethyl)-1-piperazinyl)-methanone phosphate

Molecolar Formula: C22H33N4O5P

Molecular Weight: 464.5 g/mol

CAS: 1270138-41-4

Purity: Technical / Research Grade ≥99%

General Properties 

Form: Liquid Solution

Color: Clear / Slightly opalescent

Total Content: 1650 mg in 100 mL (16.50 mg/mL total concentration)

Concentration per mL:  J-147: 4.50 mg; NSI-189 Phosphate: 12 mg

Vehicle / Carrier System: Proprietary carrier system

Storage Temperature: 4°C (Do not freeze)

Source: Synthetic

Safety classification: Standard handling

DESCRIPTION

Neuro Regeneration 1 is a structured multi-component formulation designed to support research into the coordinated biological processes involved in neuronal survival, synaptic plasticity, mitochondrial stability, and structural neural adaptation under stress conditions. Neural decline does not occur through a single isolated pathway. Whether triggered by metabolic stress, oxidative burden, protein aggregation, ischemic challenge, chronic inflammation, or age-associated mitochondrial dysfunction, neuronal compromise follows a recognizable biological cascade:

• Mitochondrial instability and reduced ATP production
• Increased reactive oxygen species (ROS) and redox imbalance
• Activation of pro-apoptotic signaling pathways
• Synaptic destabilization and dendritic spine loss
• Reduced neurotrophic support
• Impaired neurogenesis within hippocampal regions
• Progressive network-level dysfunction

Effective neural adaptation requires coordination across multiple structural and metabolic domains simultaneously. This formulation reflects the biological reality that neuronal resilience depends on synchronized regulation of:

• Mitochondrial bioenergetics
• Anti-apoptotic signaling networks
• Synaptic architecture maintenance
• Neurotrophic factor expression
• Redox balance
• Neurogenesis and circuit remodeling

Rather than focusing on a single molecular mechanism, Neuro Regeneration Complex is structured to explore how these domains interact when addressed in parallel. The integrated structure focuses on:

• Mitochondrial stabilization and ATP regulation
• Reduction of oxidative stress burden
• Modulation of apoptosis-related pathways
• Preservation of synaptic structure and plasticity
• Activation of neurotrophic cascades (BDNF-related signaling)
• Support of hippocampal neurogenesis
• Regulation of inflammatory and stress-associated signaling

Mitochondrial Stability and Cellular Energy Regulation

Neurons are among the most energy-dependent cells in the body. ATP production supports synaptic transmission, vesicle recycling, dendritic spine maintenance, axonal transport, and membrane potential stability. When mitochondrial function declines:

• ATP production decreases
• ROS production increases
• Membrane potential destabilizes
• Pro-apoptotic cascades become activated

Several components in this formulation have been investigated for their interaction with mitochondrial bioenergetics, ATP synthase modulation, redox balance, and adaptive metabolic signaling. Stabilizing mitochondrial function supports:

• Synaptic energy availability
• Reduced oxidative amplification
• Improved cellular stress tolerance
• Preservation of neuronal structure

Energy regulation is foundational to neural resilience.

Regulation of Apoptotic Signaling

Programmed cell death in neurons is tightly regulated by mitochondrial and cytosolic signaling networks involving BCL-2 family proteins, cytochrome c release, caspase activation, and JAK/STAT-associated pathways. Under proteotoxic or ischemic stress, these pathways can become amplified, leading to neuronal loss.  Humanin-family peptides and related constructs have been studied for interaction with apoptosis-regulating protein networks and survival-associated gene expression. Modulation of these pathways supports:

• Limitation of stress-induced cell death
• Maintenance of neuronal population density
• Protection against metabolic collapse

Balanced apoptosis regulation is central to long-term neural integrity.

Synaptic Plasticity and Structural Maintenance

Cognitive performance depends on synaptic integrity. Dendritic spines, postsynaptic density proteins, receptor turnover, and cytoskeletal organization define synaptic strength and adaptability. Under stress conditions:

• Spine density may decline
• LTP (long-term potentiation) becomes impaired
• Glutamatergic signaling destabilizes
• Hippocampal network coordination weakens

Components in this formulation have been associated with preservation of synaptic protein phosphorylation patterns, dendritic spine density, and restoration of LTP amplitude in experimental paradigms. Synaptic stabilization supports:

• Learning-associated signaling
• Memory encoding processes
• Network-level plasticity
• Circuit resilience under stress

Neuroregeneration is not only cell survival, it is synaptic architecture preservation.

Neurotrophic Support and BDNF-Associated Cascades

Brain-derived neurotrophic factor (BDNF) plays a central role in neuronal survival, dendritic growth, synaptic strengthening, and neurogenesis. Activation of BDNF/TrkB signaling engages:

• PI3K/Akt survival pathways
• MAPK/ERK plasticity cascades
• CREB-related transcriptional programs
• Cytoskeletal remodeling processes

Several molecules in this complex have been associated with increased hippocampal BDNF expression and enhanced downstream signaling activity. Neurotrophic support contributes to:

• Structural plasticity
• Synaptic resilience
• Integration of newly formed neurons
• Adaptive network remodeling

Oxidative Stress and Redox Balance

Neural tissue is highly susceptible to oxidative stress due to elevated metabolic demand and lipid-rich membranes. Excess ROS contributes to:

• Lipid peroxidation
• Protein oxidation
• DNA damage
• Activation of inflammatory transcription factors

Components in this formulation have been investigated for their influence on:

• ROS modulation
• Lipid peroxidation reduction
• Redox-sensitive transcription factor activity
• Neuroinflammatory marker attenuation

Redox balance supports long-term neuronal stability and synaptic preservation.

Hippocampal Neurogenesis and Structural Adaptation

The hippocampus retains the capacity for adult neurogenesis, particularly within the dentate gyrus. Chronic stress, glucocorticoid exposure, metabolic dysfunction, and inflammatory states are associated with reduced neurogenesis and hippocampal volume decline. NSI-189 and neurotrophic-associated mechanisms have been studied for:

• Increased progenitor cell proliferation
• Enhanced survival of newly formed neurons
• Improved integration into hippocampal circuits
• Expansion of dendritic networks

Structural adaptation at the hippocampal level influences:

• Contextual memory processing
• Emotional regulation circuits
• Stress resilience

Neuroregeneration involves not only protecting existing neurons but supporting structural renewal.

Integrated Neural Resilience Framework

Neurodegenerative processes are multi-factorial. They involve metabolic disruption, mitochondrial decline, oxidative stress amplification, apoptotic activation, synaptic instability, and reduced neurogenesis occurring concurrently. Addressing only one domain leaves other destabilizing factors active. Neuro Regeneration Complex reflects a coordinated strategy exploring:

• Mitochondrial energy stabilization
• Anti-apoptotic network support
• Synaptic structural preservation
• Neurotrophic activation
• Redox regulation
• Hippocampal structural renewal

The goal is not isolated pathway modulation but integrated neural resilience.

Integrated Conclusion

Neuronal survival, synaptic plasticity, and cognitive network stability depend on synchronized regulation of mitochondrial function, oxidative balance, apoptosis control, and neurotrophic signaling. Neuro Regeneration Complex is structured to support advanced research into these coordinated mechanisms governing neuronal structural maintenance and adaptive neural remodeling under stress conditions.

Individual Component Roles

• Colivelin: Colivelin is a 26–amino-acid synthetic hybrid peptide derived from the humanin (HN) family. It combines a modified humanin segment with a fragment of activity-dependent neurotrophic factor (ADNF), allowing simultaneous engagement of convergent neuroprotective signaling pathways. It has been investigated for modulation of beta-amyloid–associated neuronal stress and resistance to apoptosis. Research has explored its influence on STAT3 and JAK/STAT signaling, pathways associated with survival gene expression and neuronal resilience. In amyloid-related and ischemia models, Colivelin has been examined for effects on synaptic plasticity, axonal integrity, neuroinflammatory markers, and stress-responsive gene regulation.
• Cortagen: Cortagen is a tetrapeptide studied for modulation of neuronal functional activity in both central and peripheral nervous tissues. Observations associate it with normalization of metabolic parameters, enhancement of antioxidant defenses, and improvement of electrophysiological indices. It has demonstrated reduction of lipid and protein peroxidation within cortical tissue under oxidative stress conditions. In craniocerebral injury models, Cortagen has been evaluated for influence on motor coordination, learning performance, and neuromuscular recovery. In peripheral nerve compression paradigms, it has been associated with improved electrophysiological regeneration parameters. Exploratory cognitive observations have described improvements in attention, short-term memory, and psychophysiological indices.
• Humanin G: Humanin G is a mitochondrial-derived cytoprotective micro-peptide belonging to the humanin family. It has been investigated for anti-apoptotic signaling and mitochondrial stabilization under proteotoxic and oxidative stress conditions. A central mechanism involves interaction with apoptosis-regulating protein networks, including BCL-2 family members, limiting mitochondrial initiation of programmed cell death. In amyloid-related research models, Humanin analogs have been examined for attenuation of beta-amyloid toxicity and preservation of synaptic stability. It has also been studied in vascular stress contexts for association with reduced oxidative damage. Low Humanin levels have been reported in association with mitochondrial dysfunction, aging, metabolic dysregulation, and neurodegenerative conditions. Reported effects include modulation of JAK2–STAT3 and ERK1/2 pathways, improved ATP production, and inhibition of pro-apoptotic proteins.
• J-147: J-147 was developed to protect neurons under metabolic and proteotoxic stress typical of aging-related decline. The α-subunit of mitochondrial ATP synthase (ATP5A) has been identified as a functional target, with modulation influencing ATP production, proton flux, and mitochondrial membrane stability. Associated effects include reduced excessive ROS production, stabilization of membrane potential, and decreased pro-apoptotic signaling. Through modulation of the AMP/ATP ratio, J-147 has been linked to AMPK activation, mitochondrial biogenesis support, and adaptive metabolic regulation. In amyloid-accumulation paradigms, it has been associated with reduced soluble Aβ species and preservation of hippocampal synaptic architecture. Increased hippocampal BDNF expression, improved synaptic protein phosphorylation patterns, and stabilization of dendritic spine density have also been reported.
• NSI-189 Phosphate: NSI-189 is a synthetic small molecule developed to investigate hippocampal neurogenesis and structural decline under chronic stress conditions. It has been associated with increased proliferation of neuronal progenitor cells, enhanced survival of newly formed neurons, and improved synaptic integration within hippocampal circuits. Chronic exposure in experimental paradigms has been linked to increased hippocampal volume, consistent with expanded dendritic density and synaptic network development. Proposed mechanisms include modulation of glucocorticoid receptor–related pathways and increased neurotrophic marker expression, including BDNF-associated signaling. Beyond neurogenesis, changes in glutamatergic and monoaminergic circuitry have been discussed in relation to structural and functional network adaptation.

REFERENCES

M. Yamada et al., "Nasal Colivelin Treatment Ameliorates Memory Impairment Related to Alzheimer's Disease" [Nature]

M. Matsuoka et al., "Humanin and colivelin: neuronal-death-suppressing peptides for Alzheimer's disease and amyotrophic lateral sclerosis" [PubMed]

K. Oikawa et al., "P2-328: The role of colivelin, a novel neuroprotective peptide, on hippocampal synaptic plasticity" [The Journal of the Alzheimer's Association]

V. Khavinson et al., "Tetrapeptide stimulating functional activity of neurones, pharmacological agent based thereon and method of use thereof" [USP]

D.V. Kurkin et al., "Neuroprotective action of Cortexin, Cerebrolysin and Actovegin in acute or chronic brain ischemia in rats" [PubMed]

Shabanov, Vislobokov "Neuronoprotective action of cortexin and cortagen" [Reviews on Clinical Pharmacology and Drug Therapy]

M. Matsuoka "Humanin; a defender against Alzheimer's disease?" [PubMed]

P.G. Sreekumar et al., "The Mitochondrial-Derived Peptide Humanin Protects RPE Cells From Oxidative Stress, Senescence, and Mitochondrial Dysfunction" [ResearchGate]

S.C. Zàrate et al., "Humanin, a Mitochondrial-Derived Peptide Released by Astrocytes, Prevents Synapse Loss in Hippocampal Neurons" [PubMed]

A.R. White et al., "Sublethal concentrations of prion peptide PrP106-126 or the amyloid beta peptide of Alzheimer's disease activates expression of proapoptotic markers in primary cortical neurons" [PubMed]

P.A. Lapchak et al., "J-147 a Novel Hydrazide Lead Compound to Treat Neurodegeneration: CeeTox™ Safety and Genotoxicity Analysis" [PubMed]

D. Kepchia et al., "The Alzheimer's disease drug candidate J147 decreases blood plasma fatty acid levels via modulation of AMPK/ACC1 signaling in the liver" [PubMed]

M. Prior et al., "The neurotrophic compound J147 reverses cognitive impairment in aged Alzheimer's disease mice" [PubMed]

R. Jin et al., "J147 treatment protects against traumatic brain injury by inhibiting neuronal endoplasmic reticulum stress potentially via the AMPK/SREBP-1 pathway" [PubMed]

F. Qiu et al., "Current evidence for J147 as a potential therapeutic agent in nervous system disease: a narrative review" [PMC]

N. Tajiri et al., "NSI-189, a small molecule with neurogenic properties, exerts behavioral, and neurostructural benefits in stroke rats" [PubMed]

R.S. McIntyre et al., "The neurogenic compound, NSI-189 phosphate: a novel multi-domain treatment capable of pro-cognitive and antidepressant effects" [PubMed]

C.G. Jolivalt et al., "Amelioration of Both Central and Peripheral Neuropathy in Mouse Models of Type 1 and Type 2 Diabetes by the Neurogenic Molecule NSI-189" [PubMed]

DISCLAIMER

This product is intendend for lab research and development use only. These studies are performed outside of the body. This product is not medicines or drugs and has not been approved by the FDA or EMA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law. This product should only be handled by licensed, qualified professionals.

All product information provided on this website is for informational and educational purposes only.