Colivelin (Peptide) – Product Details

Colivelin (CLN) is a potent fusion peptide derived from neuroprotective compounds ADNF and AGA-(C8R)HNG17. It stands out for its exceptional neuroprotective effects, surpassing other derivatives of Humanin (HN) by exhibiting the most potent safeguarding abilities for neurons. 

This protein, designed with three consecutive leucine residues in its structure, showcases extraordinary potency in shielding brain cells, notably preventing cell death induced by Alzheimer’s disease-related genes and Aβ proteins, even at extremely low concentrations as low as 100 femtomolar (fM). 

Its outstanding effectiveness positions Colivelin as a highly valuable tool in the research and potential treatment of neurodegenerative diseases, making it a subject of great interest for scientific investigations.

• CAS Number: 867021-83-8
• Molar Mass: 2645.1 g/mol
• Chemical Structure: C119H206N32O35
• IUPAC Name: L-seryl-L-alanyl-L-leucyl-L-leucyl-L-arginyl-L-seryl-L-isoleucyl-L-prolyl-L-alanyl-L-prolyl-L-alanyl-glycyl-L-alanyl-L-seryl-L-arginyl-L-leucyl-L-leucyl-L-leucyl-L-leucyl-L-threonyl-glycyl-L-alpha-glutamyl-L-isoleucyl-L-alpha-aspartyl-L-leucyl-L-proline
• Synonym: CST (C-terminal Seryl-threonyl)-Ovalbumin_294-305 (CST-Ova)

What is Colivelin?

Colivelin, a fusion peptide crafted from the compounds ADNF and AGA-(C8R)HNG17, holds significant attention in the scientific realm due to its exceptional neuroprotective abilities. This peptide, derived from Humanin (HN), stands out for its effectiveness in shielding neurons from the damaging effects linked with conditions like Alzheimer’s disease (AD). [R]

Researchers originally identified HN as a peptide with promising capabilities in safeguarding neurons. Building upon this discovery, they engineered Colivelin, a novel neuroprotective protein that surpasses the efficacy of its precursor compounds, ADNF and AGA-(C8R)HNG17.

What sets Colivelin apart is its remarkable potency. Even at incredibly low concentrations—down to 100 femtomolar (fM)—it can prevent cell death induced by genes associated with AD and Aβ proteins. Its unparalleled effectiveness makes Colivelin an invaluable asset for scientific investigations into neurodegenerative diseases. [R]

Structurally, Colivelin’s distinction lies in the preservation of three consecutive leucine residues in its central region, a configuration that has been identified to maintain its potent neuroprotective activity. This characteristic has been a focal point of further structural characterization and optimization.

In essence, Colivelin’s outstanding neuroprotective properties position it as a promising candidate for potential treatments and as a vital tool for advancing research aimed at understanding and combating neurodegenerative diseases.

How Does Colivelin Work?

Colivelin’s mechanism of action in exerting its powerful neuroprotective effects has been investigated through various studies, shedding light on its functionality at a molecular level.

In one study, researchers delved into Colivelin’s impact on hippocampal long-term potentiation (LTP), an essential process for memory formation and synaptic plasticity. [R]

Their findings were significant: pretreatment with Colivelin effectively prevented cognitive function impairments observed in mice with the APP/PS1 mutation. More importantly, Colivelin demonstrated a remarkable ability to reverse the suppression of hippocampal LTP, which is crucial for maintaining cognitive abilities. [R]

Separate research demonstrated that Colivelin activates two distinct molecular pathways crucial for neuronal survival: STAT3 and CaMKIV pathways. [R]

By activating these pathways, Colivelin empowers neurons to withstand insults relevant to Alzheimer’s disease (AD) and helps them maintain their functionality. This multifaceted approach to protecting neurons sets Colivelin apart from other compounds and underscores its potential as a crucial asset for future research endeavors aimed at understanding and treating neurodegenerative conditions. [R]

Essentially, Colivelin’s prowess lies in its ability to prevent impairments in cognitive functions and its capacity to reverse existing damage by activating specific molecular pathways crucial for neuronal survival and function. This dual-action approach makes Colivelin a promising candidate for further exploration and potential therapeutic interventions in neurodegenerative diseases like Alzheimer’s.

Colivelin Potential Benefits

Colivelin and Brain Injury Research

Colivelin is a research compound that shows promise for protecting nerve cells from damage caused by reduced blood flow to the brain (ischemic brain injury), such as during a stroke.

Recent research tested Colivelin in a mouse model of ischemic stroke. The study found that when given Colivelin, the mice activated genes that prevent cell death and turned on a signaling pathway called JAK/STAT3. These responses are important for cell survival. [R]

In mice given Colivelin, fewer nerve cells died, there was less damage to cell structures called axons, and axons were better able to regrow and repair themselves after injury. This regeneration process is crucial for restoring brain function.

These positive results suggest Colivelin may someday be a treatment for ischemic stroke and other brain circulation conditions in humans. The ability to activate protective genes and signaling pathways makes Colivelin stand out as having the potential to reduce brain tissue damage and loss of function after injury involving blood flow reduction.

More research is still needed to fully understand exactly how Colivelin rescues dying nerve cells at the molecular level. However, the discoveries so far provide a promising early foundation for developing Colivelin as a therapy.

Colivelin and Alzheimer’s Disease Research

Alzheimer’s disease (AD) is a neurodegenerative condition that lacks effective treatments. A peptide called Colivelin (CLN) has shown promise in protecting nerve cells from death caused by amyloid beta (Aβ) protein buildup in the brain, which is a key feature of AD.

Previous research injecting CLN into the hippocampus (memory center) of rat brains showed it could prevent nerve cell loss, protect memory and learning functions, and alleviate spatial memory deficits caused by AD-like pathology. [R]

Based on these promising results, scientists tested long-term nasal administration of CLN in a mouse model of AD. They evaluated effects on memory, levels of pathological proteins, and brain cell communication/signaling.

As a neuroprotective peptide that can cross into the brain from blood, CLN has significant potential to reduce nerve cell death and cognitive decline associated with memory loss in AD. Understanding its protective mechanisms could inform the development of AD therapies.

However, it is important to note that Colivelin is currently intended only for research. It should not be self-administered by individuals with memory deficits or other neurological conditions, as safety and efficacy have not been established. More research is still needed before CLN can become an approved medical treatment.

Colivelin and ALS Treatment

Amyotrophic lateral sclerosis (ALS) is a progressive neurological disease that affects nerve cells responsible for controlling muscle movement. There are no cures yet.

A protein called activity-dependent neurotrophic factor (ADNF) showed some promise in improving symptoms in an ALS mouse model when injected into the brain but did not extend lifespan.

However, recent research found that injecting another compound called Colivelin into the brains of ALS mice prolonged their survival and improved their motor abilities compared to untreated ALS mice. [R]

More research is still needed to understand exactly how Colivelin provides these benefits and to evaluate its safety and effectiveness in human clinical trials.

However, these early results suggest Colivelin could represent a significant advance toward developing much-needed treatments that slow disease progression and improve the quality of life for people living with ALS.

The research is still in the early experimental stages. Colivelin should not be self-administered by patients, as appropriate dosing and effects in humans are still unknown. However, it marks encouraging initial progress in the search for more effective ALS therapies.

Colivelin and Spinal Cord Injury Research

Spinal cord injury (SCI) is a complex condition lacking effective treatments. A compound called colivelin can strongly activate a cell signaling pathway called STAT3, which drew interest in using it to promote recovery after SCI.

Recent research explored combining colivelin with another compound called wogonin, which has shown protective effects in nervous system injuries. The study looked at impacts in a rat model of SCI. [R]

Rats were divided into a control group, SCI-only group, SCI + wogonin group, and SCI + wogonin + colivelin group.

Unexpectedly, the addition of colivelin appeared to reverse the benefits that wogonin displayed when used alone after SCI. Activation of the STAT3 pathway by colivelin seems to interfere with wogonin’s helpful effects.

This indicates colivelin may not provide additional gains when paired with certain promising neuroprotective compounds for SCI, despite initial thoughts it could enhance recovery via STAT3 signaling.

More research is still needed, but these findings shed light on complex interactions between cell signaling pathways in the injured spinal cord that influence treatment outcomes.

Colivelin and Endothelial Dysfunction Research

Sepsis is a dangerous whole-body infection that can lead to the failure of multiple organs. In sepsis, the lining of blood vessels called the endothelium can become damaged, contributing to worse outcomes.

Specifically, sepsis disrupts the protective glycocalyx layer that shields endothelial cells. A compound called colivelin has shown an ability to guard cells against oxidative damage.

Emerging research found that injury to the glycocalyx occurs early in sepsis and is an important part of endothelial dysfunction. The study also provided additional evidence that colivelin may have therapeutic potential to treat the endothelial problems arising from sepsis. [R]

These findings add to growing support for investigating colivelin as a possible treatment for the blood vessel damage of sepsis. More research is still needed on exactly how colivelin protects endothelial cells and the best dosing strategies.

However, protecting the glycocalyx could help maintain the integrity of blood vessels in this dangerous infection. Exploring colivelin as an endothelial protectant in sepsis models appears promising.

Frequently Asked Questions

Is Colivelin legal?

Colivelin is an experimental compound still under investigation in preclinical studies – it has not undergone formal safety and efficacy testing for use in humans through clinical trials.

The research on Colivelin so far has been limited to laboratory experiments, animal models, and in vitro studies. Testing in human subjects has not been reported.

Without sufficient clinical testing and approval by regulatory bodies like the FDA, no drug can be legally marketed or prescribed to patients, including Colivelin.

Since it is still considered investigational, Colivelin would only be available for carefully controlled and monitored research studies, not routine clinical use.

Is Colivelin safe?

Colivelin is currently considered an experimental research compound with unproven safety and efficacy in humans. Its effects and appropriate usage in people are still under investigation in restricted research studies only.

Conclusion

In conclusion, Colivelin stands out as a promising compound with remarkable potential for protecting brain cells from damage, particularly in conditions like Alzheimer’s disease and ischemic stroke. Its exceptional ability to shield neurons, promote survival pathways and stimulate regrowth marks it as a valuable asset in the pursuit of treatments for neurodegenerative diseases and brain injuries. 

While more research is needed to fully grasp its mechanisms and optimize its therapeutic use, Colivelin represents a beacon of hope in the quest for effective interventions against brain-related disorders, offering prospects for improved outcomes and better quality of life for affected individuals in the future.

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Strength	100mg