Description

Colivelin – Product Information

Colivelin is a synthetic peptide derived from the protein humanin, which is naturally produced in the body. It was first identified in a study exploring the neuroprotective properties of humanin in the brain.

• Colivelin is offered in 100mg lyophilized powder.

Lyophilized peptide powders above 50mg may require more than the regular amount of bacteriostatic water for complete dissolution. Insufficient bacteriostatic water volume may lead to some powder remaining undissolved.

Colivelin
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

What is Colivelin?

The fusion peptide named Colivelin (CLN) was derived from the neuroprotective compounds Adeno-associated nuclear factor (ADNF) and AGA-(C8R)HNG17. Notably, CLN has exhibited the most potent neuroprotective effect among the discovered derivatives of Humanin (HN). Maintaining three consecutive leucine residues in the central region, as opposed to four, preserves the activity of CLN, according to further structural characterization [R].

Colivelin stands out due to its extraordinary neuroprotective properties, making it a subject of great interest for scientific investigation. Initially, HN was identified as a peptide with exceptional capabilities in safeguarding neurons against the toxic effects associated with conditions like Alzheimer’s disease (AD). Building upon this knowledge, researchers developed Colivelin, a novel neuroprotective protein that surpasses the effectiveness of ADNF and AGA-(C8R)HNG17.[R]

The efficacy of Colivelin is truly remarkable, as it has been shown to prevent cell death induced by AD-related genes and Aβ proteins even at remarkably low concentrations. In fact, concentrations as low as 100 femtomolar (fM) have demonstrated the ability to confer significant neuroprotection. Such exceptional potency positions Colivelin as a valuable tool for research purposes in the investigation and potential treatment of neurodegenerative diseases [R]

How Does Colivelin Work?

The mode of action of CLN’s neuroprotective effects was explored in a study by examining hippocampal long-term potentiation (LTP) using in vivo recordings. The findings revealed that pretreatment with CLN successfully prevented impairments in multiple cognitive functions observed in the APP/PS1 mice. Notably, CLN demonstrated the ability to reverse the suppression of hippocampal LTP, which is crucial for memory formation and synaptic plasticity. [R]

Colivelin’s capacity to activate both STAT3- and CaMKIV-mediated prosurvival pathways was demonstrated in a separate study. Colivelin enables neurons to resist AD-relevant insults and preserve their functionality by activating these molecular pathways. This diverse approach to neuroprotection distinguishes Colivelin from other compounds and highlights its potential as a key asset for future research efforts.[R]

Colivelin Research

Numerous animal and human studies have been conducted on the potential application of Colivelin. Below follows some of the relevant findings:

Colivelin on Spinal Cord Injury

Colivelin, a powerful activator of the STAT3 signal pathway, has garnered significant attention in the field of spinal cord injury (SCI) research. SCI is a complex traumatic condition that affects the central nervous system, necessitating effective therapeutic interventions for promoting recovery. In recent studies, the potential therapeutic benefits of colivelin in SCI have been explored in combination with other compounds. The study investigates the effects of colivelin in conjunction with wogonin, a natural compound known for its neuroprotective properties, on SCI and the underlying molecular mechanisms. Rats were divided into different groups, including a control group (Sham), a group with SCI, a group receiving wogonin treatment after SCI, and a group receiving both wogonin and colivelin after SCI.

The experimental results revealed that colivelin, as an activator of the STAT3 pathway, played a significant role in reversing the therapeutic effects of wogonin. These findings indicated that the activation of the STAT3 signal pathway by colivelin interfered with the beneficial effects of wogonin on SCI.[R]

While colivelin’s activation of the STAT3 signal pathway has shown potential therapeutic effects in other contexts, its administration in combination with wogonin hindered the functional recovery observed with wogonin alone. Further investigation is required to fully understand the intricate molecular mechanisms and interactions involved in SCI treatment.

Colivelin on Fetus Alcohol Exposure

The human brain is a complex organ that undergoes remarkable development during fetal stages. However, exposure to alcohol during pregnancy can have severe consequences, leading to detrimental effects on the developing brain.

The discovery of Colivelin (CLN) and its ability to counteract alcohol-induced neuronal apoptosis presents a promising avenue for future research. By inhibiting caspase-3 activation and maintaining normal levels of cytochrome c, CLN showcases its potential as a neuroprotective agent. However, it is crucial to emphasize that CLN should be regarded solely as a research chemical, with its applications restricted to laboratory investigations aimed at unraveling the mysteries surrounding fetal alcohol syndrome. [R] Continued research in this area holds the key to developing innovative strategies to combat the detrimental effects of alcohol exposure during pregnancy and safeguard the developing brain.

Colivelin Peptide for ALS Treatment

Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disease, and effective therapies are still lacking. In recent research, it was discovered that the intracerebroventricular injection of activity-dependent neurotrophic factor (ADNF) improved motor performance in ALS mice but did not significantly extend survival. However, the latest research shows that when injected i.c.v., Colivelin prolongs survival and enhances motor performance in ALS mice. [R]

Further research is needed to understand the mechanisms of Colivelin and assess its safety and efficacy in human trials. Nevertheless, Colivelin represents a significant potential advancement in the search for effective therapies for individuals living with ALS.

Colivelin on Brain Injury

Colivelin, a promising compound, has shown the ability to shield nerve cells from damage caused by ischemic brain injury, prompting scientists to investigate its mechanisms of action. In a recent study, researchers examined the effects of administering Colivelin in a mouse model of transient focal cerebral ischemia and reperfusion-a condition that mimics an ischemic stroke. The study revealed that Colivelin activated anti-apoptotic genes and triggered the JAK/STAT3 signaling pathway in response to an ischemic stroke. Consequently, Colivelin exhibited the ability to prevent neuronal death, halt axonal damage, and promote axonal growth. These findings highlight the potential of Colivelin as a potential treatment for ischemic stroke.[R]

However, further research is necessary to fully understand how colivelin rescues ischemic neurons.

Colivelin Potential Neuroprotective Peptide for Alzheimer’s Disease

Alzheimer’s disease (AD), is a neurodegenerative disease condition that lacks effective treatment options or no treatment at all. However, Colivelin (CLN) has shown promising results in preventing cell death induced by genes associated with aβ deposition neuronal in the brain, a hallmark of AD. Previous studies using a hippocampal injection of CLN have demonstrated its ability to counteract neuronal loss and protect against Aβ-induced memory and synaptic plasticity deficits, as well as alleviate impairments in spatial working memory in hippocampus-induced rats. Based on these findings, researchers investigated the effects of long-term nasal administration of CLN in AD mice, specifically evaluating cognitive behaviors, pathological markers, and the underlying electrophysiological mechanisms.[R]

CLN, as a neuroprotective peptide capable of crossing the blood-brain barrier, holds significant potential as it antagonizes neuronal loss and improves cognitive function, particularly in relation to memory impairment associated with AD. The ongoing research and exploration of CLN’s mechanisms of action may contribute to the development of potential therapeutic strategies for individuals affected by AD and other neurodegenerative diseases.

However, it is crucial to emphasize that Colivelin is strictly intended for research use only and should not be consumed by individuals with neurological deficits and plasticity deficits in neurodegenerative
disease.

Colivelin on Endothelial Dysfunction Associated with Sepsis

During sepsis, a life-threatening systemic infection, endothelial dysfunction is essential for the development of multiple organ failure. During an infection, the glycocalyx layer that protects blood vessels is especially susceptible to injury. Colivelin has demonstrated potent cytoprotective properties under oxidative conditions. Research highlights the early involvement of glycocalyx injury in sepsis and provides additional evidence supporting the potential therapeutic value of colivelin in the management of sepsis-related endothelial dysfunction. [R]

These results contribute to the growing collection of proof supporting the investigation of colivelin as a potential treatment for endothelial dysfunction caused by sepsis. The mechanisms underlying its action and the optimal administration strategies for colivelin in the context of sepsis require further investigation.

Precautions

The information presented here is for educational purposes only and should not be construed as medical advice. Colivelin is intended for laboratory research use only and is not intended for human consumption.

Summary of Colivelin

Colivelin (CLN) is a brain-penetrant neuroprotective peptide derived from neuroprotective compounds ADNF and AGA-(C8R)HNG17. It surpasses other derivatives of Humanin (HN) in terms of neuroprotective efficacy. CLN as a potent activator has shown possibilities in preventing cell death induced by Alzheimer’s disease (AD)-related genes and Aβ proteins, even at low concentrations. The mode of action of CLN involves reversing impairments in cognitive functions, including spatial working memory induced by AD.

It holds great potential for research and the potential treatment of neurodegenerative diseases. CLN’s mode of action includes reversing impairments in cognitive functions and activating prosurvival pathways, such as STAT3 and CaMKIV. Studies have explored its applications in spinal cord injury, fetal alcohol exposure, ALS, brain injury, and endothelial dysfunction associated with sepsis. However, further research is required to understand its mechanisms fully and evaluate its safety and neurological outcomes in human trials. It is essential to note that CLN is strictly for research purposes and not for human consumption. The FDA has not approved any treatments for AD-specific behavioral and psychotic symptoms, and more research is needed to determine CLN’s benefits.

FAQ

What is the molecular weight?

The molecular weight of Colivelin is 2645.1 g/mol.

Is Alzheimer’s curable?

While some studies have shown neuroprotective effects, there is currently no cure for Alzheimer’s disease. Available treatments aim to slow down the progression of the disease rather than provide a complete cure.

Is Colivelin safe?

As of now, there isn’t much information about the safety of using CLN to treat the behavioral and psychotic symptoms of AD. Because CLN works in a unique way and has a unique structure, more research is needed to figure out what benefits and risks it might have in this situation. Clinical trials are needed to find out what the best dose of CLN is for treating AD symptoms, how safe it is over the long term, and what side effects it might have.

It is important to know that the FDA has not approved any treatments for AD-specific behavioral and psychotic symptoms. [R]

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Disclaimer

This information is for educational purposes only and does not constitute medical advice. THE PRODUCTS DESCRIBED HEREIN ARE FOR LABORATORY AND RESEARCH USE ONLY. All clinical research must be conducted with oversight from the appropriate Institutional Review Board (IRB). All preclinical research must be conducted with oversight from the appropriate Institutional Animal Care and Use Committee (IACUC) following the guidelines of the Animal Welfare Act (AWA).

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