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The products offered on this website (except supplements) are furnished for in-vitro studies only. In-vitro studies are performed outside of the body. These products are not medicines or drugs and have 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.
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COLIVELIN SPRAY - 10ml/100mg
COSP10100
New product
Colivelin is a neuroprotective humanin family peptide with potent long-term capacity against Aβ deposition, neuronal apoptosis, and synaptic plasticity deficits in neurodegenerative disease.
Nasal Colivelin treatment ameliorates memory impairment related to Alzheimer's Disease.
FRESHLY PREPARED SOLUTION
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Colivelin is a brain penetrant neuroprotective peptide and a potent activator of STAT3, suppresses neuronal death by activating STAT3 in vitro.
Colivelin exhibits long-term beneficial effects against neurotoxicity, Aβ deposition, neuronal apoptosis, and synaptic plasticity deficits in neurodegenerative disease. Colivelin has the potential for the treatment of alzheimer's disease and ischemic brain injury.
This hybrid peptide was synthesized to potentiate the neuroprotective effect of humanin (HN). Colivelin is composed of Activity-Dependent Neurotrophic Factor (ADNF) C-terminally fused to AGA-(C8R) HNG17, a potent HN derivative.
Colivelin completely suppresses cell death induced by overexpressed Familial Alzheimer's disease (FAD)-causative genes and beta-amyloid. Colivelin administration decreased the neurological deficits and infarct lesion induced by brain ischemia.
Colivelin inhibited axonal damage and neuronal death in brain tissue, which was associated with elevated anti-apoptotic gene expression in ischemic neurons as well as increased axonal growth up until two-weeks post-stroke.
Moreover, Colivelin activated STAT3 signaling, which may partially contribute to its beneficial effect against neuronal death and axon growth. In conclusion, Colivelin induce anti-apoptotic genes up-regulation, and activate JAK/STAT3 signaling after ischemic stroke, which may contribute to its effects of rescuing ischemic neuronal death and axonal remodeling.
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REFERENCES:
https://www.nature.com/articles/1301591
https://pubmed.ncbi.nlm.nih.gov/17928813
https://pubmed.ncbi.nlm.nih.gov/16958985
https://www.jneurosci.org/content/25/44/10252
https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1016/j.jalz.2008.05.1405